ArticleThe Journal of biological chemistry2008
Focal adhesion kinase as a RhoA-activable signaling scaffold mediating Akt activation and cardiomyocyte protection.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 110 citations in OpenAlex.
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- Deciphering the association between Sirt2 modulation and non-canonical Wnt/planar cell polarity-dependent splenic junctional priming: a comparative study of two Sirt2 modulators in murine endotoxemia.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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- Remodeling of intracellular architecture during SARS-CoV-2 infection of human endothelium.Scientific reports · 2024Article
- Untangling the role of RhoA in the heart: protective effect and mechanism.Cell death & disease · 2024Review
- Overexpression of miR-22-3p and miR-29c-3p in CFU-Hill colonies is related to senescence process among children with low birth weight.Pediatric research · 2024Article
- Gα12 signaling regulates transcriptional and phenotypic responses that promote glioblastoma tumor invasion.Scientific reports · 2023Article
- A bioactive material with dual integrin-targeting ligands regulates specific endogenous cell adhesion and promotes vascularized bone regeneration in adult and fetal bone defects.Bioactive materials · 2023Article
- RhoA signaling increases mitophagy and protects cardiomyocytes against ischemia by stabilizing PINK1 protein and recruiting Parkin to mitochondria.Cell death and differentiation · 2022Article
- Review
- An optogenetic model reveals cell shape regulation through FAK and fascin.Journal of cell science · 2021Article
- 0.5‑Gy X‑ray irradiation induces reorganization of cytoskeleton and differentiation of osteoblasts.Molecular medicine reports · 2021Article
- RhoA: a dubious molecule in cardiac pathophysiology.Journal of biomedical science · 2021Review
- PKN1 kinase-negative knock-in mice develop splenomegaly and leukopenia at advanced age without obvious autoimmune-like phenotypes.Scientific reports · 2019Article
- Protective transcriptional mechanisms in cardiomyocytes and cardiac fibroblasts.Journal of molecular and cellular cardiology · 2019Review
- Disruption of both ROCK1 and ROCK2 genes in cardiomyocytes promotes autophagy and reduces cardiac fibrosis during aging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Yes-associated protein (YAP) mediates adaptive cardiac hypertrophy in response to pressure overload.The Journal of biological chemistry · 2019Article
- Gastric cancer cells escape metabolic stress via the DLC3/MACC1 axis.Theranostics · 2019Article
- ARAP2 inhibits Akt independently of its effects on focal adhesions.Biology of the cell · 2018Article
- RhoA regulates Drp1 mediated mitochondrial fission through ROCK to protect cardiomyocytes.Cellular signalling · 2018Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
RhoA a small G-protein that has an established role in cell growth and in regulation of the actin cytoskeleton. Far less is known about whether RhoA can modulate cell fate. We previously reported that sustained RhoA activation induces cardiomyocyte apoptosis (Del Re, D. P., Miyamoto, S., and Brown, J. H. (2007) J. Biol. Chem. 282, 8069-8078). Here we demonstrate that less chronic RhoA activation affords a survival advantage, protecting cardiomyocytes from apoptotic insult induced by either hydrogen peroxide treatment or glucose deprivation. Under conditions where RhoA is protective, we observe Rho kinase-dependent cytoskeletal rearrangement and activation of focal adhesion kinase (FAK). Activation of endogenous cardiomyocyte FAK leads to its increased association with the p85 regulatory subunit of phosphatidylinositol-3-kinase (PI3K) and to concomitant activation of Akt. Treatment of isolated perfused hearts with sphingosine 1-phosphate recapitulates this response. The pathway by which RhoA mediates cardiomyocyte Akt activation is demonstrated to require Rho kinase, FAK and PI3K, but not Src, based on studies with pharmacological inhibitors (Y-27632, LY294002, PF271 and PP2) and inhibitory protein expression (FAK-related nonkinase). Inhibition of RhoA-mediated Akt activation at any of these steps, including inhibition of FAK, prevents RhoA from protecting cardiomyocytes against apoptotic insult. We further demonstrate that stretch of cardiomyocytes, which activates endogenous RhoA, induces the aforementioned signaling pathway, providing a physiologic context in which RhoA-mediated FAK phosphorylation can activate PI3K and Akt. We suggest that RhoA-mediated effects on the cardiomyocyte cytoskeleton provide a novel mechanism for protection from apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.