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O papel da FAK (Focal Adhesion Kinase) na biogênese mitocondrial cardíaca induzida por estresse mecânico; A role for Focal Adhesion Kinase in cardiac mitochondrial biogenesis induced by mechanical stress

Thaís Franchini Tornatore
Fonte: Biblioteca Digital da Unicamp Publicador: Biblioteca Digital da Unicamp
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 12/01/2011 PT
Relevância na Pesquisa
66.08%
Estudamos o gene da FAK (focal adhesion kinase) na mitocondriogênese cardíaca induzida por estresse mecânico. O estresse prolongado (2-12 hs) de miócitos do ventrículo esquerdo de ratos neonatos(NRVM) aumentou a expressão do regulador transcricional mitocondrial PGC-1? (peroxisome proliferator activated receptor coactivator-1), NRF-1 (nuclear respiratory factor) e o Tfam (mitochondrial transcription factor A). A ativação da cascata transcricional mitocondrial em cardiomiócitos estirados foi acompanhada pelo aumento da mitocondriogênese (aumento da densidade mitocondrial e número de cópias do DNA - mtDNA) e hipertrofia(tamanho da célula e transcrição do ANP). Estresse mecânico também aumentou a fosforilação da FAK, a localização nuclear e associação com PGC1-?. FAK C-terminal Recombinante, mas não a N-terminal ou domínio kinase, precipitaram PGC-1? em extratos nucleares de NRVMs. Além disso, a inibição da expressão da FAK por RNA de interferência suprimiu a hiper regulação do PGC-1? e NRF-1, e atenuou o aumento da mitocondriogênese e hipertrofia em cardiomiócitos. Ao mesmo tempo, a inibição da FAK reduziu os níveis de ATP em cardiomiócitos estirados. Estudos complementares em ventrículos esquerdo de camundongos adultos revelaram aumento da expressão de PGC-1?...

Effect of mechanical stress on biofilms challenged by different chemicals

Simões, M.; Pereira, Maria Olívia; Vieira, M. J.
Fonte: Elsevier Publicador: Elsevier
Tipo: Artigo de Revista Científica
Publicado em /12/2005 ENG
Relevância na Pesquisa
56.09%
In this study a methodology was applied in order to ascertain the mechanical stability of biofilms, by using a stainlesssteel (SS) rotating device immersed in a biological reactor where biofilms formed by Pseudomonas fluorescens were allowed to grow for 7 days at a Reynolds number of agitation of 2400. The biofilms developed with this system were characterised in terms of amount of total, extracellular and intracellular proteins and polysaccharides, amount of mass, metabolic activity and mechanical stability, showing that the biofilms were active, had a high content of extracellular constituents and an inherent mechanical stability. In order to assess the role of chemical agents on the mechanical stability, the biofilms were exposed to chemical agents followed by mechanical treatments by submission to increase Reynolds number of agitation. Seven different chemical agents were tested (two non-oxidising biocides, three surfactants and two oxidising biocides) and their effects on the biofilm mechanical stability were evaluated. The increase in the Reynolds number increased the biofilm removal, but total biofilm removal was not found for all the conditions tested. For the experiment without chemical addition (only mechanical treatment)...

Polymeric piezoelectric actuator substrate for osteoblast mechanical stimulation.

Frias, C; Reis, J; Capela e Silva, F; Potes, J; Simões, J; Marques, AT
Fonte: Polymeric piezoelectric actuator substrate for osteoblast mechanical stimulation. Publicador: Polymeric piezoelectric actuator substrate for osteoblast mechanical stimulation.
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
55.93%
Bone mass distribution and structure are dependent on mechanical stress and adaptive response at cellular and tissue levels. Mechanical stimulation of bone induces new bone formation in vivo and increases the metabolic activity and gene expression of osteoblasts in culture. A wide variety of devices have been tested for mechanical stimulation of cells and tissues in vitro. The aim of this work was to experimentally validate the possibility to use piezoelectric materials as a mean of mechanical stimulation of bone cells, by converse piezoelectric effect. To estimate the magnitude and the distribution of strain, finite numerical models were applied and the results were complemented with the optical tests (Electronic Speckle Pattern Interferometric Process). In this work, osteoblasts were grown on the surface of a piezoelectric material, both in static and dynamic conditions at low frequencies, and total protein, cell viability and nitric oxide measurement comparisons are presented.

Periodic mechanical stress activates MEK1/2-ERK1/2 mitogenic signals in rat chondrocytes through Src and PLCγ1

Ren,Kewei; Ma,Yimin; Huang,Yumin; Liang,Wenwei; Liu,Feng; Wang,Qing; Cui,Weiding; Liu,Zhengyu; Yin,Guoyong; Fan,Weimin
Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/12/2011 EN
Relevância na Pesquisa
66.26%
The mitogenic effects of periodic mechanical stress on chondrocytes have been studied extensively but the mechanisms whereby chondrocytes sense and respond to periodic mechanical stress remain a matter of debate. We explored the signal transduction pathways of chondrocyte proliferation and matrix synthesis under periodic mechanical stress. In particular, we sought to identify the role of the MEK1/2-ERK1/2 signaling pathway in chondrocyte proliferation and matrix synthesis following cyclic physiologic mechanical compression. Under periodic mechanical stress, both rat chondrocyte proliferation and matrix synthesis were significantly increased (P < 0.05) and were associated with increases in the phosphorylation of Src, PLCγ1, MEK1/2, and ERK1/2 (P < 0.05). Pretreatment with the MEK1/2-ERK1/2 selective inhibitor, PD98059, and shRNA targeted to ERK1/2 reduced periodic mechanical stress-induced chondrocyte proliferation and matrix synthesis (P < 0.05), while the phosphorylation levels of Src-Tyr418 and PLCγ1-Tyr783 were not inhibited. Proliferation, matrix synthesis and phosphorylation of MEK1/2-Ser217/221 and ERK1/2-Thr202/Tyr204 were inhibited after pretreatment with the PLCγ1 inhibitor U73122 in chondrocytes in response to periodic mechanical stress (P < 0.05)...

Spatial Patterning of Cell Proliferation and Differentiation Depends on Mechanical Stress Magnitude

Li, Bin; Li, Fang; Puskar, Kathleen M.; Wang, James H-C.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
46.23%
Mechanical stress has been proposed as a major regulator of tissue morphogenesis; however, it remains unclear what is the exact mechanical signal that leads to local tissue pattern formation. We explored this question by using a micropatterned cell aggregate model in which NIH 3T3 fibroblasts were cultured on micropatterned adhesive islands and formed cell aggregates (or “cell islands”) of triangular, square, and circular shapes. We found that the cell islands generated high levels of mechanical stresses at their perimeters compared to their inner regions. Regardless of the shape of cell islands, the mechanical stress patterns corresponded to both cell proliferation and differentiation patterns, meaning that high level of cell proliferation and differentiation occurred at the locations where mechanical stresses were also high. When mechanical stretching was applied to cell islands to elevate overall mechanical stress magnitudes, cell proliferation and differentiation generally increased with the relatively higher mechanical stresses, but neither cell proliferation nor differentiation patterns followed the new mechanical stress pattern. Thus, our findings indicate that a certain range of mechanical stress magnitudes, termed window stress threshold...

The Chitinase-like Protein YKL-40 Is Secreted by Airway Epithelial Cells at Base Line and in Response to Compressive Mechanical Stress*

Park, Jin-Ah; Drazen, Jeffrey M.; Tschumperlin, Daniel J.
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
46.18%
The chitinase-like protein YKL-40, encoded by the CHI3L1 gene, is a biomarker and functional effector of chronic inflammatory and allergic diseases. In the lung it is associated with asthma severity and reduced lung function. The cellular sources of YKL-40 in human airways and the mechanisms regulating YKL-40 expression are poorly understood. We previously showed that mechanical stress similar to that experienced during bronchoconstriction triggers epithelial cell signaling through epidermal growth factor receptor (EGFR), fibrotic mediator release, and goblet cell hyperplasia consistent with airway remodeling in asthma. We now show that well differentiated normal human bronchial epithelial cells express CHI3L1 and secrete YKL-40 under base-line culture conditions. Mechanical stress (30-cm H2O transcellular compressive stress) applied for 3 h induces CHI3L1 expression by ∼4-fold compared with time matched controls, resulting in increased secretion of YKL-40 by 3.6-fold 24 h after onset of the 3-h stimulus. Inhibition of EGFR or MEK1/2 (ERK kinase) significantly but incompletely attenuates mechanical stress-induced up-regulation of CHI3L1 expression in normal human bronchial epithelial cells. Direct activation of EGFR utilizing EGF-family ligands induces CHI3L1 expression. Our results reveal that human airway epithelial cells are a source of YKL-40 and demonstrate that mechanical stress potently induces CHI3L1 expression leading to increased secretion of YKL-40 protein in an EGFR and MEK1/2-dependent pathway. In the asthmatic airway mechanical stress may contribute to enhanced YKL-40 levels.

Cells Respond to Mechanical Stress by Rapid Disassembly of Caveolae

Sinha, Bidisha; Köster, Darius; Ruez, Richard; Gonnord, Pauline; Bastiani, Michele; Abankwa, Daniel; Stan, Radu. V.; Butler-Browne, Gillian; Vedie, Benoit; Johannes, Ludger; Morone, Nobuhiro; Parton, Robert G.; Raposo, Graça; Sens, Pierre; Lamaze, Chris
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 04/02/2011 EN
Relevância na Pesquisa
46.18%
The precise role of caveolae, the characteristic plasma membrane invaginations present in many cells, still remains debated. The high density of caveolae in cells experiencing mechanical stress led us to investigate their role in membrane-mediated mechanical response. Acute mechanical stress induced by cell osmotic swelling or by uniaxial stretching results in the immediate disappearance of caveolae, which is associated with a reduced caveolin/Cavin1 interaction, and an increase of free caveolins at the plasma membrane. Tether pulling force measurements in live cells and in plasma membrane spheres demonstrate that caveola flattening and disassembly is the primary actin and ATP-independent cell response which buffers membrane tension surges during mechanical stress. Conversely, stress release leads to complete caveola reassembly in an actin and ATP-dependent process. The absence of a functional caveola reservoir in myotubes from muscular dystrophic patients enhanced membrane fragility under mechanical stress. Our findings support a new role for caveolae as a physiological membrane reservoir that allows cells to quickly accommodate sudden and acute mechanical stresses.

Static Mechanical Stress Induces Apoptosis in Rat Endplate Chondrocytes through MAPK and Mitochondria-Dependent Caspase Activation Signaling Pathways

Kong, Dechao; Zheng, Tiansheng; Zhang, Ming; Wang, Daode; Du, Shihao; Li, Xiang; Fang, Jiahu; Cao, Xiaojian
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 19/07/2013 EN
Relevância na Pesquisa
46.19%
Mechanical stress has detrimental effects on cartilaginous endplate chondrocytes due to apoptosis in vivo and in vitro. In this study, we investigated the possible apoptosis signaling pathways induced by mechanical stress in cultured rat cervical endplate chondrocytes. Static mechanical load significantly reduced cell viability in a time- and load-dependent manner, as demonstrated by the Cell Counting Kit-8 (CCK-8) assay. Chondrocyte apoptosis induced by mechanical stress was confirmed by annexin V/propidium iodide (PI) staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Western blot analysis revealed that static load-induced chondrocyte apoptosis was accompanied by increased phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 mitogen-activated protein kinase (MAPK). The loss of mitochondrial membrane potential (ΔΨm), increased Cytochrome c release, and activated Caspase-9 and Caspase-3, indicating that the mitochondrial pathway is involved in mechanical stress-induced chondrocyte apoptosis. Treatment with inhibitors of JNK (SP600125), p38 MAPK (SB203580), and ERK (PD98059) prior to mechanical stimulation reversed both the static load-induced chondrocyte apoptosis and the activation of JNK...

Angiopoietin-Like Protein 2 Induced by Mechanical Stress Accelerates Degeneration and Hypertrophy of the Ligamentum Flavum in Lumbar Spinal Canal Stenosis

Nakamura, Takayuki; Okada, Tatsuya; Endo, Motoyoshi; Kadomatsu, Tsuyoshi; Taniwaki, Takuya; Sei, Akira; Odagiri, Haruki; Masuda, Tetsuro; Fujimoto, Toru; Nakamura, Takafumi; Oike, Yuichi; Mizuta, Hiroshi
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 17/01/2014 EN
Relevância na Pesquisa
46.19%
Chronic inflammation and subsequent fibrosis induced by mechanical stress play an important role in ligamentum flavum (LF) hypertrophy and degeneration in patients with lumbar spinal canal stenosis (LSCS). Angiopoietin-like protein 2 (Angptl2) is a chronic inflammatory mediator induced under various pathological conditions and increases the expression of TGF-β1, which is a well-characterized mediator in LF hypertrophy. We investigated whether Angptl2 is induced by mechanical stress, and whether it contributes to LF hypertrophy and degeneration by activating the TGF-β1 signaling cascade. In this study, we investigated human LF tissue and LF fibroblasts isolated from patients who underwent lumbar surgery. We found that Angptl2 was abundantly expressed in fibroblasts of hypertrophied LF tissues at both the mRNA and protein levels. This expression was not only positively correlated with LF thickness and degeneration but also positively correlated with lumbar segmental motion. Our in vitro experiments with fibroblasts from hypertrophied LF tissue revealed that mechanical stretching stress increases the expression and secretion of Angptl2 via activation of calcineurin/NFAT pathways. In hypertrophied LF tissue, expression of TGF-β1 mRNA was also increased and TGF-β1/Smad signaling was activated. Angptl2 expression in LF tissue was positively correlated with the expression of TGF-β1 mRNA...

Mechanical Stress Promotes Cisplatin-Induced Hepatocellular Carcinoma Cell Death

Ziko, Laila; Riad, Sandra; Amer, Momen; Zdero, Radovan; Bougherara, Habiba; Amleh, Asma
Fonte: Hindawi Publishing Corporation Publicador: Hindawi Publishing Corporation
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
46.21%
Cisplatin (CisPt) is a commonly used platinum-based chemotherapeutic agent. Its efficacy is limited due to drug resistance and multiple side effects, thereby warranting a new approach to improving the pharmacological effect of CisPt. A newly developed mathematical hypothesis suggested that mechanical loading, when coupled with a chemotherapeutic drug such as CisPt and immune cells, would boost tumor cell death. The current study investigated the aforementioned mathematical hypothesis by exposing human hepatocellular liver carcinoma (HepG2) cells to CisPt, peripheral blood mononuclear cells, and mechanical stress individually and in combination. HepG2 cells were also treated with a mixture of CisPt and carnosine with and without mechanical stress to examine one possible mechanism employed by mechanical stress to enhance CisPt effects. Carnosine is a dipeptide that reportedly sequesters platinum-based drugs away from their pharmacological target-site. Mechanical stress was achieved using an orbital shaker that produced 300 rpm with a horizontal circular motion. Our results demonstrated that mechanical stress promoted CisPt-induced death of HepG2 cells (~35% more cell death). Moreover, results showed that CisPt-induced death was compromised when CisPt was left to mix with carnosine 24 hours preceding treatment. Mechanical stress...

Excessive Mechanical Stress Increases HMGB1 Expression in Human Lung Microvascular Endothelial Cells Via STAT3

Wolfson, Rachel K.; Mapes, Brandon; Garcia, Joe G.N.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
46.18%
Ventilator-induced lung injury (VILI) occurs when the lung parenchyma and vasculature are exposed to repetitive and excessive mechanical stress via mechanical ventilation utilized as supportive care for the adult respiratory distress syndrome (ARDS). VILI induces gene expression and systemic release of inflammatory mediators that contribute to the multi-organ dysfunction and morbidity and mortality of ARDS. HMGB1, an intracellular transcription factor with cytokine properties, is a late mediator in sepsis and ARDS pathobiology, however, the role of HMGB1 in VILI remains poorly described. We now report HMGB1 expression in human lung microvessel endothelial cells (EC) exposed to excessive, equibiaxial mechanical stress, an in vitro correlate of VILI. We determined that high amplitude cyclic stretch (18% CS) increased HMGB1 expression (2-4 fold) via a signaling pathway with critical involvement of the transcription factor, STAT3. Concomitant exposure to 18% CS and oxidative stress (H2O2) augmented HMGB1 expression (~13 fold increase) whereas lipopolysaccharide (LPS) challenge increased HMGB1 expression in static EC, but not in 18% CS-challenged EC. In contrast, physiologic, low amplitude cyclic stretch (5% CS) attenuated both oxidative H2O2- and LPS-induced increases in HMGB1 expression...

Plasma Membrane Mechanical Stress Activates TRPC5 Channels

Shen, Bing; Wong, Ching-On; Lau, On-Chai; Woo, Theodosia; Bai, Suwen; Huang, Yu; Yao, Xiaoqiang
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 07/04/2015 EN
Relevância na Pesquisa
46.21%
Mechanical forces exerted on cells impose stress on the plasma membrane. Cells sense this stress and elicit a mechanoelectric transduction cascade that initiates compensatory mechanisms. Mechanosensitive ion channels in the plasma membrane are responsible for transducing the mechanical signals to electrical signals. However, the mechanisms underlying channel activation in response to mechanical stress remain incompletely understood. Transient Receptor Potential (TRP) channels serve essential functions in several sensory modalities. These channels can also participate in mechanotransduction by either being autonomously sensitive to mechanical perturbation or by coupling to other mechanosensory components of the cell. Here, we investigated the response of a TRP family member, TRPC5, to mechanical stress. Hypoosmolarity triggers Ca2+ influx and cationic conductance through TRPC5. Importantly, for the first time we were able to record the stretch-activated TRPC5 current at single-channel level. The activation threshold for TRPC5 was found to be 240 mOsm for hypoosmotic stress and between −20 and −40 mmHg for pressure applied to membrane patch. In addition, we found that disruption of actin filaments suppresses TRPC5 response to hypoosmotic stress and patch pipette pressure...

Translocation of TRPV2 channel induced by focal administration of mechanical stress

Nagasawa, Masahiro; Kojima, Itaru
Fonte: BlackWell Publishing Ltd Publicador: BlackWell Publishing Ltd
Tipo: Artigo de Revista Científica
Publicado em 13/02/2015 EN
Relevância na Pesquisa
46.22%
The effect of focal mechanical stress on the localization of TRPV2 was investigated in HT1080 cells, where only mRNA for TRPV2 was detected among members of the TRPV channel family. Mechanical stress was applied by adding negative pressure using a glass pipette. When focal mechanical stress was applied, subplasma membrane Ca2+ concentration ([Ca2+]s) was increased beneath the pipette, which propagated throughout the cell. The increase in [Ca2+]s was blocked by ruthenium red or by knocking down TRPV2. Elevation of [Ca2+]s was not observed by removal of extracellular Ca2+, by an addition of a phosphatidylinositol 3-kinase inhibitor LY29034, and by transfection of dominant-negative Rac. In cells expressing GFP-TRPV2 and RFP-Akt, administration of focal mechanical stress induced accumulation of GFP-TRPV2 beneath the pipette. RFP-Akt was also accumulated to the same site. Gadolinium blocked the elevation of [Ca2+]s induced by focal mechanical stress and also attenuated accumulation of TRPV2. When GFP-TRPV1, GFP-TRPV3, GFP-TRPV4, GFP-TRPV5, or GFP-TRPV6 was transfected ectopically in HT1080 cells, only GFP-TRPV4 was accumulated beneath the pipette in response to the focal mechanical stress. These results indicate that TRPV2 translocates to the site receiving a focal mechanical stress and increases [Ca2+]s.

Micro-Environmental Mechanical Stress Controls Tumor Spheroid Size and Morphology by Suppressing Proliferation and Inducing Apoptosis in Cancer Cells

Cheng, Gang; Tse, Janet; Jain, Rakesh K.; Munn, Lance Leon
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
EN_US
Relevância na Pesquisa
56.2%
Background: Compressive mechanical stress produced during growth in a confining matrix limits the size of tumor spheroids, but little is known about the dynamics of stress accumulation, how the stress affects cancer cell phenotype, or the molecular pathways involved. Methodology/Principal Findings: We co-embedded single cancer cells with fluorescent micro-beads in agarose gels and, using confocal microscopy, recorded the 3D distribution of micro-beads surrounding growing spheroids. The change in micro-bead density was then converted to strain in the gel, from which we estimated the spatial distribution of compressive stress around the spheroids. We found a strong correlation between the peri-spheroid solid stress distribution and spheroid shape, a result of the suppression of cell proliferation and induction of apoptotic cell death in regions of high mechanical stress. By compressing spheroids consisting of cancer cells overexpressing anti-apoptotic genes, we demonstrate that mechanical stress-induced apoptosis occurs via the mitochondrial pathway. Conclusions/Significance: Our results provide detailed, quantitative insight into the role of micro-environmental mechanical stress in tumor spheroid growth dynamics, and suggest how tumors grow in confined locations where the level of solid stress becomes high. An important implication is that apoptosis via the mitochondrial pathway...

Stimulation of angiogenesis through collagen gel by applying shear stress and interstitial flow

Ranka, Mitun P
Fonte: Massachusetts Institute of Technology Publicador: Massachusetts Institute of Technology
Tipo: Tese de Doutorado Formato: 38 leaves; 1906657 bytes; 1906202 bytes; application/pdf; application/pdf
ENG
Relevância na Pesquisa
56.15%
The induction of angiogenesis has been documented in many diseases such as cancer, arthritis, and diabetes. Angiogenesis can be stimulated by a variety of signals including a mechanical stress applied to the apical side of endothelial cells. To get a better understanding of this mechanical stimulus, a parallel plate flow chamber was designed and tested to elicit a constant laminar flow onto a monolayer of endothelial cells. The goal of this research was to develop a more physiologically similar in vitro system to study the effects of shear stress on endothelial cells. Unlike prior flow chamber apparatus, this chamber allows the cells to be seeded on collagen gel rather than a rigid substrate to more closely mimic in vivo environment. A shear stress of I Pa was applied to the endothelial cells for a duration of 36 hours. Results show that after flow was initiated for this duration, a change in shape of the endothelial cells can be seen when compared to the static condition. Elongation and alignment of cells plated on collagen gel can be seen in the direction of flow, though not at pronounced as the elongation typically seen from cells plated on rigid substrates. Nuclear and F-actin staining also revealed similar results.; (cont.) The nuclear staining revealed a confluent monolayer formation occurred prior to flow and was maintained throughout the experiment. A change in organization of the F-actin fibers...

Microstructure, residual stress, and mechanical properties of thin film materials for a microfabricated solid oxide fuel cell

Quinn, David John, Sc. D. Massachusetts Institute of Technology
Fonte: Massachusetts Institute of Technology Publicador: Massachusetts Institute of Technology
Tipo: Tese de Doutorado Formato: 184 p.
ENG
Relevância na Pesquisa
46.2%
The microstructure and residual stress of sputter-deposited films for use in microfabricated solid oxide fuel cells are presented. Much of the work focuses on the characterization of a candidate solid electrolyte: Yttria Stabilized Zirconia (YSZ). Stress and structure of reactive RF sputtered YSZ films are explored as a function of thickness (5nm - 1000nm), deposition pressure (5mtorr - 1OOmtorr), and substrate temperature (room temperature, 3000C and 6000C). Microstructure is characterized by x-ray diffraction (XRD), transmission electron microscopy (TEM), and scanning electron microscopy (SEM). Film composition, specifically impurity content, is investigated with secondary ion mass spectroscopy (SIMS). Results indicate that YSZ films likely have a columnar structure with fully cubic crystalline phases of (100) texture with mixed amorphous/crystalline phases. Residual stress is measured via substrate curvature techniques. Results indicate that the as-deposited residual stress of YSZ ranges from -1.4 GPa to 400MPa with variations in sputtering conditions. Transitions from compressive to tensile stress are identified with variations in working pressure and film thickness.; (cont.) The origins and variations in as-deposited stress are determined to be from two primary mechanisms: tensile stress due to grain coalescence/growth and compressive stresses due to forward sputtering of target atoms (also known as "atomic peening" stresses). Due to the expected high-temperature operation (-1 0000C) of microfabricated solid oxide fuel cells...

Periostin Responds to Mechanical Stress and Tension by Activating the MTOR Signaling Pathway

Rosselli-Murai, Luciana K.; Almeida, Luciana O.; Zagni, Chiara; Galindo-Moreno, Pablo; Padial-Molina, Miguel; Volk, Sarah L.; Murai, Marcelo J.; R??os, H??ctor F.; Squarize, Cristiane H.; Castilho, Rogerio M.
Fonte: Public Library of Science (PLOS) Publicador: Public Library of Science (PLOS)
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
66%
Current knowledge about Periostin biology has expanded from its recognized functions in embryogenesis and bone metabolism to its roles in tissue repair and remodeling and its clinical implications in cancer. Emerging evidence suggests that Periostin plays a critical role in the mechanism of wound healing; however, the paracrine effect of Periostin in epithelial cell biology is still poorly understood. We found that epithelial cells are capable of producing endogenous Periostin that, unlike mesenchymal cell, cannot be secreted. Epithelial cells responded to Periostin paracrine stimuli by enhancing cellular migration and proliferation and by activating the mTOR signaling pathway. Interestingly, biomechanical stimulation of epithelial cells, which simulates tension forces that occur during initial steps of tissue healing, induced Periostin production and mTOR activation. The molecular association of Periostin and mTOR signaling was further dissected by administering rapamycin, a selective pharmacological inhibitor of mTOR, and by disruption of Raptor and Rictor scaffold proteins implicated in the regulation of mTORC1 and mTORC2 complex assembly. Both strategies resulted in ablation of Periostin-induced mitogenic and migratory activity. These results indicate that Periostin-induced epithelial migration and proliferation requires mTOR signaling. Collectively...

Estudio de la regulación de la expresión y activación de factores relevantes en la involución mamaria y el desarrollo tumoral. El rol del estrés mecánico en estos procesos; Expression and activity regulation of factors involved in mammary involution and tumorigenesis. Role of mechanical stress in these processes

Quaglino, Ana
Fonte: Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires Publicador: Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires
Tipo: info:eu-repo/semantics/doctoralThesis; tesis doctoral; info:eu-repo/semantics/publishedVersion Formato: application/pdf
Publicado em //2009 SPA
Relevância na Pesquisa
55.94%
En la mama normal, LIF es el principal activador del factor de transcripción STAT3,responsable de inducir la apoptosis del epitelio secretorio durante la involución. En el cáncer de mama STAT3 se encuentra frecuentemente activo aunque su rol biológico es aún controversial. En este trabajo nos propusimos evaluar si el LIF producido localmente es responsable de la activación de STAT3 en tumores mamarios murinos. Por estudios in vivo e in vitro determinamos que LIF se sobre-expresa en estos tumores, donde actúa como principal activador de STAT3. Encontramos además que LIF ejerce un efecto opuesto en células normales y tumorales, inhibiendo e induciendo, respectivamente, la supervivencia celular. A continuación, decidimos evaluar si el estrés mecánico inducido por la acumulación de leche al final del amamantamiento dispara la expresión de factores relevantes en la involución y tumorigénesis mamaria. Para ello, diseñamos un dispositivo que permite “estirar” radialmente células creciendo en cultivo sobre membranas elásticas. Encontramos que el estímulo mecánico es capaz de disparar en células mamarias la activación de cascadas de señales y la expresión de genes fundamentales en la involución y el desarrollo tumoral. En conjunto...

The effects of mechanical stress on photographic emulsions

Weiss, Dennis A.
Fonte: Rochester Instituto de Tecnologia Publicador: Rochester Instituto de Tecnologia
Tipo: Tese de Doutorado
EN_US
Relevância na Pesquisa
66.17%
The effects of mechanical stress on a photographic emulsion, namely Kodak Royal-X Panchromatic, has been investigated. The effects are related to the phenomenon of "Kink Desensitization" of the photographic emulsion. Despite the numerous experiments, results and explanations by previous authors on this phenomenon, a model relating the effects of mechanical stress on emulsions and dislocation theory of strained crystals still evades the photographic scientist. Strips of emulsion were axially stressed, using a Dillon tensiometer modified for compression. To analyze the changes in photo graphic sensitivity of the emulsion, the characteristic curves of the developed internal and external images were compared as a function of the applied stress. Both surface and deep internal developers were utilized to analyze changes in the position of latent image formation in a strained crystal. The parameter used to correlate the effect of stress on the emulsion was the change in optical density, AD, between the stressed and unstressed portion of the emulsion. Then, aging experiments were conducted on the stressed samples to investigate the effect of time on surface desensitization . Aging experiments were conducted in the temperature range between 249K and 318K. This allowed the calculation of the activation energy of the aging process which was found to be 0.42 0.03 eV. In general...

Iron Overload in a Murine Model of Hereditary Hemochromatosis Is Associated with Accelerated Progression of Osteoarthritis Under Mechanical Stress

Camacho, A; Simão, M; Ea, H-K; Cohen-Solal, M; Richette, P; Branco, J; Cancela, M L
Fonte: Elsevier Publicador: Elsevier
Tipo: Artigo de Revista Científica
Publicado em 25/09/2015 ENG
Relevância na Pesquisa
66%
OBJECTIVE: Hereditary hemochromatosis (HH) is a disease caused by mutations in the Hfe gene characterised by systemic iron overload and associated with an increased prevalence of osteoarthritis (OA) but the role of iron overload in the development of OA is still undefined. To further understand the molecular mechanisms involved we have used a murine model of HH and studied the progression of experimental OA under mechanical stress. DESIGN: OA was surgically induced in the knee joints of 10-week-old C57BL6 (wild-type) mice and Hfe-KO mice. OA progression was assessed using histology, micro CT, gene expression and immunohistochemistry at 8 weeks after surgery. RESULTS: Hfe-KO mice showed a systemic iron overload and an increased iron accumulation in the knee synovial membrane following surgery. The histological OA score was significantly higher in the Hfe-KO mice at 8 weeks after surgery. Micro CT study of the proximal tibia revealed increased subchondral bone volume and increased trabecular thickness. Gene expression and immunohistochemical analysis showed a significant increase in the expression of matrix metallopeptidase 3 (MMP-3) in the joints of Hfe-KO mice compared with control mice at 8 weeks after surgery. CONCLUSIONS: HH was associated with an accelerated development of OA in mice. Our findings suggest that synovial iron overload has a definite role in the progression of HH-related OA