Burn injuries frequently result in
hypertrophic scars (HTSs), specifically when excision and grafting are delayed due to limited resources or patient complications. In patient populations with dark baseline pigmentation, one symptom of HTS that often occurs is dyspigmentation. The mechanism behind dyspigmentation has not been explored, and, as such, prevention and treatment strategies for this morbidity are lacking. The mechanism by which cells make pigment is controlled at the apex of the pathway by
pro-opiomelanocortin (
POMC), which is cleaved to its products
alpha-melanocyte-stimulating hormone (α-
MSH) and
adrenocorticotropin hormone (
ACTH). α-
MSH and
ACTH secreted by keratinocytes bind to
melanocortin 1 receptor (MC1R), expressed on melanocytes, to initiate melanogenesis.
POMC protein expression is upregulated in hyperpigmented
scar compared to hypopigmented
scar by an unknown mechanism in a Duroc pig model of HTS.
POMC RNA levels, as well as the
POMC gene promoter methylation status were investigated as a possible mechanism.
DNA was isolated from biopsies obtained from distinct areas of hyper- or hypopigmented
scar and normal skin.
DNA was
bisulfite-converted, and amplified using two sets of primers to observe methylation patterns in two different CpG islands near the
POMC promoter. Amplicons were then sequenced and methylation patterns were evaluated.
POMC gene expression was significantly downregulated in hypopigmented
scar compared to normal skin, consistent with previously reported
protein expression levels. There were significant changes in methylation of the
POMC promoter; however, none that would account for the development of hyper- or
hypopigmentation. Future work will focus on other areas of
POMC transcriptional regulation.