Calcitonin Inhibits
Phenotypic Switching of Aortic
Smooth Muscle Cells and Neointimal Hyperplasia through the AMP-Activated
Protein Kinase/Mechanistic Target of Rapamycin Pathway
Calcitonin (CT) is a peptide hormone secreted by the
parafollicular
C cells of the thyroid gland, salmon calcitonin was originally extracted
from the hind cheek of salmon. Neointimal hyperplasia refers to the
excessive proliferation and migration of vascular smooth muscle cells
(VSMCs). In this study, a rat model of restenosis was employed to
explore the impact of calcitonin on neointima proliferation. Calcitonin
was administered via continuous injections for a duration of 14 days
postsurgery, and the expression of proteins associated with proliferation,
migration, and phenotypic switching was assessed using the vascular
smooth muscle cells. Additionally, metabolomic analyses were conducted
to shed light on the mechanisms that underlie the role of calcitonin
in the development of cardiovascular disease. In our study, we found
that calcitonin possesses the capability to dispute the proliferation,
migration, and phenotypic transformation of VSMCs induced by platelet-derived
growth factor-BB (PDGF-BB) and 15% fetal bovine serum in vitro. Calcitonin
has demonstrated a favorable impact on smooth muscle cells, both in
vitro and in vivo. More specifically, it has been observed to mitigate
phenotypic switching, proliferation, and migration of these cells.
Moreover, calcitonin has been identified as a protective factor against
phenotypic switching and the formation of neointima, operating through
the AMP-activated protein kinase/mechanistic target of rapamycin (mTOR)
pathway.