Formation of Actin Stress Fibers and Focal Adhesions Enhanced by Rho-Kinase

Amano, Mutsuki; Chihara, Kazuyasu; Kimura, Kei; Fukata, Yuko; Nakamura, Nao; Matsuura, Yoshiharu; Kaibuchi, Kozo

doi:10.1126/science.275.5304.1308

Cited by 1,000 publications

(837 citation statements)

References 29 publications

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“…RhoA/Rho-associated kinase (ROCK) Recent studies have shown that the ROCK family, one of the several small GTPase Rho effectors, has major roles in actin cytoskeleton organization, 94 smooth muscle contraction 95 and gene expression. 96 Results of previous studies have shown that ROCK has a role in the contraction of vascular smooth muscle cells.…”

Section: Tetrahydrobiopterin (Bh 4 )mentioning

confidence: 99%

Endothelial dysfunction and hypertension in aging

2012

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Hypertension is one of the common diseases in the elderly. The prevalence of hypertension markedly increases with advancing age. Both aging and hypertension have a critical role in cardiovascular and cerebrovascular complications. Although aging and hypertension, either independently or collectively, impair endothelial function, aging and hypertension may have similar cascades for the pathogenesis and development of endothelial dysfunction. Nitric oxide (NO) has an important role in regulation of vascular tone. Decrease in NO bioavailability by endothelial dysfunction would lead to elevation of blood pressure. An imbalance of reduced production of NO or increased production of reactive oxygen species, mainly superoxide, may promote endothelial dysfunction. One possible mechanism by which the prevalence of hypertension is increased in relation to aging may be advancing endothelial dysfunction associated with aging through an increase in oxidative stress. In addition, endothelial cell senescence is also involved in aging-related endothelial dysfunction. In this review, we focus on recent findings and interactions between endothelial function, oxidative stress and hypertension in aging.

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Section: Tetrahydrobiopterin (Bh 4 )mentioning

confidence: 99%

Endothelial dysfunction and hypertension in aging

2012

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“…Two substrates of ROCK, myosin light chain (MLC) and myosin-binding subunit (MBS) of MLC phosphatase are thought to be important regulators of actin-myosin filament assembly (Bishop and Hall, 2000). ROCK stimulates actomyosin contractility either by direct phosphorylation of MLC or indirectly by inactivating MLC phosphatase (Amano et al, 1996(Amano et al, , 1997Kimura et al, 1996). The resulting increase in force at focal complexes triggers the transition of these structures into focal contacts.…”

Section: Cellular Mechanotransductionmentioning

confidence: 99%

Mechanoregulation of gene expression in fibroblasts

Wang

Thampatty

Lin

et al. 2007

Gene

225

187

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Mechanical loads placed on connective tissues alter gene expression in fibroblasts through mechanotransduction mechanisms by which cells convert mechanical signals into cellular biological events, such as gene expression of extracellular matrix components (e.g., collagen). This mechanical regulation of ECM gene expression affords maintenance of connective tissue homeostasis. However, mechanical loads can also interfere with homeostatic cellular gene expression and consequently cause the pathogenesis of connective tissue diseases such as tendinopathy and osteoarthritis. Therefore, the regulation of gene expression by mechanical loads is closely related to connective tissue physiology and pathology. This article reviews the effects of various mechanical loading conditions on gene regulation in fibroblasts and discusses several mechanotransduction mechanisms. Future research directions in mechanoregulation of gene expression are also suggested.

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“…ROCK can increase MLC phosphorylation through direct effect on MLC or indirectly by inactivating MLC phosphatase. The increased MLC phosphorylation results in stimulation of actomyosin contractility [2,55,73]. Inactivation of MLC phosphatase by ROCK plays an important physiological role such as agonist-induced Ca 2+ sensitization in smooth muscle contraction [28,29,141].…”

Section: Substrates Of Rockmentioning

confidence: 99%

Rho kinase in the regulation of cell death and survival

Shi

Wei

2007

Arch. Immunol. Ther. Exp.

214

183

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SummaryRho kinase (ROCK) belongs to a family of serine/threonine kinases that are activated via interaction with Rho GTPases. ROCK is involved in a wide range of fundamental cellular functions such as contraction, adhesion, migration, and proliferation. Recent studies have shown that ROCK plays an important role in the regulation of apoptosis in various cell types and animal disease models. Two ROCK isoforms, ROCK1 and ROCK2, are assumed to be function redundant, based largely on kinase construct overexpression, and chemical inhibitors (Y27632 and fasudil), which inhibit both ROCK1 and ROCK2. Gene targeting and RNA interference approaches allow further dissection of distinct cellular, physiological and patho-physiological functions of the two ROCK isoforms. This review, based on recent molecular, cellular and animal studies, focuses on the current understanding of ROCK signaling in the regulation of apoptosis and highlights the new findings from recently generated ROCK-deficient mice.

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Formation of Actin Stress Fibers and Focal Adhesions Enhanced by Rho-Kinase

Cited by 1,000 publications

References 29 publications

Endothelial dysfunction and hypertension in aging

Endothelial dysfunction and hypertension in aging

Mechanoregulation of gene expression in fibroblasts

Rho kinase in the regulation of cell death and survival

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