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Suppression of injury-induced epithelial-mesenchymal transition in a mouse lens epithelium lacking tenascin-C
Sai-ichi Tanaka1, Takayoshi Sumioka, Norihito Fujita
1Department of Ophthalmology, Wakayama Medical University, Wakayama, Japan. s-tanaka@wakayama-med.ac.jp
Purpose:
To investigate the role of tenascin-C in epithelial-mesenchymal transition (EMT) of the lens epithelium during wound healing in mice. Tenascin-C is a component of the extracellular matrix in patients having post-operative capsular opacification.
Methods:
The crystalline lens was injured by needle puncture in tenascin-C null (KO, n=56) and wild-type (WT, n=56) mice in a C57BL/6 background. The animals were killed at day 2, 5, or 10 post-injury. Immunohistochemistry was employed to detect alpha-smooth muscle actin (alphaSMA), a marker of EMT, collagen type I, transforming growth factor beta1 (TGFbeta1), phospho-Smad2, phospho-adducin, and phospho-myosin light chain 9 (MLC9). The expression levels of phospho-adducin and phospho-MLC9 were used as markers for the activation of protein kinase C and Rho kinase, respectively.
Results:
The expression of tenascin-C was upregulated in WT lens epithelial cells adjacent to the capsular break at day 5. The results showed that injury-induced EMT of the mouse lens epithelium, as evaluated by histology and the expression patterns of alphaSMA and fibronectin, was attenuated in the absence of tenascin-C. Upregulation of TGFbeta1 expression in the epithelium was also inhibited, and loss of tenascin-C attenuated the phosphorylation of Smad2 and adducin in epithelial cells adjacent to the capsular break. The expression of phospho-adducin was suppressed, while the expression level of phospho-MLC9 was unchanged, in the healing epithelium in the absence of tenascin C.
Conclusions:
Tenascin-C is required for injury-induced EMT in the mouse lens epithelium. The mechanism behind this might involve impaired activation of cytoplasmic signaling cascades; i.e., TGFbeta/Smad and protein kinase C-adducing signaling, in the absence of tenascin-C.
Insights
Tenascin-C is essential for lens epithelial cells to undergo epithelial-mesenchymal transition (EMT) after injury. Its absence impairs key signaling pathways involved in wound healing.
Area of Science:
- Ophthalmology
- Cell Biology
- Extracellular Matrix Biology
Background:
- Epithelial-mesenchymal transition (EMT) is crucial for wound healing in the lens epithelium.
- Post-operative capsular opacification is associated with tenascin-C, an extracellular matrix component.
Purpose of the Study:
- To investigate the role of tenascin-C in lens epithelial EMT during wound healing in mice.
- To explore the underlying molecular mechanisms of tenascin-C's function in this process.
Main Methods:
- Needle puncture injury was performed on the crystalline lens of tenascin-C null and wild-type mice.
- Immunohistochemistry was used to detect markers of EMT (alphaSMA), TGFbeta1, and signaling pathway components (phospho-Smad2, phospho-adducin, phospho-MLC9).
Main Results:
- Injury-induced EMT in the lens epithelium was attenuated in tenascin-C null mice.
- Upregulation of TGFbeta1 and phosphorylation of Smad2 and adducin were inhibited in tenascin-C deficient mice.
- Tenascin-C deficiency suppressed phospho-adducin expression, indicating impaired protein kinase C signaling.
Conclusions:
- Tenascin-C is required for injury-induced EMT in the mouse lens epithelium.
- The mechanism involves impaired activation of TGFbeta/Smad and protein kinase C signaling cascades.
