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Updated: Jun 17, 2026
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Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
HIVAN phenotype: consequence of epithelial mesenchymal transdifferentiation
Anju Yadav1, Sridevi Vallabu, Dileep Kumar
1Immunonlogy Center, Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, New York, USA.
American Journal of Physiology. Renal Physiology
|December 18, 2009
Summary
Epithelial mesenchymal transdifferentiation (EMT) drives cell proliferation in Human Immunodeficiency Virus (HIV)-1-associated nephropathy (HIVAN). Blocking the AT1 receptor with telmisartan reduced EMT and proliferation in HIVAN mouse models.
Area of Science:
- Nephrology
- Virology
- Cell Biology
Background:
- Human Immunodeficiency Virus (HIV)-1-associated nephropathy (HIVAN) is characterized by abnormal proliferation of renal epithelial cells.
- The role of epithelial mesenchymal transdifferentiation (EMT) in the pathogenesis of HIVAN remains to be fully elucidated.
Purpose of the Study:
- To investigate the contribution of EMT to the development of the HIVAN phenotype in a mouse model.
- To evaluate the therapeutic potential of targeting EMT in HIVAN.
Main Methods:
- Immunohistochemical analysis of renal cortical sections from control (FVB/N) and HIVAN (Tg26) mice.
- Assessment of cell proliferation markers (PCNA) and EMT markers (alpha-SMA, FSP1, E-cadherin, ZEB2).
- Treatment of Tg26 mice with telmisartan (an AT1 receptor blocker) or saline, followed by renal tissue evaluation.
Main Results:
- Tg26 mice exhibited increased expression of EMT markers and decreased E-cadherin, indicating EMT.
- Significant increases in parietal epithelial cell (PEC)-PGC and tubular cell (TC)-PTC proliferation were observed in Tg26 mice.
- Telmisartan treatment attenuated PEC-PGC and TC-PTC proliferation and reduced EMT marker expression in Tg26 mice.
Conclusions:
- EMT plays a significant role in the proliferative phenotype observed in HIVAN.
- Targeting the AT1 receptor with telmisartan may be a viable therapeutic strategy for mitigating HIVAN progression by inhibiting EMT.
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