Abstract
The present study aims to explore the roles of calcitonin gene-related peptide (CGRP) in the hypertrophic scar and its underlying mechanism. The levels of CGRP were determined in human hypertrophic scar and mouse cutaneous scar using ELISA and Western blot. In in vivo studies, A cutaneous excision mouse model was established and treated with exogenous CGRP or CGRP antagonist. In in vitro studies, bone marrow-derived macrophages (BMDMs) were isolated and treated with exogenous CGRP in the presence of lipopolysaccharide (LPS). qRT-PCR and Western blot were applied to determine the mRNA and protein levels of scar formation and inflammation-related genes, respectively. Flow cytometry was operated to determine the populations of macrophages in the scar. Elevated levels of CGRP were observed in the hypertrophic scar. In the cutaneous excision mouse model, treatment of exogenous CGRP or CGRP antagonist-affected scar formation-related genes including Col1, Tgfb1, and α-SMA, inflammation-related genes including Il1b, Il6, Tnfa, and Ccl2, and CD45+F4/80+ macrophage. In LPS-induced BMDMs, treatment of exogenous CGRP also altered inflammation-related genes by regulating NF-κB and ERK signaling pathways. The ameliorated effects of CGRP on inflammation in hypertrophic scar formation are associated with its regulative effects on NF-κB and ERK signaling pathways.
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