Purchase this article with an account.
Eri Kubo, Teppei Shibata, Etsuko Kiyokawa, Masahito Ikawa, Dhirendra P Singh, Hiroshi Sasaki; Tropomyosin is required for normal lens development and differentiation. Invest. Ophthalmol. Vis. Sci. 2018;59(9):890. doi: https://doi.org/.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Tropomyosin (Tpm) 1 and 2 are involved in the regulation of posterior capsule opacification (PCO). Knock-out of Tpm2 in mice, generated via the clustered regularly interspaced short palindromic repeat/Cas9 (CRISPR/Cas9) system, promoted progression of cataract with aging and inhibited wound healing. To further investigate how Tpm1 regulates lens differentiation, we generated and characterized mice in which Tpm1 was conditionally deleted in the lens.
Floxed alleles of the Tpm1 were conditionally deleted in the lens by using Pax6-cre transgenic mice (Tpm1-CKO). Lenses of age-matched animals were dissected and photographed. Postnatal lenses were fixed, paraffin embedded, sectioned, and stained with hematoxylin-eosin. Expressions of Tpm2 and α smooth muscle actin (αSMA) were examined by real-time RT-PCR and western blotting.
Expression of Tpm1 mRNA was significantly reduced in Tpm1-CKO (p<0.001). Lens-specific deletion of Tpm1 resulted in a significant reduction of lens size, with compromising lens clarity. Lnes opacity, swelling of lens fibers, and formation of vacuoles were observed from 11 weeks-old in Tpm1-CKO. Levels of Tpm2 and α smooth muscle actin (αSMA) mRNAs were unchanged in Tpm1 deleted lenses compared to wild type lenses.
Our results highlight the significance of Tpm1 function in lens fiber formation, which is necessary for maintaining an intact lens structure.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
This PDF is available to Subscribers Only