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HIV-1 gp120-induced neuroinflammation: relationship to neuron loss and protection by rSV40-delivered antioxidant enzymes.
Exp Neurol. 2010 Jan; 221(1):231-45.EN

Abstract

HIV-1 gp120 neurotoxicity and oxidant injury are well documented, but consequent neuroinflammation is less understood. Rat caudate-putamens (CPs) were challenged with 100-500 ng HIV-1BaL gp120, with or without prior rSV40-delivered superoxide dismutase or glutathione peroxidase. CD11b-positive microglia were increased 1 day post-challenge; Iba-1- and ED1-positive cells peaked at 7 days and 14 days. Astrocyte infiltration was maximal at 7-14 days. MIP-1alpha was produced immediately, mainly by neurons. ED1- and GFAP-positive cells correlated with neuron loss and gp120 dose. We also tested the effect of more chronic gp120 exposure on neuroinflammation using an experimental model of continuing gp120 exposure. SV(gp120), a recombinant SV40-derived gene transfer vector was inoculated into the rat CP, leading to chronic expression of gp120, ongoing apoptosis in microglia and neurons, and oxidative stress. Increase in microglia and astrocytes was seen following intra-CP SV(gp120) injection, suggesting that continuing gp120 production increased neuroinflammation. SV(SOD1) or SV(GPx1) significantly reduced MIP-1alpha and limited neuroinflammation following gp120 administration into the CP, as well as microglia and astrocytes proliferation after injection of SV(gp120) in the striatum. Thus, gp120-induced CNS injury, neuron loss and inflammation may be mitigated by antioxidant gene delivery.

Authors+Show Affiliations

Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Room 255, Philadelphia, PA 19107, USA. jplouboutin@hotmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19913017

Citation

Louboutin, Jean-Pierre, et al. "HIV-1 Gp120-induced Neuroinflammation: Relationship to Neuron Loss and Protection By rSV40-delivered Antioxidant Enzymes." Experimental Neurology, vol. 221, no. 1, 2010, pp. 231-45.
Louboutin JP, Reyes BA, Agrawal L, et al. HIV-1 gp120-induced neuroinflammation: relationship to neuron loss and protection by rSV40-delivered antioxidant enzymes. Exp Neurol. 2010;221(1):231-45.
Louboutin, J. P., Reyes, B. A., Agrawal, L., Van Bockstaele, E. J., & Strayer, D. S. (2010). HIV-1 gp120-induced neuroinflammation: relationship to neuron loss and protection by rSV40-delivered antioxidant enzymes. Experimental Neurology, 221(1), 231-45. https://doi.org/10.1016/j.expneurol.2009.11.004
Louboutin JP, et al. HIV-1 Gp120-induced Neuroinflammation: Relationship to Neuron Loss and Protection By rSV40-delivered Antioxidant Enzymes. Exp Neurol. 2010;221(1):231-45. PubMed PMID: 19913017.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - HIV-1 gp120-induced neuroinflammation: relationship to neuron loss and protection by rSV40-delivered antioxidant enzymes. AU - Louboutin,Jean-Pierre, AU - Reyes,Beverly A S, AU - Agrawal,Lokesh, AU - Van Bockstaele,Elisabeth J, AU - Strayer,David S, Y1 - 2009/11/11/ PY - 2009/07/20/received PY - 2009/10/17/revised PY - 2009/11/04/accepted PY - 2009/11/17/entrez PY - 2009/11/17/pubmed PY - 2010/2/17/medline SP - 231 EP - 45 JF - Experimental neurology JO - Exp Neurol VL - 221 IS - 1 N2 - HIV-1 gp120 neurotoxicity and oxidant injury are well documented, but consequent neuroinflammation is less understood. Rat caudate-putamens (CPs) were challenged with 100-500 ng HIV-1BaL gp120, with or without prior rSV40-delivered superoxide dismutase or glutathione peroxidase. CD11b-positive microglia were increased 1 day post-challenge; Iba-1- and ED1-positive cells peaked at 7 days and 14 days. Astrocyte infiltration was maximal at 7-14 days. MIP-1alpha was produced immediately, mainly by neurons. ED1- and GFAP-positive cells correlated with neuron loss and gp120 dose. We also tested the effect of more chronic gp120 exposure on neuroinflammation using an experimental model of continuing gp120 exposure. SV(gp120), a recombinant SV40-derived gene transfer vector was inoculated into the rat CP, leading to chronic expression of gp120, ongoing apoptosis in microglia and neurons, and oxidative stress. Increase in microglia and astrocytes was seen following intra-CP SV(gp120) injection, suggesting that continuing gp120 production increased neuroinflammation. SV(SOD1) or SV(GPx1) significantly reduced MIP-1alpha and limited neuroinflammation following gp120 administration into the CP, as well as microglia and astrocytes proliferation after injection of SV(gp120) in the striatum. Thus, gp120-induced CNS injury, neuron loss and inflammation may be mitigated by antioxidant gene delivery. SN - 1090-2430 UR - https://www.unboundmedicine.com/medline/citation/19913017/HIV_1_gp120_induced_neuroinflammation:_relationship_to_neuron_loss_and_protection_by_rSV40_delivered_antioxidant_enzymes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4886(09)00460-9 DB - PRIME DP - Unbound Medicine ER -