ArticleMedical science monitor : international medical journal of experimental and clinical research2016
Chemokine-Like Receptor 1 Regulates the Proliferation and Migration of Vascular Smooth Muscle Cells.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Tanshinone I, tanshinone IIA, and cryptotanshinone: key bioactive components modulating vascular smooth muscle cell function.Frontiers in pharmacology · 2025Review
- Inconsequential role for chemerin-like receptor 1 in the manifestation of ozone-induced lung pathophysiology in male mice.Physiological reports · 2024Article
- A novel method to obtain rat aortic media for primary culture of rat aortic smooth muscle cells.In vitro cellular & developmental biology. Animal · 2021Article
- Chemerin Added to Endothelin-1 Promotes Rat Pulmonary Artery Smooth Muscle Cell Proliferation and Migration.Frontiers in physiology · 2020Article
- Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoEBioMed research international · 2019Article
- Primary Culture of Rat Aortic Vascular Smooth Muscle Cells: A New Method.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND We aimed to explore how chemokine-like receptor 1 (CMKLR1) influences the proliferation and migration of vascular smooth muscle cells (VSMCs). MATERIAL AND METHODS Normal VSMCs, negative control VSMCs interfered by CMKLR1 gene, and VSMCs with stable knockdown of CMKLR1 gene were divided into the control group, PDGF group, negative-shRNA group, and CMKLR1-shRNA group. Both cell number counting and BrdU incorporation assays were employed to investigate the proliferation status of VSMCs. Transwell migration assay was used to measure the migration status of VSMCs. Inflammation markers, including cytokines IL-1β, IL-6, TNF-α, and chemokines MCP-1 in VSMCs, were detected by real-time quantitative RT-PCR. Western blotting assay was used to detect protein expressions of the MAPK pathway in VSMCs. RESULTS The number of VSMCs and the OD value of BrdU in PDGF group were significantly higher than those in the control group (both P<0.05). Compared with the control and negative-shRNA group, the CMKLR1-shRNA group exhibited significantly reduced VSMCs number and BrdU OD value (both P<0.05). Transwell migration assay indicated that PDGF-BB promoted whereas CMKLR1-shRNA inhibited the migration of VSMCs. The expression of IL-1β, IL-6, TNF-α, and MCP-1 were up-regulated in the PDGF group but down-regulated in the CMKLR1-shRNA group. Compared with normal VSMCs, the protein level of p-ERK1/2 was up-regulated in VSMCs treated with PDGF-BB, while it was down-regulated in the CMKLR1-shRNA group. CONCLUSIONS CMKLR1 exacerbated the proliferation and migration of VSMCs by activating ERK1/2.
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