HIV-1 Tat-Mediated Neurotoxicity in Retinal Cells

被引:11
作者
Chatterjee, Nivedita [1 ]
Callen, Shannon [3 ]
Seigel, Gail M. [2 ]
Buch, Shilpa J. [3 ]
机构
[1] Vis Res Fdn, Dept Ocular Pathol, Madras 600006, Tamil Nadu, India
[2] SUNY Buffalo, Ctr Hearing & Deafness, Buffalo, NY 14214 USA
[3] Univ Nebraska Med Ctr, Dept Pharmacol & Expt Neurosci, Nebraska Med Ctr, Omaha, NE 68198 USA
关键词
Retina; HIV; Chemokine; VIRUS TYPE-1 TAT; ACTIVE ANTIRETROVIRAL THERAPY; CENTRAL-NERVOUS-SYSTEM; NECROSIS-FACTOR-ALPHA; HIV-1-ASSOCIATED DEMENTIA; PROTEASOME INHIBITION; CEREBROSPINAL-FLUID; INTERFERON-GAMMA; BETA-CHEMOKINES; TRANSGENIC MICE;
D O I
10.1007/s11481-011-9257-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The current study was aimed at investigating the effect of HIV-1 protein Tat on the retinal neurosensory cell line R28. Exposure of Tat resulted in induction of pro-inflammatory mediators such as CXCL10 and TNF-alpha in addition to the activation marker GFAP in these cells. Conditioned media from Tat-treated R28 cells was able to induce monocyte migration, an effect that was blocked by CXCR3 antagonist. Complementary studies in the HIV-1 Tat-transgenic mice, showed a complete absence of the nuclear layer and the outer photoreceptor segments of the retina with a concomitant increase in glial activation. These findings lend support to the observation in post-HAART era of increased incidence of immune response-mediated retinal degeneration. These findings have direct relevance to diseases such as immune response uveitis and patients recovering from CMV retinitis.
引用
收藏
页码:399 / 408
页数:10
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