HIV-1 Expression Induces Tubular Cell G2/M Arrest and Apoptosis

Himanshu Vashistha Immunology and Inflammation Center, Feinstein Institute for Medical Research, Manhasset, New York, USA; Department of Medicine, North Shore University Hospital and Long Island Jewish Medical Center, New Hyde Park, New York, USA

Mohammad Husain Immunology and Inflammation Center, Feinstein Institute for Medical Research, Manhasset, New York, USA; Department of Medicine, North Shore University Hospital and Long Island Jewish Medical Center, New Hyde Park, New York, USA

Dileep Kumar Immunology and Inflammation Center, Feinstein Institute for Medical Research, Manhasset, New York, USA; Department of Medicine, North Shore University Hospital and Long Island Jewish Medical Center, New Hyde Park, New York, USA

Anju Yadav Immunology and Inflammation Center, Feinstein Institute for Medical Research, Manhasset, New York, USA; Department of Medicine, North Shore University Hospital and Long Island Jewish Medical Center, New Hyde Park, New York, USA

Shitij Arora Immunology and Inflammation Center, Feinstein Institute for Medical Research, Manhasset, New York, USA; Department of Medicine, North Shore University Hospital and Long Island Jewish Medical Center, New Hyde Park, New York, USA

Pravin C. Singhal Department of Medicine, North Shore University Hospital and Long Island Jewish Medical Center, New Hyde Park, New York, USACorrespondence[email protected]

Abstract

Human renal biopsy studies suggest the presence of HIV-1 and associated signs of injury in renal tubular epithelial cells. Because renal epithelial cells lack conventional HIV-1 receptors, the modus operandi of HIV-1 in the induction of tubular cell injury remains a mystery. In the present study, we evaluated the role of HIV-1 gene expression in human proximal tubular cell apoptosis and cell cycle progression. HIV-1- or vector-transduced cells were assayed for cellular injury and cell cycle defect. HIV-1-transduced cells showed the progressive loss of viability in a time-dependent manner. Similarly, HIV-1-transduced cells showed greater apoptosis when compared with vector-transduced cells. A higher number of HIV-1 expressing cells showed cell cycle arrest at G2/M phase and enhanced tubular cell expression of phospho-p53(ser15), phospho-cdc-2(Tyr 15), and phospho-chk-2 (Thr 68). These findings suggest that in addition to the activation of apoptotic pathway, HIV-1-induced G2/M arrest may also contribute to tubular cell injury.

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HIV-1 Expression Induces Tubular Cell G2/M Arrest and Apoptosis

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HIV-1 Expression Induces Tubular Cell G2/M Arrest and Apoptosis

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