ArticleJournal of cellular and molecular medicine2014
Inflammatory cytokines promote growth of intestinal smooth muscle cells by induced expression of PDGF-Rβ.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 65 citations in OpenAlex.
- Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Intestinal muscularis in health and disease.Communications biology · 2026Review
- Macrophage Immune-Competent Colon Assembloids for Functional Interrogation of Neuroinflammation-Induced Colonic Dysmotility.Gastro hep advances · 2026Article
- Obesity induces phenotypic switching of gastric smooth muscle cells through the activation of the PPARD/PDK4/ANGPTL4 pathway.Journal of biomedical science · 2025Article
- The Crosstalk Between Endothelial Cells, Smooth Muscle Cells, and Macrophages in Atherosclerosis.International journal of molecular sciences · 2025Review
- Advanced In Vitro Models for Preclinical Drug Safety: Recent Progress and Prospects.Current issues in molecular biology · 2024Review
- Prevention of colon enlargement by TNF-α antagonist in a streptozotocin-induced diabetic rat model.Histology and histopathology · 2024Article
- Muscular hyperplasia in Crohn's disease strictures: through thick and thin.American journal of physiology. Cell physiology · 2024Review
- Pancreatic Tumor Organoid-Derived Factors from Cachectic Patients Disrupt Contractile Smooth Muscle Cells.Cancers · 2024Article
- Identification of Angiogenesis-Related Gene Signatures and Prediction of Potential Therapeutic Targets in Ulcerative Colitis Using Integrated Bioinformatics.Journal of inflammation research · 2024Article
- Colonic dysmotility regulated by downregulation of PDGFRα+ cells / SK3 channel in DSS-induced colitis mice.PloS one · 2024Article
- Recent Advances in Liver Tissue Engineering as an Alternative and Complementary Approach for Liver Transplantation.Current issues in molecular biology · 2023Review
- HLA-DQA1*05 and upstream variants of PPARGC1B are associated with infliximab persistence in Japanese Crohn's disease patients.The pharmacogenomics journal · 2023Article
- Reconsideration of the Gastroparetic Syndrome.Current gastroenterology reports · 2023Review
- Nintedanib regulates intestinal smooth muscle hyperplasia and phenotype in vitro and in TNBS colitis in vivo.Scientific reports · 2022Article
- Experimental Intestinal Stenosis Alters Crohn's Disease-Like Intestinal Inflammation in Ileitis-Prone Mice.Digestive diseases and sciences · 2022Article
- The Interplay between Nutrition, Innate Immunity, and the Commensal Microbiota in Adaptive Intestinal Morphogenesis.Nutrients · 2021Review
- Phenotypic switch of smooth muscle cells in paediatric chronic intestinal pseudo-obstruction syndrome.Journal of cellular and molecular medicine · 2021Article
- Small intestine remodeling in male Goto-Kakizaki rats.Physiological reports · 2021Article
- Activation of α7nAChR Protects Against Gastric Inflammation and Dysmotility in Parkinson's Disease Rats.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thickening of the inflamed intestinal wall involves growth of smooth muscle cells (SMC), which contributes to stricture formation. Earlier, the growth factor platelet-derived growth factor (PDGF)-BB was identified as a key mitogen for SMC from the rat colon (CSMC), and CSMC growth in colitis was associated with both appearance of its receptor, PDGF-Rβ and modulation of phenotype. Here, we examined the role of inflammatory cytokines in inducing and modulating the growth response to PDGF-BB. CSMC were enzymatically isolated from Sprague-Dawley rats, and the effect of tumour necrosis factor (TNF)-α, interleukin (IL)-1β, transforming growth factor (TGF), IL-17A and IL-2 on CSMC growth and responsiveness to PDGF-BB were assessed using proliferation assays, PCR and western blotting. Conditioned medium (CM) was obtained at 48 hrs of trinitrobenzene sulphonic acid-induced colitis. Neither CM alone nor cytokines caused proliferation of early-passage CSMC. However, CM from inflamed, but not control colon significantly promoted the effect of PDGF-BB. IL-1β, TNF-α and IL-17A, but not other cytokines, increased the effect of PDGF-BB because of up-regulation of mRNA and protein for PDGF-Rβ without change in receptor phosphorylation. PDGF-BB was identified in adult rat serum (RS) and RS-induced CSMC proliferation was inhibited by imatinib, suggesting that blood-derived PDGF-BB is a local mitogen in vivo. In freshly isolated CSMC, CM from the inflamed colon as well as IL-1β and TNF-α induced the early expression of PDGF-Rβ, while imatinib blocked subsequent RS-induced cell proliferation. Thus, pro-inflammatory cytokines both initiate and maintain a growth response in CSMC via PDGF-Rβ and serum-derived PDGF-BB, and control of PDGF-Rβ expression may be beneficial in chronic intestinal inflammation.
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