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Blood, 1 August 2001, Vol. 98, No. 3, pp. 541-547
CHEMOKINES
HIV-1 glycoprotein 120 induces the MMP-9 cytopathogenic factor
production that is abolished by inhibition of the p38 mitogen-activated
protein kinase signaling pathway
Dorothée Missé,
Pierre-Olivier Esteve,
Benoit Renneboog,
Michel Vidal,
Martine Cerutti,
Yves St
Pierre,
Hans Yssel,
Marc Parmentier, and
Francisco Veas
From the Laboratoire d'Immunologie Rétrovirale
et Moléculaire, the Institut de Recherche pour le
Développement and the Centre National de la Recherche
Scientifique, Montpellier, France; INRS-Institut Armand Frappier,
Centre de Recherches en Immunologie, Montreal, QC, Canada; Institut de
Recherche en Biologie Humaine et Nucléaire, Faculté de
Médecine, ULB, Bruxelles, Belgique; Université de
Montpellier II, Montpellier, France; and Institut National de la
Recherche Médicale (INSERM) U 454, Montpellier, France.
It has been previously shown that the HIV-1 envelope glycoprotein
120 (gp120) activates cell signaling by CXCR4, independently of CD4.
The present study examines the involvement of different intracellular
signaling pathways and their physiopathologic consequences following
the CD4-independent interaction between CXCR4 or CCR5 and gp120 in
different cell types: primary T cells,
CD4 /CXCR4+/CCR5+ T cells, or
glioma cells. These interactions were compared with those obtained with
natural ligands, stromal cell-derived factor 1  (SDF-1)
(CXCL12) and macrophage inflammatory protein 1  (MIP-1) (CCL4) of
their respective coreceptors. Thus, both p38 and SAPK/Jun N-terminal
kinase mitogen-activated protein kinases (MAPKs) are activated on
stimulation of these cells with either T- or M-tropic gp120, as well as
with SDF-1 or MIP-1. In contrast, extracellular signal-related
kinase 1 and 2 MAPKs are only activated by MIP-1 but not by M-tropic
gp120. Importantly, T- and M-tropic gp120 are able to induce the
secretion of matrix metalloproteinase 9 (MMP-9), an extracellular
metalloproteinase present in cerebrospinal fluid of patients with HIV-1
by T cells or glioma cells. Specific inhibition of MAPK p38 activation
resulted in a complete abrogation of the induction of the MMP-9
pathogenic factor expression by gp120 or chemokines in both cell types.
Because neurodegenerative features in acquired immune deficiency
syndrome dementia may involve demyelinization by MMP-9, the specific
targeting of p38 could provide a novel means to control HIV-induced
cytopathogenic effects and cell homing to viral replication sites.
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