ArticleCellular signalling2009
Differential requirement for MEK/ERK and SMAD signaling in PAI-1 and CTGF expression in response to microtubule disruption.
Article in Cellular signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
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- Mechanical programming of arterial smooth muscle cells in health and ageing.Biophysical reviews · 2021Review
- Oleanolic acid induces migration in Mv1Lu and MDA-MB-231 epithelial cells involving EGF receptor and MAP kinases activation.PloS one · 2017Article
- The GTPase ARF6 Controls ROS Production to Mediate Angiotensin II-Induced Vascular Smooth Muscle Cell Proliferation.PloS one · 2016Article
- Characterization of twenty-five ovarian tumour cell lines that phenocopy primary tumours.Nature communications · 2015Article
- A Novel Microtubule-Disrupting Agent Induces Endoplasmic Reticular Stress-Mediated Cell Death in Human Hepatocellular Carcinoma Cells.PloS one · 2015Article
- Paclitaxel reduces formation of hypertrophic scars in the rabbit ear model.Therapeutics and clinical risk management · 2015Article
- The dynamics of Rho GTPase signaling and implications for targeting cancer and the tumor microenvironment.Small GTPases · 2015Review
- Poldip2 controls vascular smooth muscle cell migration by regulating focal adhesion turnover and force polarization.American journal of physiology. Heart and circulatory physiology · 2014Article
- The AMPK-related kinase SNARK regulates hepatitis C virus replication and pathogenesis through enhancement of TGF-β signaling.Journal of hepatology · 2013Article
- Control of myofibroblast differentiation by microtubule dynamics through a regulated localization of mDia2.The Journal of biological chemistry · 2013Article
- Cellular functions regulated by phosphorylation of EGFR on Tyr845.International journal of molecular sciences · 2013Review
- Uterine fibroids and current clinical challenges.Journal of the Turkish German Gynecological Association · 2013Review
- A systematic evaluation of multi-gene predictors for the pathological response of breast cancer patients to chemotherapy.PloS one · 2012Article
- Fibroin and sericin from Bombyx mori silk stimulate cell migration through upregulation and phosphorylation of c-Jun.PloS one · 2012Article
- Salvianolic Acid B Inhibits ERK and p38 MAPK Signaling in TGF-β1-Stimulated Human Hepatic Stellate Cell Line (LX-2) via Distinct Pathways.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- Low-dose paclitaxel ameliorates fibrosis in the remnant kidney model by down-regulating miR-192.The Journal of pathology · 2011Article
- Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) integrates developmental signals for eyelid closure.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Colchicine and nocodazole, both established microtubule disruptors, are useful tools to investigate cytoskeletal-dependent signaling cascades and the associated downstream transcriptional targets. Since cytoskeletal events impact pathophysiologic consequences in the vascular system, the signaling requirements underlying colchicine-stimulated expression of PAI-1 and CTGF, two prominent cell deformation-sensitive fibrosis-initiating proteins, were evaluated in vascular smooth muscle cells. Microtubule disruption rapidly induced EGFR transactivation (at the src kinase-sensitive EGFR(Y845) site) in a ROS-dependent manner. Genetic deficiency of EGFR, inhibition of EGFR signaling with AG1478 or introduction of a kinase-deficient EGFR construct effectively blocked colchicine-stimulated PAI-1 and CTGF expression. MEK/ERK involvement downstream of ROS generation was critical for PAI-1, but not CTGF, expression following cytoskeletal perturbation suggesting bifurcation of signaling pathways downstream of EGFR activation. Colchicine also stimulated SMAD2/3 phosphorylation by a Rho/ROCK-dependent mechanism independent of TGF-beta1 release or receptor activity. Rho/ROCK signaling initiated by tubulin network collapse was required for both CTGF and PAI-1 induction. Colchicine-initiated SMAD3 phosphorylation, however, was essential for PAI-1, but not CTGF, expression further highlighting divergence of signaling events downstream of Rho/ROCK that mediate microtubule deformation-associated changes in profibrotic gene transcription.
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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.