ArticleJournal of cellular and molecular medicine2010
Cross-talk between calcineurin/NFAT and Jak/STAT signalling induces cardioprotective alphaB-crystallin gene expression in response to hypertrophic stimuli.
Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Function and therapeutic value of astrocytes in neurological diseases.Nature reviews. Drug discovery · 2022Review
- Alpha B-Crystallin in Muscle Disease Prevention: The Role of Physical Activity.Molecules (Basel, Switzerland) · 2022Review
- LncRNA Chaer Prevents Cardiomyocyte Apoptosis From Acute Myocardial Infarction Through AMPK Activation.Frontiers in pharmacology · 2021Article
- JAK-Inhibitors for the Treatment of Rheumatoid Arthritis: A Focus on the Present and an Outlook on the Future.Biomolecules · 2020Review
- Leptin-induced cardiomyocyte hypertrophy is associated with enhanced mitochondrial fission.Molecular and cellular biochemistry · 2019Article
- AG490 suppresses EPO-mediated activation of JAK2-STAT but enhances blood flow recovery in rats with critical limb ischemia.Journal of inflammation (London, England) · 2016Article
- Secondhand smoke exposure toxicity accelerates age-related cardiac disease in old hamsters.BMC cardiovascular disorders · 2014Article
- Pressure overload-induced cardiac hypertrophy response requires janus kinase 2-histone deacetylase 2 signaling.International journal of molecular sciences · 2014Article
- Epigenomic model of cardiac enhancers with application to genome wide association studies.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2013Article
- Review
- Profiling CCK-mediated pancreatic growth: the dynamic genetic program and the role of STATs as potential regulators.Physiological genomics · 2012Article
- RAGE-dependent activation of the oncoprotein Pim1 plays a critical role in systemic vascular remodeling processes.Arteriosclerosis, thrombosis, and vascular biology · 2011Article
- Signal transducers and activators of transcription-3/pim1 axis plays a critical role in the pathogenesis of human pulmonary arterial hypertension.Circulation · 2011Article
- Constitutively active calcineurin induces cardiac endoplasmic reticulum stress and protects against apoptosis that is mediated by alpha-crystallin-B.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- JAK redux: a second look at the regulation and role of JAKs in the heart.American journal of physiology. Heart and circulatory physiology · 2009Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Among the stress proteins that are up-regulated in the heart due to imposed biomechanical stress, alphaB-crystallin (CryAB) is the most abundant and pivotal in rendering protection against stress-induced cell damage. Cardiomyocyte-specific expression of the CryAB gene was shown to be dependent upon an intact alphaBE4 cis-element located in the CryAB enhancer. To date, there is no evidence on the identity of regulatory proteins and associated signalling molecules that control CryAB expression in cardiomyocytes. In this study, we define a mechanism by which the calcineurin/NFAT and Jak/STAT pathways regulate CryAB gene expression in response to a hypertrophic agonist endothelin-1 (En-1), in hypertrophic hearts of mice with pressure overload (TAC) and in heart-targeted calcineurin over-expressing mice (MHC-CnA). We observed that in response to various hypertrophic stimuli the transcription factors NFAT, Nished and STAT3 form a dynamic ternary complex and interact with the alphaBE4 promoter element of the CryAB gene. Both dominant negative NFAT and AG490, an inhibitor of the Jak2 phosphorylation, inhibited CryAB gene transcription in transient transfection assays. AG490 was also effective in blocking the nuclear translocation of NFAT and STAT3 in cardiomyocytes treated with En-1. We observed a marked increase in CryAB gene expression in MHC-CnA mouse hearts accompanied with increased phosphorylation of STAT3. We conclude that hypertrophy-dependent CryAB gene expression can be attributed to a functional linkage between the Jak/STAT and calcineurin/NFAT signalling pathways, each of which are otherwise known to be involved independently in the deleterious outcome in cardiac hypertrophy.
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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.