ArticleJournal of molecular and cellular cardiology2007
Stretch-induced MAP kinase activation in cardiac myocytes: differential regulation through beta1-integrin and focal adhesion kinase.
Article in Journal of molecular and cellular cardiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 90 citations in OpenAlex.
- Adhesion-derived condensates control component availability to regulate adhesion dynamics.Nature communications · 2026Article
- The spectrum of pregnancy-induced cardiac remodeling: transitioning from healthy adaptive hypertrophy to peripartum cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
- Molecular Regulation of Cardiomyocyte Maturation.Current cardiology reports · 2025Review
- Inhibition of Integrin-Associated Kinases FAK and ILK on the In Vitro Model of Skin Wound Healing.Applied biochemistry and biotechnology · 2024Article
- Differential sensitivity to longitudinal and transverse stretch mediates transcriptional responses in mouse neonatal ventricular myocytes.American journal of physiology. Heart and circulatory physiology · 2024Article
- Regulation of collagen deposition in the trout heart during thermal acclimation.Current research in physiology · 2022Article
- Integrins in cardiac hypertrophy: lessons learned from culture systems.ESC heart failure · 2021Review
- Review
- The tumour microenvironment in pancreatic cancer - clinical challenges and opportunities.Nature reviews. Clinical oncology · 2020Review
- Short-term cyclical stretch phosphorylates p38 and ERK1/2 MAPKs in cultured fibroblasts from the hearts of rainbow trout,Biology open · 2020Article
- Extracellular Matrix in Regulation of Contractile System in Cardiomyocytes.International journal of molecular sciences · 2019Review
- Cardiomyocyte-specific deletion of GSK-3β leads to cardiac dysfunction in a diet induced obesity model.International journal of cardiology · 2018Article
- Biological Aspect of Pathophysiology for Frozen Shoulder.BioMed research international · 2018Review
- Caveolar remodeling is a critical mechanotransduction mechanism of the stretch-induced L-type CaPflugers Archiv : European journal of physiology · 2017Article
- Regulation of the microenvironment for cardiac tissue engineering.Regenerative medicine · 2017Review
- Article
- β1 integrin signaling in asymmetric migration of keratinocytes under mechanical stretch in a co-cultured wound repair model.Biomedical engineering online · 2016Article
- Hydrostatic Compress Force Enhances the Viability and Decreases the Apoptosis of Condylar Chondrocytes through Integrin-FAK-ERK/PI3K Pathway.International journal of molecular sciences · 2016Article
- Extracellular matrix-mediated cellular communication in the heart.Journal of molecular and cellular cardiology · 2016Review
- The role of endothelial mechanosensitive genes in atherosclerosis and omics approaches.Archives of biochemistry and biophysics · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Mitogen-activated protein (MAP) kinases have been implicated in hemodynamic load induced heart failure. Both angiotensin II (Ang II) and mechanical stretch activate MAP kinases in cardiac myocytes. In this study, we used a neonatal rat ventricular myocyte (NRVM) model to determine the role of focal-adhesion kinase (FAK) in beta1 integrin mediated MAP kinase activation in response to mechanical stretch in presence and absence of Ang II receptor blockade (ATB). NRVM plated on deformable membranes coated with collagen IV were exposed to 20% equiaxial static-stretch. beta1 integrin signaling was blocked by adenovirus-mediated expression of a dominant-negative form of beta1D integrin (tac-beta1D). FAK signaling was disrupted by infecting NRVM with adenovirus expressing FAK-related non-kinase (FRNK). Western blot analysis was used to assess the phosphorylation of MAP kinases. In the presence and absence of ATB, mechanical stretch caused maximal phosphorylation of ERK, p38 and JNK at 5 min, which was significantly attenuated in NRVM expressing tac-beta1D. In the presence of ATB, FRNK overexpression significantly increased basal phosphorylation of ERK (40.2+/-8.6% P<0.05), p38 (39.5+/-11.7%, P<0.05), JNK (86+/-29.4%, P<0.05) and stretch-induced p38 (48.1+/-8.7%, P<0.05) and JNK (85.0+/-19.4%, P<0.05) phosphorylation. However, in the absence of ATB, FRNK overexpression significantly reduced basal and stretch-induced phosphorylation of only ERK. Examination of FAK activation revealed that beta1 integrin was required for stretch-induced phosphorylation of FAK at Y397 and Y925, but not Y861. In summary, mechanical stretch-activated ERK1/2, p38 and JNK through FAK independent and dependent mechanisms. Beta1 integrin was required for FAK independent activation of all three MAP kinases, whereas cross-talk between beta1 integrin and Ang II receptors mediated FAK dependent regulation of ERK1/2.
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