THE MODE OF ACTION OF PROSTAGLANDIN (PG) I-1 ANALOG, SM-10906, ON FIBROBLASTS OF HYPERTROPHIC SCARS IS SIMILAR TO PGE(1) IN ITS POTENTIAL ROLE OF PREVENTING SCAR FORMATION

Citation
Lj. Zhou et al., THE MODE OF ACTION OF PROSTAGLANDIN (PG) I-1 ANALOG, SM-10906, ON FIBROBLASTS OF HYPERTROPHIC SCARS IS SIMILAR TO PGE(1) IN ITS POTENTIAL ROLE OF PREVENTING SCAR FORMATION, Experimental dermatology, 6(6), 1997, pp. 314-320
Citations number
29
Categorie Soggetti
Dermatology & Venereal Diseases
Journal title
ISSN journal
09066705
Volume
6
Issue
6
Year of publication
1997
Pages
314 - 320
Database
ISI
SICI code
0906-6705(1997)6:6<314:TMOAOP>2.0.ZU;2-R
Abstract
The effects of prostaglandin (PG) I-1 analog, SM-10906 (SM-6) and PGE( 1) on extracellular matrix formation and the release of cytokines by c ultured normal human dermal fibroblasts (NDF) and hypertrophic scar fi broblasts (HSF) were compared in order to evaluate the clinical effica cy of PGs in preventing scar formation. In the present study, we measu red type I collagen synthesis, collagenase activity production of inte rleukin (IL)-6, IL-8, and transforming growth factor (TGF)-beta(1) and levels of adenosine 3, 5-cyclic monophosphate (cAMP) in NDF and HSF c ultured with or without PGs. The results demonstrated that HSF culture supernatants has a significantly higher level of type I collagen and TGF-beta(1) than those of NDE However, the levels of collagenase activ ity and IL-8 in HSF were significantly lower in comparison to that of NDE There was no substantial difference in IL-6 production between two types of culture cells. On the other hand, PGE(1) and SM-6 significan tly enhanced collagenase activity and raised the collagenase/type I co llagen ratio in the HSF supernatants. In addition, both PGE(1) and SM- 6 increased production of TGF-beta(1), IL-8 and IL-6 and levels of cAM P in both cell types. However, they had no effect on the type I collag en synthesis of either types. These results suggest that, the stable P GI(1) analog, SM-6, similarly acts as PGE(1) in HSF by increasing the activity of collagenase.