ENHANCED BIOSYNTHESIS OF EXTRACELLULAR-MATRIX PROTEINS AND TGF-BETA-1BY POLYINOSINIC-POLYCYTIDYLIC ACID DURING CUTANEOUS WOUND-HEALING IN-VIVO

In our previous study, we have shown that polyinosinic-polycytidylic a cid (poly I:C), a double-stranded RNA, and a potent inducer of interfe ron, enhanced the wound healing in rats and mice. Increased levels of laminin and collagen, and greater influx of dermal fibroblasts were ob served in poly I:C-treated wounds as compared to untreated wounds (Bha rtiya et al., 1992, J. Cell. Physiol., 150:312-319). In this study, we have explored the mechanism of enhanced wound healing by poly I:C in rats. Poly I:C (1 mg/kg) in phosphate buffered saline was injected int raperitoneally 18 h prior to wound healing, and the animals were sacri ficed on day 3 postwounding. Immunofluorescence studies showed increas ed expression of adhesion molecules that includes ICAM-1 (intercellula r adhesion molecule-1; CD54) and VCAM-1 (vascular cell adhesion molecu le; CD 106) in poly I:C-treated wounds as compared to untreated contro l. Poly I:C treatment resulted in an increase in the mRNA levels of co llagen type 1(alpha), collagen III, laminin B1, and transforming growt h factor-beta 1 (TGF-beta 1) in wounds compared to untreated wounds as demonstrated by in situ hybridization and PCR analysis. These studies suggests that poly I:C upregulates the biosynthesis of adhesion molec ules, extracellular matrix proteins (ECM), and TGF-beta 1 in the wound bed. Adhesion molecules and ECM play a major role in wound healing, a nd TGF-beta 1 has been known to be a potent wound healer. Therefore, t he increased expression of these molecules may play a role in the enha nced healing by poly I:C observed in rats. (C) 1996 Wiley-Liss, Inc.