ArticleJournal of cellular biochemistry2007
Smooth muscle alpha-actin expression and myofibroblast differentiation by TGFbeta are dependent upon MK2.
Article in Journal of cellular biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
61 citing papers in PubMed, 94 citations in OpenAlex.
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- Cell sources and engineering strategies for cultured meat production: a critical comparative review.Frontiers in nutrition · 2026Review
- Nanoperlite Particles Enhance Fibrogenesis in Thyroid Orbital Fibroblasts: A Potential Activated Cell Source for Ocular Tissue Engineering.BioMed research international · 2026Article
- Nanoperlite Particles Enhance Fibrogenesis in Thyroid Orbital Fibroblasts: A Potential Activated Cell Source for Ocular Tissue Engineering.BioMed research international · 2026Article
- Article
- RNA-sequencing demonstrates transcriptional differences between human vocal fold fibroblasts and myofibroblasts.BMC genomics · 2025Article
- Targeted degradation of MK2 is insufficient to block inflammatory cytokine production in human cells due to cooperativity with MK3 and MK5.Frontiers in immunology · 2025Article
- Skin repair and infection control in diabetic, obese mice using bioactive laser-activated sealants.Biomaterials · 2024Article
- Hepatocyte Growth Factor Modulates Corneal Endothelial Wound Healing In Vitro.International journal of molecular sciences · 2024Article
- Resveratrol inhibits arecoline-induced fibrotic properties of buccal mucosal fibroblasts via miR-200a activation.Journal of dental sciences · 2024Article
- Transcriptomics ofMicroorganisms · 2024Article
- Trimetazidine Alleviates Bleomycin-Induced Pulmonary Fibrosis by Targeting the Long Noncoding RNA CBR3-AS1-Mediated miRNA-29 and Resistin-Like Molecule alpha 1: Deciphering a Novel Trifecta Role of LncRNA CBR3-AS1/miRNA-29/FIZZ1 Axis in Lung Fibrosis.Drug design, development and therapy · 2024Article
- Associations of Tissue and Soluble LOX-1 with Human Abdominal Aortic Aneurysm.Journal of the American Heart Association · 2023Article
- Combination of Niclosamide and Pirfenidone Alleviates Pulmonary Fibrosis by Inhibiting Oxidative Stress and MAPK/Nf-κB and STATs Regulated Genes.Pharmaceuticals (Basel, Switzerland) · 2023Article
- The Incidence of Urgent Tube Shunt Surgery for Diabetic Neovascular Glaucoma at a Tertiary Academic Medical Center.Clinical medicine insights. Endocrinology and diabetes · 2023Article
- Phosphorylation of the small heat shock protein HspB1 regulates cytoskeletal recruitment and cell motility.Molecular biology of the cell · 2022Article
- Mitogen-activated protein kinase-activated protein kinase-2 (MK2) and its role in cell survival, inflammatory signaling, and migration in promoting cancer.Molecular carcinogenesis · 2022Article
- The extended effect of adsorbed damage-associated molecular patterns and Toll-like receptor 2 signaling on macrophage-material interactions.Frontiers in bioengineering and biotechnology · 2022Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Fibroblasts play a major role in processes such as wound repair, scarring, and fibrosis. Differentiation into myofibroblasts, characterized by upregulation of smooth muscle alpha-actin (smalpha) in response to profibrotic agents such as TGFbeta is believed to be an important step in fibrosis. Therefore, elucidating mechanisms of myofibroblast differentiation might reveal novel targets in treating diseases such as idiopathic pulmonary fibrosis (IPF). MK2 is a kinase substrate of p38 MAP kinase that mediates some effects of p38 activation on the actin cytoskeleton. Using mouse embryonic fibroblasts (MEF) from MK2 knockout (MK2(-/-)) mice, we demonstrate that disrupting expression of MK2 expression reduces filamentous actin and stress fibers. It also causes MK2(-/-) MEF to express less smalpha than their corresponding wild-type (WT) MEF at baseline and in response to TGFbeta. Furthermore, TGFbeta causes downregulation of smalpha in MK2(-/-) MEF, instead of upregulation observed in WT MEF. Expression of other fibroblast markers, such as collagen, is not altered in MK2(-/-) MEF. Our results further suggest that downregulation of smalpha in MK2(-/-) MEF is not due to lack of activation of serum responsive promoter elements, but probably due to reduced smalpha message stability in these cells. These results indicate that MK2 plays a key role in regulation of smalpha expression, and that targeting MK2 might present a therapeutic approach in managing conditions such as pulmonary fibrosis.
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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.