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TGF-β2 induces transdifferentiation and fibrosis in human lens epithelial cells via regulating gremlin and CTGF

Bo Ma1, Qianyan Kang2, Li Qin2

  • 1Medical School of Xi'an Jiaotong University, First Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an 710061, China.

Biochemical and Biophysical Research Communications
|April 24, 2014
PubMed

Insights

Transforming growth factor-β2 (TGF-β2), gremlin, and connective tissue growth factor (CTGF) drive epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) synthesis. Silencing gremlin and CTGF blocks TGF-β2-induced EMT and ECM synthesis via the Smad pathway.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Ophthalmology

Background:

  • Transforming growth factor-β2 (TGF-β2), gremlin, and connective tissue growth factor (CTGF) are implicated in epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) synthesis.
  • The specific interactions between gremlin, CTGF, and TGF-β2 in human lens epithelial cells (HLECs) regarding EMT and ECM synthesis are not fully understood.

Purpose of the Study:

  • To investigate the functional relationship among gremlin, CTGF, and TGF-β2 in inducing EMT and ECM synthesis in HLECs.
  • To elucidate the role of the Smad signaling pathway in these processes.

Main Methods:

  • Treatment of HLECs with TGF-β2, CTGF, and gremlin to assess the expression of EMT and ECM markers (α-SMA, Fn, COL-I) and Smad proteins (Smad2, Smad3).
  • Utilizing blockade strategies for CTGF, gremlin, Smad2, and Smad3 to determine their necessity in TGF-β2-induced responses.
  • Employing gene silencing techniques for CTGF and gremlin.

Main Results:

  • TGF-β2, CTGF, and gremlin individually induced the expression of α-smooth muscle actin (α-SMA), fibronectin (Fn), collagen type I (COL-I), Smad2, and Smad3 in HLECs.
  • Blocking CTGF and gremlin significantly inhibited TGF-β2-induced expression of α-SMA, Fn, COL-I, Smad2, and Smad3.
  • Blocking Smad2 and Smad3 effectively inhibited CTGF and gremlin-induced expression of α-SMA, Fn, and COL-I.

Conclusions:

  • TGF-β2, CTGF, and gremlin are key mediators of EMT and ECM synthesis in HLECs through the activation of the Smad signaling pathway.
  • Targeting CTGF and gremlin can effectively inhibit TGF-β2-induced EMT and ECM synthesis by disrupting Smad pathway activation.
Keywords:
Connective tissue growth factorExtracellular matrixGremlinHuman lens epithelial cellsSmad signaling pathwayTransforming growth factor β2

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