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American Journal of Pathology, Vol 147, 25-32, Copyright © 1995 by American Society for Investigative Pathology

REGULAR ARTICLES

Human immunodeficiency virus-1 gp120 and gp160 envelope proteins modulate mesangial cell gelatinolytic activity

PC Singhal, S Sagar, D Chandra and P Garg
Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, New York 11040, USA.

Patients with human immunodeficiency virus (HIV) infection often develop glomerular lesions (mesangial expansion and sclerosis). Modulation of matrix degradation may be important in the expansion of the mesangium. We studied the effect of HIV sera and HIV-1 envelope glycoproteins on gelatinolytic activity of human mesangial cells. HIV serum-treated cells showed lower (P < 0.01) gelatinolytic activity when compared with cells treated with control serum (control serum, 4.3 +/- 0.1 versus HIV serum, 3.3 +/- 0.1 micrograms gelatin degraded/mg protein). Mesangial cells incubated with HIV-1 gp120 protein also showed decreased (P < 0.01) gelatinolytic activity (control, 4.6 +/- 0.2 versus HIV-1 gp120 protein, 1.7 +/- 0.2 micrograms gelatin degraded/mg protein). HIV-1 gp160 protein also inhibited (P < 0.05) mesangial cell gelatinolytic activity as judged by a biotin-avidin assay as well as by a 3H gelatin degradation assay. In contrast, gp alpha-1 acid, a nonviral glycoprotein, did not modulate mesangial cell gelatinolytic activity. These results suggest that the serum contents of HIV patients decrease gelatinolytic activity of mesangial cells. This effect of HIV sera seems to be mediated through HIV-1 gp proteins.


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A. A. Kapasi, S. Fan, and P. C. Singhal
Role of 14-3-3{epsilon}, c-Myc/Max, and Akt phosphorylation in HIV-1 gp 120-induced mesangial cell proliferation
Am J Physiol Renal Physiol, February 1, 2001; 280(2): F333 - F342.
[Abstract] [Full Text] [PDF]


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Copyright © 1995 by the American Society for Investigative Pathology.