Document Detail


HIV-1 viral protein r induces ERK and caspase-8-dependent apoptosis in renal tubular epithelial cells.
MedLine Citation:
PMID:  20404718     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: HIV-associated nephropathy (HIVAN) is the most common cause of end-stage renal disease in persons with HIV/AIDS and is characterized by focal glomerulosclerosis and dysregulated renal tubular epithelial cell (RTEC) proliferation and apoptosis. HIV-1 viral protein r (Vpr) has been implicated in HIV-induced RTEC apoptosis but the mechanisms of Vpr-induced RTEC apoptosis are unknown. The aim of this study was therefore to determine the mechanisms of Vpr-induced apoptosis in RTEC.
METHODS: Apoptosis and caspase activation were analyzed in human RTEC (HK2) after transduction with Vpr-expressing and control lentiviral vectors. Bax and BID were inhibited with lentiviral shRNA, and ERK activation was blocked with the MEK1,2 inhibitor, U0126.
RESULTS: Vpr induced apoptosis as indicated by caspase 3/7 activation, PARP-1 cleavage and mitochondrial injury. Vpr activated both caspases-8 and 9. Inhibition of Bax reduced Vpr-induced apoptosis, as reported in other cell types. Additionally, Vpr-induced cleavage of BID to tBID and suppression of BID expression prevented Vpr-induced apoptosis. Since sustained ERK activation can activate caspase-8 in some cell types, we studied the role of ERK in Vpr-induced caspase-8 activation. Vpr induced sustained ERK activation in HK2 cells and incubation with U0126 reduced Vpr-induced caspase-8 activation, BID cleavage and apoptosis. We detected phosphorylated ERK in RTEC in HIVAN biopsy specimens by immunohistochemistry.
CONCLUSIONS: These studies delineate a novel pathway of Vpr-induced apoptosis in RTEC, which is mediated by sustained ERK activation, resulting in caspase 8-mediated cleavage of BID to tBID, thereby facilitating Bax-mediated mitochondrial injury and apoptosis.
Authors:
Alexandra Snyder; Zygimantas C Alsauskas; Jeremy S Leventhal; Paul E Rosenstiel; Pengfei Gong; Justin J K Chan; Kevin Barley; John C He; Mary E Klotman; Michael J Ross; Paul E Klotman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  AIDS (London, England)     Volume:  24     ISSN:  1473-5571     ISO Abbreviation:  AIDS     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-27     Completed Date:  2011-03-31     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  8710219     Medline TA:  AIDS     Country:  England    
Other Details:
Languages:  eng     Pagination:  1107-19     Citation Subset:  IM; X    
Affiliation:
Department of Nephrology, Mount Sinai School of Medicine, New York, New York 10029, USA.
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MeSH Terms
Descriptor/Qualifier:
AIDS-Associated Nephropathy / genetics,  metabolism*,  virology
Apoptosis / genetics,  physiology*
Caspase 8 / genetics,  metabolism*
Cell Proliferation
Extracellular Signal-Regulated MAP Kinases / metabolism*
Gene Expression Regulation, Viral
Gene Products, vpr / genetics,  metabolism*
HIV-1*
Humans
Kidney Failure, Chronic / genetics,  metabolism*,  virology
Kidney Tubules / virology
RNA, Viral
Virus Replication
Grant Support
ID/Acronym/Agency:
P01 DK056492-09/DK/NIDDK NIH HHS; P01DK056492/DK/NIDDK NIH HHS; R01 DK078510-03/DK/NIDDK NIH HHS; R01 DK078510-04/DK/NIDDK NIH HHS; R01DK078510/DK/NIDDK NIH HHS; //Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
0/Gene Products, vpr; 0/RNA, Viral; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.-/Caspase 8
Comments/Corrections

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