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Related Experiment Video

Updated: May 22, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Albumin-induced epithelial mesenchymal transformation.

J Ibrini¹, S Fadel, R S Chana

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).

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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.