ArticleAmerican journal of respiratory cell and molecular biology2007
Lack of MK2 inhibits myofibroblast formation and exacerbates pulmonary fibrosis.
Article in American journal of respiratory cell and molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- Inhibition of macrophage migration inhibitory factor attenuates bleomycin-induced murine pulmonary fibrosis via the MAPK pathway.Respiratory research · 2026Article
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- Long QT syndrome type 3 gain-of-function of NaCommunications biology · 2025Article
- Fibroblasts facilitate lymphatic vessel formation in transplanted heart.Theranostics · 2024Article
- MK2 drives progression of pancreas and colon cancers by suppressing CD8Frontiers in immunology · 2023Article
- 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
- Regulators of cardiac fibroblast cell state.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- Loss of FOXM1 in macrophages promotes pulmonary fibrosis by activating p38 MAPK signaling pathway.PLoS genetics · 2020Article
- Article
- Mesenchymal MAPKAPK2/HSP27 drives intestinal carcinogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Deletion of SMARCA4 impairs alveolar epithelial type II cells proliferation and aggravates pulmonary fibrosis in mice.Genes & diseases · 2017Article
- Tracking Adventitial Fibroblast Contribution to Disease: A Review of Current Methods to Identify Resident Fibroblasts.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
- Redefining the identity of cardiac fibroblasts.Nature reviews. Cardiology · 2017Review
- Stress-dependent phosphorylation of myocardin-related transcription factor A (MRTF-A) by the p38(MAPK)/MK2 axis.Scientific reports · 2016Article
- Molecular networks underlying myofibroblast fate and fibrosis.Journal of molecular and cellular cardiology · 2016Review
- Targeting Mitogen-Activated Protein Kinase-Activated Protein Kinase 2 (MAPKAPK2, MK2): Medicinal Chemistry Efforts To Lead Small Molecule Inhibitors to Clinical Trials.Journal of medicinal chemistry · 2016Review
- Normal endothelial but impaired arterial development in MAP-Kinase activated protein kinase 2 (MK2) deficient mice.Vascular cell · 2016Article
- Pivotal Role of Mitogen-Activated Protein Kinase-Activated Protein Kinase 2 in Inflammatory Pulmonary Diseases.Current protein & peptide science · 2016Review
- Anthrax lethal toxin-induced lung injury and treatment by activating MK2.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Article
- Stem Cell-Based Therapy in Idiopathic Pulmonary Fibrosis.Stem cell reviews and reports · 2015Review
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7 authors at 2 institutions in 2 countries.
Funding
Abstract
Fibroblasts play a major role in tissue repair and remodeling. Their differentiation into myofibroblasts, marked by increased expression of smooth muscle-specific alpha-actin (alpha-SMA), is believed to be important in wound healing and fibrosis. We have recently described a role for MK2 in this phenotypic differentiation in culture. In this article, we demonstrate that MK2 also regulates myofibroblasts in vivo. Disruption of MK2 in mice prevented myofibroblast formation in a model of pulmonary fibrosis. However, MK2 disruption and consequent lack of myofibroblast formation exacerbated fibrosis rather than ameliorated it as previously postulated. When mice lacking MK2 (MK2-/-) were exposed to bleomycin, more collagen accumulated and more fibroblasts populated fibrotic regions in their lungs than in similarly treated wild-type mice. While there were many vimentin-positive cells in the bleomycin-treated MK2-/- mouse lungs, few alpha-SMA-positive cells were observed in these lungs compared with wild-type mouse lungs. siRNA against MK2 reduced alpha-SMA expression in wild-type mouse embryonic fibroblasts (MEF), consistent with its suppression in MK2-/- MEF. On the other hand expressing constitutively active MK2 in MK2-/- MEF significantly increased alpha-SMA expression. MK2-/-MEF proliferated at a faster rate and produced more collagen; however, they migrated at a slower rate than wild-type MEF. Overexpressing phosphomimicking HSP27, a target of MK2, did not reverse the effect of MK2 disruption on fibroblast migration. MK2 disruption did not affect Smad2 activation by transforming growth factor-beta. Thus, MK2 appears to mediate myofibroblast differentiation, and inhibiting that differentiation might contribute to fibrosis rather than protect against it.
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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.