Biochem Biophys Res Commun. 1994 Nov 15;204(3):1272-8.

Modulations of 92kDa gelatinase B and its inhibitors are associated with HIV-1 infection in human macrophage cultures.

Chapel C, Camara V, Clayette P, Salvat S, Mabondzo A, Leblond V, Marcé D, Lafuma C, Dormont D.

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Laboratoire de Neuropathologie expérimentale et Neurovirologie, CEA/DSV/DPTE/SSA, Fontenay aux Roses, France.

Abstract

The macrophage-secreted 92-kDa type IV collagenase and metalloproteinases play a critical role in cell microenvironment regulation and cell movement. HIV infection of macrophages might be capable of deregulating the expression of these gelatinases. Hence, human monocyte-derived-macrophages were infected by lymphotropic HIV-1/Lai and monocytropic HIV-1/DAS isolates. Gelatinase activity and gelatinase and inhibitor (TIMP, alpha 2M) biosyntheses were evaluated in supernatants and cellular extracts. Our data suggest that HIV infection facilitates gelatinase secretion and intracellular inhibitor retention. These argue for the increase of free proteinase that could degrade barriers, which would permit cell movement and viral dissemination into tissues.

PMID:: 7980605; [PubMed - indexed for MEDLINE]

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Modulations of 92kDa gelatinase B and its inhibitors are associated with HIV-1 infection in human macrophage cultures.

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