ArticleThe Journal of biological chemistry2011
Opposing actions of extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3) in regulating microtubule stabilization during cardiac hypertrophy.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Runx2 Regulated Airway Homeostasis Is Disrupted in Asthma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Cardiomyocyte Janus kinase 1 (JAK1) signaling is required for cardiac homeostasis and cytokine-dependent activation of STAT3.Journal of molecular and cellular cardiology · 2025Article
- Article
- Cardiomyocyte-derived YOD1 promotes pathological cardiac hypertrophy by deubiquitinating and stabilizing STAT3.Science advances · 2025Article
- Emerging urinary alpha-synuclein and miRNA biomarkers in Parkinson's disease.Metabolic brain disease · 2022Review
- The microtubule cytoskeleton in cardiac mechanics and heart failure.Nature reviews. Cardiology · 2022Review
- Inflammatory Glycoprotein 130 Signaling Links Changes in Microtubules and Junctophilin-2 to Altered Mitochondrial Metabolism and Right Ventricular Contractility.Circulation. Heart failure · 2022Article
- Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 to Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution.Pharmacological reviews · 2020Review
- Protein Quality Control Activation and Microtubule Remodeling in Hypertrophic Cardiomyopathy.Cells · 2019Article
- An Update on the Multifaceted Roles of STAT3 in the Heart.Frontiers in cardiovascular medicine · 2019Review
- Traditional Chinese medicine suppresses left ventricular hypertrophy by targeting extracellular signal-regulated kinases signaling pathway in spontaneously hypertensive rats.Scientific reports · 2017Article
- Opposing roles for JNK and Aurora A in regulating the association of WDR62 with spindle microtubules.Journal of cell science · 2015Article
- cAMP-dependent protein kinase and c-Jun N-terminal kinase mediate stathmin phosphorylation for the maintenance of interphase microtubules during osmotic stress.The Journal of biological chemistry · 2014Article
- Dancing rhinos in stilettos: The amazing saga of the genomic and nongenomic actions of STAT3 in the heart.JAK-STAT · 2013Review
- WD40-repeat protein 62 is a JNK-phosphorylated spindle pole protein required for spindle maintenance and timely mitotic progression.Journal of cell science · 2012Article
- Local axonal function of STAT3 rescues axon degeneration in the pmn model of motoneuron disease.The Journal of cell biology · 2012Article
- Selective STAT3-α or -β expression reveals spliceform-specific phosphorylation kinetics, nuclear retention and distinct gene expression outcomes.The Biochemical journal · 2012Article
- Cytoskeletal role in protection of the failing heart by β-adrenergic blockade.American journal of physiology. Heart and circulatory physiology · 2012Article
- Phosphoinositide 3-kinase (PI3K(p110alpha)) directly regulates key components of the Z-disc and cardiac structure.The Journal of biological chemistry · 2011Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive proliferation and stabilization of the microtubule (MT) array in cardiac myocytes can accompany pathological cardiac hypertrophy, but the molecular control of these changes remains poorly characterized. In this study, we examined MT stabilization in two independent murine models of heart failure and revealed increases in the levels of post-translationally modified stable MTs, which were closely associated with STAT3 activation. To explore the molecular signaling events contributing to control of the cardiac MT network, we stimulated cardiac myocytes with an α-adrenergic agonist phenylephrine (PE), and observed increased tubulin content without changes in detyrosinated (glu-tubulin) stable MTs. In contrast, the hypertrophic interleukin-6 (IL6) family cytokines increased both the glu-tubulin content and glu-MT density. When we examined a role for ERK in regulating cardiac MTs, we showed that the MEK/ERK-inhibitor U0126 increased glu-MT density in either control cardiac myocytes or following exposure to hypertrophic agents. Conversely, expression of an activated MEK1 mutant reduced glu-tubulin levels. Thus, ERK signaling antagonizes stabilization of the cardiac MT array. In contrast, inhibiting either JAK2 with AG490, or STAT3 signaling with Stattic or siRNA knockdown, blocked cytokine-stimulated increases in glu-MT density. Furthermore, the expression of a constitutively active STAT3 mutant triggered increased glu-MT density in the absence of hypertrophic stimulation. Thus, STAT3 activation contributes substantially to cytokine-stimulated glu-MT changes. Taken together, our results highlight the opposing actions of STAT3 and ERK pathways in the regulation of MT changes associated with cardiac myocyte hypertrophy.
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