ArticlePloS one2012
HIV-1 promotes renal tubular epithelial cell protein synthesis: role of mTOR pathway.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- HIV-1 Tat Activates Akt/mTORC1 Pathway and AICDA Expression by Downregulating Its Transcriptional Inhibitors in B Cells.International journal of molecular sciences · 2021Article
- Modulation of mTORC1 Signaling Pathway by HIV-1.Cells · 2020Review
- Polyploidy and Mitotic Cell Death Are Two Distinct HIV-1 Vpr-Driven Outcomes in Renal Tubule Epithelial Cells.Journal of virology · 2018Article
- Broad-spectrum antiviral agents.Frontiers in microbiology · 2015Review
- eEF2 and Ras-GAP SH3 domain-binding protein (G3BP1) modulate stress granule assembly during HIV-1 infection.Nature communications · 2014Article
- Review
- Renin angiotensin system modulates mTOR pathway through AT2R in HIVAN.Experimental and molecular pathology · 2014Article
- mTOR plays a critical role in p53-induced oxidative kidney cell injury in HIVAN.American journal of physiology. Renal physiology · 2013Article
- MicroRNAs in HIV-associated nephropathy (HIVAN).Experimental and molecular pathology · 2013Article
- Sirolimus modulates HIVAN phenotype through inhibition of epithelial mesenchymal transition.Experimental and molecular pathology · 2012Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Tubular cell HIV-infection has been reported to manifest in the form of cellular hypertrophy and apoptosis. In the present study, we evaluated the role of mammalian target of rapamycin (mTOR) pathway in the HIV induction of tubular cell protein synthesis. Mouse proximal tubular epithelial cells (MPTECs) were transduced with either gag/pol-deleted NL4-3 (HIV/MPTEC) or empty vector (Vector/MPTEC). HIV/MPTEC showed enhanced DNA synthesis when compared with Vector/MPTECs by BRDU labeling studies. HIV/MPTECs also showed enhanced production of β-laminin and fibronection in addition to increased protein content per cell. In in vivo studies, renal cortical sections from HIV transgenic mice and HIVAN patients showed enhanced tubular cell phosphorylation of mTOR. Analysis of mTOR revealed increased expression of phospho (p)-mTOR in HIV/MPTECs when compared to vector/MPTECs. Further downstream analysis of mTOR pathway revealed enhanced phosphorylation of p70S6 kinase and associated diminished phosphorylation of eEF2 (eukaryotic translation elongation factor 2) in HIV/MPTECs; moreover, HIV/MPTECs displayed enhanced phosphorylation of eIF4B (eukaryotic translation initiation factor 4B) and 4EBP-1 (eukaryotic 4E binding protein). To confirm our hypothesis, we evaluated the effect of rapamycin on HIV-induced tubular cell downstream signaling. Rapamycin not only attenuated phosphorylation of p70S6 kinase and associated down stream signaling in HIV/MPTECs but also inhibited HIV-1 induced tubular cell protein synthesis. These findings suggest that mTOR pathway is activated in HIV-induced enhanced tubular cell protein synthesis and contributes to tubular cell hypertrophy.
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