Tropomyosin 2 heterozygous knockout in mice using CRISPR-Cas9 system displays the inhibition of injury-induced epithelial-mesenchymal transition, and lens opacity

Teppei Shibata, Shinsuke Shibata, Yasuhito Ishigaki, Etsuko Kiyokawa, Masahito Ikawa, Dhirendra P. Singh, Hiroshi Sasaki, Eri Kubo

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

The process of epithelial–mesenchymal transition (EMT) of lens epithelial cells (LECs) after cataract surgery contributes to tissue fibrosis, wound healing and lens regeneration via a mechanism not yet fully understood. Here, we show that tropomyosin 2 (Tpm2) plays a critical role in wound healing and lens aging. Posterior capsular opacification (PCO) after lens extraction surgery was accompanied by elevated expression of Tpm2. Tpm2 heterozygous knockout mice, generated via the clustered regularly interspaced short palindromic repeat/Cas9 (CRISPR/Cas9) system showed promoted progression of cataract with age. Further, injury-induced EMT of the mouse lens epithelium, as evaluated histologically and by the expression patterns of Tpm1 and Tpm2, was attenuated in the absence of Tpm2. In conclusion, Tpm2 may be important in maintaining lens physiology and morphology. However, Tpm2 is involved in the progression of EMT during the wound healing process of mouse LECs, suggesting that inhibition of Tpm2 may suppress PCO.

Original languageEnglish (US)
Pages (from-to)24-30
Number of pages7
JournalMechanisms of Ageing and Development
Volume171
DOIs
StatePublished - Apr 2018

Keywords

  • Cataract
  • Epithelial-mesenchymal transition
  • Lens
  • Posterior capsular opacification
  • Tropomyosin

ASJC Scopus subject areas

  • Aging
  • Developmental Biology

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