Abstract:
:The contractile to synthetic phenotypic switching of vascular smooth muscle cells (VSMCs) in response to fibroblast growth factor (FGF) has been previously described. However, the role of the inflammatory response induced by FGF signaling in VSMCs and its occurrence in atherosclerosis remains unclear. In the present study, FGF signaling promoted a contractile to secretory phenotypic transition in VSMCs. VSMCs (primary human aortic smooth muscle cells) treated with FGF exhibited a decrease in the protein expression levels of factors involved in contractility and the secretion of various chemokines was increased, as assessed by reverse transcription‑quantitative PCR and ELISA. Additionally, inhibition of FGF signaling by silencing FGF receptor substrate 2 (FRS2) decreased the protein expression levels of various chemokines. Furthermore, VSMCs in the medial layers of arteries from apolipoprotein E‑deficient mice and human atherosclerotic samples exhibited an increase in FGF signaling that was identified to be associated with an increase in the protein expression levels of pro‑inflammatory molecules, including C‑C motif chemokine ligand 2, C‑X‑C motif chemokine ligand (CXCL) 9, CXCL10 and CXCL11, compared with wild‑type mice and healthy control samples, respectively. The present results suggested that FGF signaling induced dedifferentiation of contractile VSMCs and the transition to a secretory phenotype, which may be involved in the progression of atherosclerosis. Collectively, the present results suggested that the FGF signaling pathway may represent a novel target for the treatment of atherosclerosis.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Qi M,Xin Sdoi
10.3892/mmr.2019.10249subject
Has Abstractpub_date
2019-07-01 00:00:00pages
162-170issue
1eissn
1791-2997issn
1791-3004journal_volume
20pub_type
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