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Updated: May 22, 2026
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Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Albumin-induced epithelial mesenchymal transformation
1Sheffield Kidney Institute and Academic Nephrology Unit, University of Sheffield, Sheffield, UK.
Nephron. Experimental Nephrology
|May 23, 2012
Summary
Albumin exposure transforms kidney tubular epithelial cells (TECs) into myofibroblasts, a key process in kidney fibrosis. This albumin-induced epithelial mesenchymal transformation (EMT) may be driven by transforming growth factor-beta 1 (TGF-β1).
Area of Science:
- Nephrology
- Cell Biology
- Biochemistry
Background:
- Progressive chronic kidney disease is characterized by albuminuria and renal fibrosis.
- Renal fibrosis involves the accumulation of myofibroblasts, which originate from cells like tubular epithelial cells (TECs) via epithelial mesenchymal transformation (EMT).
Purpose of the Study:
- To investigate the hypothesis that albumin exposure induces EMT in TECs.
- To explore the role of transforming growth factor-beta 1 (TGF-β1) in albumin-induced EMT.
Main Methods:
- Rat TECs (NRK52E) were cultured and exposed to de-lipidated bovine serum albumin (dBSA).
- Assessed albumin binding/uptake, morphological changes, and expression of markers for TECs (E-cadherin) and myofibroblasts (α-SMA, FSP-1).
- Measured TGF-β1 expression, activity, and utilized a neutralizing antibody to assess its role in EMT.
Main Results:
- dBSA exposure led to albumin uptake and fibroblastic morphological changes in TECs.
- A time-dependent decrease in E-cadherin and increase in α-SMA and FSP-1 expression were observed.
- Albumin increased TGF-β1 expression and activity, and TGF-β1 neutralization significantly inhibited EMT.
Conclusions:
- In vitro, albumin induces TECs to transform into cells with myofibroblast characteristics.
- This albumin-induced EMT process appears to be dependent on TGF-β1.
