It was found that HTscar formation coincided with a prolonged decreased expression of inflammatory genes (TNFα, IL-1α, IL-1RN, CCL2, CCL3, CXCL2, CXCR2, C3 and IL-10) and an extended increased expression of ECM-related genes (PLAU, Col3A1, TGFβ3).
When combined with 10 ng/mL TNF-α, a PLVX-TRADD-EGFP lentivirus transfection could inhibit cell proliferation, promote apoptosis, and reduce the secretion of type I collagen in HSFb, thereby reducing HS formation.
The coordinated overexpression of IL-1β and TNF-α type I receptor may maintain the fibrogenic phenotypes of hypertrophic scars, even those in "remission".
The present study sought to determine the effects of continuous and transient TNF-alpha exposure on collagen and IGFBP-3 expression by cultured HS fibroblasts and to investigate the role of IGFBP-3 in collagen accretion by HS fibroblasts.