作者: Xin Che , Fanglin He , Yuan Deng , Shiqiong Xu , Xianqun Fan
DOI: 10.1371/JOURNAL.PONE.0095420
关键词:
摘要: HIV-1-associated ocular complications, such as microvasculopathies, can lead to the loss of vision in HIV-1-infected patients. Even patients under highly active antiretroviral therapy, lesions are unavoidable. Ocular complications have been demonstrated be closely related breakdown blood-retinal-barrier (BRB); however, underlying mechanism is not clear. The data from this study indicated that HIV-1 Tat protein induced apoptosis human retinal microvascular endothelial cells (HRMECs) and pigmen epithelium (RPE) cells, which compose inner BRB outer BRB, respectively. In addition, found activation N-methyl-D-aspartate receptors (NMDARs) was involved RPE but it caused no changes HRMECs. Furthermore, both cell types exhibited enhanced expression Bak, Bax Cytochrome c. inhibition activity protected against by NMDAR prevented dysregulation c, revealing an important role for mitochondrial pathway Tat-induced apoptosis. Together, these findings suggest a possible may identify potential therapeutic strategy complications.