ALTERED INSULIN-LIKE GROWTH FACTOR-II (IGF-II) LEVEL AND IGF-BINDING PROTEIN-3 (IGFBP-3) PROTEASE ACTIVITY IN INTERSTITIAL FLUID TAKEN FROMTHE SKIN LESION OF PSORIASIS

Citation
S. Xu et al., ALTERED INSULIN-LIKE GROWTH FACTOR-II (IGF-II) LEVEL AND IGF-BINDING PROTEIN-3 (IGFBP-3) PROTEASE ACTIVITY IN INTERSTITIAL FLUID TAKEN FROMTHE SKIN LESION OF PSORIASIS, Journal of investigative dermatology, 106(1), 1996, pp. 109-112
Citations number
28
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
0022202X
Volume
106
Issue
1
Year of publication
1996
Pages
109 - 112
Database
ISI
SICI code
0022-202X(1996)106:1<109:AIGF(L>2.0.ZU;2-2
Abstract
In the present study, we have investigated insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) in serum and artificially raised blister fluid from uninvolved and involved areas of nine patien ts with psoriasis. Both levels of IGFs and IGFBP-3, and profiles of IG FBP in serum and fluid from the uninvolved areas of these patients wer e comparable to those seen in normal subjects, In fluid from the invol ved areas, the IGF-II but not IGF-I level was significantly elevated, Among five molecular forms of IGFBP, the density of 41.5- and 38.5-kDa forms of IGFBP-3 were apparently increased in fluid from the involved areas, shown by Western ligand blotting, Radioimmunoassay further sho wed that the IGFBP-3 concentration in the involved areas was significa ntly raised, Immunoblotting revealed that the predominant form of IGFB P-3 in fluid from the uninvolved areas was a 29-kDa proteolytically mo dified product. In contrast, intact doublet IGFBP-3 was the main form of IGFBP-3 in fluid from the involved areas, Fluid from the involved a reas but not the matched serum concentration-dependently inhibited the degradation of I-125-labeled nonglycosylated IGFBP-3 (ngIGFBP-3) caus ed by fluid from the uninvolved areas, suggesting the presence of an I GFBP-3 protease inhibitor(s) in psoriatic skin lesion, These findings suggest that the alterations in IGF/IGFBP system may contribute to the pathogenesis of psoriasis.