ArticleFrontiers in physiology2020
Chemerin Added to Endothelin-1 Promotes Rat Pulmonary Artery Smooth Muscle Cell Proliferation and Migration.
Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Superficial Parasternal Intercostal Plane Block and Full Sternotomy; A Randomized Trial.European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery · 2025Trial
- Adipokine Nesfatin-1 Mediates Endothelial Dysfunction by SuppressingJournal of the American Heart Association · 2026Article
- Vascular effects of perivascular adipose tissue-derived chemerin in obesity-associated cardiovascular disease.Cardiovascular diabetology · 2025Review
- Adipokines in pulmonary hypertension: angels or demons?Heliyon · 2023Review
- Biomarkers of haemodynamic severity of systemic sclerosis-associated pulmonary arterial hypertension by serum proteome analysis.Annals of the rheumatic diseases · 2023Article
- Role of Chemerin in Cardiovascular Diseases.Biomedicines · 2022Review
- Role of Chemerin/ChemR23 axis as an emerging therapeutic perspective on obesity-related vascular dysfunction.Journal of translational medicine · 2022Review
- Chemerin Regulates the Proliferation and Migration of Pulmonary Arterial Smooth Muscle CellsFrontiers in pharmacology · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWhile chemerin has been shown to increase proliferation and migration of systemic vascular smooth muscle cells (SMCs) contributing therefore to the development of hypertension, this remains to be clarified for the pulmonary circulation.
methodsExpression of chemerin and its three receptors (CMKRL1, CCRL2, GPR1) was examined by immunohistochemistry and RTq-PCR in lungs, pulmonary artery, and thoracic aorta from Wistar rats. Primary cultured rat pulmonary artery and thoracic aorta SMCs treated with recombinant chemerin (tested from 5.10
resultsIn pulmonary artery and thoracic aorta, CMKLR1 expression was detected in both endothelial cells and SMCs. In primary cultured pulmonary artery SMCs, chemerin and its three receptors were expressed, and CMKLR1 expression was higher than those of CCRL2 and GPR1. Chemerin added to endothelin-1 increased pulmonary artery SMC proliferation, while chemerin or endothelin-1 alone did not. This effect was less pronounced in thoracic aorta SMCs. Chemerin induced pulmonary artery and thoracic aorta SMC migration, which was exacerbated by endothelin-1 and more pronounced in thoracic aorta SMCs. Chemerin concentration-dependently reduced staurosporine-induced apoptosis in both pulmonary artery and thoracic aorta SMCs. In pulmonary artery SMCs, endothelin-1 treatment increased the expression of CMKLR1, CCRL2, and GPR1, while these expressions were not altered in thoracic aorta SMCs.
conclusionChemerin/CMKRL1 signaling, in conjunction with a key mediator in the pathogenesis of pulmonary hypertensive diseases, endothelin-1, stimulated proliferation and migration, and increased resistance to apoptosis in rat primary cultured pulmonary artery SMCs. Our results suggest that this signaling could play a role in pulmonary artery remodeling observed in pulmonary hypertension.
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