Focal Adhesion Kinase Regulation by Oxidative Stress in Different Cell Types

Mahdi, Meriem H. Ben; Andrieu, Valérie; Pasquier, Claude

doi:10.1080/713803721

Cited by 28 publications

(10 citation statements)

References 49 publications

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“…Stimulation of FAK phosphorylation has been demonstrated in response to mechanical stretch in cardiac myocytes (50,55,56) and fibroblasts (64) and in response to shear stress (30) or stretch (2) in endothelial cells. FAK phosphorylation is also increased in endothelial cells in response to oxidative stress (7,60,61). Neither high stretch (MV) nor hyperoxia (HO) alone affected FAK phosphorylation in our studies, suggesting tight regulation of FAK signaling under these conditions in vivo.…”

Section: Discussionmentioning

confidence: 42%

High tidal volume mechanical ventilation with hyperoxia alters alveolar type II cell adhesion

Desai¹,

Sinclair²,

Chapman³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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Patients with acute respiratory distress syndrome undergoing mechanical ventilation may be exposed to both high levels of stretch and high levels of oxygen. We hypothesized that the combination of high stretch and hyperoxia promotes loss of epithelial adhesion and impairs epithelial repair mechanisms necessary for restoration of barrier function. We utilized a model of high tidal volume mechanical ventilation (25 ml/kg) with hyperoxia (50% O(2)) in rats to investigate alveolar type II (AT2) cell adhesion and focal adhesion signaling. AT2 cells isolated from rats exposed to hyperoxia and high tidal volume mechanical ventilation (MVHO) exhibited significantly decreased cell adhesion and reduction in phosphotyrosyl levels of focal adhesion kinase (FAK) and paxillin compared with control rats, rats exposed to hyperoxia without ventilation (HO), or rats ventilated with normoxia (MV). MV alone increased phosphorylation of p130(Cas). RhoA activation was increased by MV, HO, and the combination of MV and HO. Treatment of MVHO cells with keratinocyte growth factor (KGF) for 1 h upon isolation reduced RhoA activity and restored attachment to control levels. Attachment and migration of control AT2 cells was significantly decreased by constitutively active RhoA or a kinase inactive form of FAK (FRNK), whereas expression of dominant negative RhoA in cells from MVHO-treated rats restored cell adhesion. Mechanical ventilation with hyperoxia promotes changes in focal adhesion proteins and RhoA in AT2 cells that may be deleterious for cell adhesion and migration.

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Section: Discussionmentioning

confidence: 42%

High tidal volume mechanical ventilation with hyperoxia alters alveolar type II cell adhesion

Desai¹,

Sinclair²,

Chapman³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Several mechanisms of ROS regulation of cancer cell migration have been proposed; most of these involve alterations of cellular cytoskeleton and adhesion molecules. For instance, ROS have been reported to regulate integrin (13,14), small GTPase Rho family proteins (15,16), focal contact-forming proteins (13,17), and extracellular matrix-degrading enzymes such as matrix metalloproteinases (14,18,19). Caveolin-1 (Cav-1) is an essential structural protein component of the plasma membrane microdomains called caveolae.…”

mentioning

confidence: 99%

Regulation of Lung Cancer Cell Migration and Invasion by Reactive Oxygen Species and Caveolin-1

Luanpitpong

Talbott

Rojanasakul

et al. 2010

Journal of Biological Chemistry

179

167

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The acquired capability of tumor cells to migrate and invade neighboring tissues is associated with high metastatic potential and advanced stage of cancers. Recently, signaling molecules such as reactive oxygen species (ROS) and caveolin-1 (Cav-1) have been implicated in the aggressive behavior of cancer cells. However, the roles of specific ROS in cancer cell migration and Cav-1 regulation are unclear. We demonstrate here that Cav-1 plays an important role in the migration and invasion of human lung carcinoma H460 cells and that these effects are differentially regulated by cellular ROS. Using various known inhibitors and donors of ROS, we found that different ROS have different effects on Cav-1 expression and cell migration and invasion. Superoxide anion and hydrogen peroxide down-regulated Cav-1 expression and inhibited cell migration and invasion, whereas hydroxyl radical up-regulated the Cav-1 expression and promoted cell migration and invasion. The down-regulating effect of superoxide anion and hydrogen peroxide on Cav-1 is mediated through a transcriptionindependent mechanism that involves protein degradation via the ubiquitin-proteasome pathway. These results indicate the essential role of different ROS in cancer cell motility and through Cav-1 expression, which may provide a key mechanism controlling tumor progression and metastasis. The upregulation of Cav-1 and cell motility by hydroxyl free radical suggests an important role of this ROS as a positive regulator of tumor progression.Cancer cell migration and invasion are initial steps in metastasis that is a primary cause of cancer-related death. During metastasis, primary tumor cells migrate and invade neighboring tissues and enter the circulation to establish new or secondary tumor sites (1-3). Increasing evidence suggests that signaling molecules presenting in the tumor microenvironment have a significant impact on the migratory properties of cancer cells (4,5 Caveolin-1 (Cav-1) is an essential structural protein component of the plasma membrane microdomains called caveolae. It has been shown to function in vesicular trafficking, signal transduction, and tumor progression. Cav-1 interacts with several signaling molecules, including Ha-Ras, Src family tyrosine kinases, G protein ␣ subunits, and protein kinase C (20 -23). Increased expression of Cav-1 has been observed in lung adenocarcinoma and prostate cancer, which are associated with their invasiveness (24 -26). In lung carcinoma, the elevated Cav-1 expression is also associated with an increase in metastatic capacity and poor survival of patients (26 -28). On the other hand, Cav-1 has been shown to have a suppressive effect on pancreatic and breast cancer cell motility (29 -31). Thus, the role of Cav-1 in cancer cell migration and metastasis remains unclear and appears to be cell type-dependent.Increased oxidative stress and ROS production have also been associated with many human metastatic tumors, including the lung (32, 33), breast (34), prostate (35), colon (36), and ovary (37). ROS such as s...

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“…To our knowledge, the ROS dependent regulation of FAK phosphorylation has not been examined in the VSMC. Ben Mahdi et al (2000) have suggested that ROS may induce FAK phosphorylation through phosphoinositide 3-kinase (PI3-K). Interestingly, we have recently demonstrated that the aortic content and activity of phosphatase and tensin homolog (PTEN), a negative regulator of PI3K signaling, is upregulated with aging in the F344/NXBN.…”

Section: Discussionmentioning

confidence: 99%

“…The factors, which influence the activation of FAK are diverse, as increases in FAK phosphorylation have been linked to a number of different stimuli including integrin engagement, growth factor stimulation, bioactive lipids, and elevated reactive oxygen species (ROS) (Ilic et al 1997;Ben Mahdi et al 2000). Given these data and previous findings from our laboratory demonstrating that ROS levels are increased in the aged F344XBN aorta (Rice et al 2006), it is intriguing that the extent of FAK phosphorylation (Tyr 925) is diminished with aging (Fig.…”

Section: Discussionmentioning

confidence: 99%

Load-induced focal adhesion mechanotransduction is altered with aging in the Fischer 344/NNiaHSd × Brown Norway/BiNia rat aorta

et al. 2006

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The focal adhesion kinase (FAK) pathway has emerged as a critical component for mediating numerous cellular responses including control of cell growth, differentiation, and adaptation. Here we compared the expression, basal activation, and the ability of increased intraluminal pressure to activate FAK and focal adhesion-associated proteins in the aorta of adult (6 months old) and very aged (36 months old) Fischer 344/NNiaHSd x Brown Norway/BiNia (F344/NXBN) rats. Immunoblot analysis showed increases in the aortic content of FAK (15%), FAK related non-kinase (p41-FRNK) (28%), Src (92%), RhoA (41%), and paxillin (23%) in the very aged aortae. Increased age significantly changed the basal phosphorylation status of FAK and paxillin. Application of aortic intraluminal pressure (200 mm Hg) amplified the phosphorylation of FAK (Tyr 925), Src (Tyr 416), and paxillin (Tyr 188) in adult animals while aortic loading in the very aged animals failed to induce FAK (Tyr 925) phosphorylation. Aging did not alter the load-induced regulation of RhoA; however, FRNK (p41) translocation between cytosolic and membrane compartments was increased. These results confirm previous observations that FAK and focal adhesion-associated proteins are mechanically regulated and expand these studies to suggest that FAK mechanotransduction is altered with aging.

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Focal Adhesion Kinase Regulation by Oxidative Stress in Different Cell Types

Cited by 28 publications

References 49 publications

High tidal volume mechanical ventilation with hyperoxia alters alveolar type II cell adhesion

High tidal volume mechanical ventilation with hyperoxia alters alveolar type II cell adhesion

Regulation of Lung Cancer Cell Migration and Invasion by Reactive Oxygen Species and Caveolin-1

Load-induced focal adhesion mechanotransduction is altered with aging in the Fischer 344/NNiaHSd × Brown Norway/BiNia rat aorta

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