Tropomyosin (Tpm) 1 and 2 are important in the epithelial mesenchymal transition of lens epithelial cells; however, the effect of Tpm1 depletion during aging remains obscure. We analyzed the age-related changes in the crystalline lens of Tpm1- conditional knockout mice (Tpm1-CKO). Floxed alleles of Tpm1 were conditionally deleted in the lens, using Pax6-cre transgenic mice. Lenses of embryonic day (ED) 14, postnatal 1-, 11-, and 48-week-old Tpm1-CKO and wild type mice were dissected to prepare paraffin sections, which subsequently underwent histological and immunohistochemical analysis. Tpm1 and α smooth muscle actin (αSMA) mRNA expression were assessed using RT-PCR. The homozygous Tpm1-CKO (Tpm1^−/−) lenses displayed a dramatic reduction in Tpm1 transcript, with no change to αSMA mRNA expression. Tpm1^−/− mice had small lenses with disorganized, vesiculated fiber cells, and loss of epithelial cells. The lenses of Tpm1^−/− mice had abnormal and disordered lens fiber cells with cortical and peri-nuclear liquefaction. Expression of filamentous-actin was reduced in the equator region of lenses derived from ED14, 1-, 11-, and 48-week-old Tpm1^−/− mice. Therefore, Tpm1 plays an integral role in mediating the integrity and fate of lens fiber differentiation and lens homeostasis during aging. Age-related Tpm1 dysregulation or deficiency may induce cataract formation.

原肌球蛋白 (Tpm) 1 和 2 在晶状体上皮细胞的上皮间充质转化中很重要；然而，老化过程中 Tpm1 耗竭的影响仍然模糊不清。我们分析了Tpm1 - 条件敲除小鼠 ( Tpm1 -CKO)晶状体的年龄相关变化。使用 Pax6-cre 转基因小鼠，有条件地删除了晶状体中Tpm1 的Floxed 等位基因。胚胎第 14 天 (ED)、出生后1、11和 48 周龄的Tpm1 - CKO 和野生型小鼠的晶状体被解剖以制备石蜡切片，随后进行组织学和免疫组织化学分析。Tpm1和α平滑肌肌动蛋白 ( αSMA) 使用 RT-PCR 评估 mRNA 表达。纯合的Tpm1 -CKO ( Tpm1 ^-/- ) 透镜显示 Tpm1 转录物显着减少，而αSMA mRNA 表达没有变化。Tpm1 ^-/-小鼠的晶状体小，纤维细胞杂乱无章，有泡状纤维细胞，上皮细胞丢失。的透镜TPM1 ^{/ - -}小鼠具有异常和无序晶状体纤维细胞与皮质和周围核液化。来自ED14、1-、11- 和 48 周龄的Tpm1 ^-/-晶状体的赤道区域中丝状肌动蛋白的表达降低老鼠。因此，Tpm1 在调节老化过程中晶状体纤维分化和晶状体稳态的完整性和命运中起着不可或缺的作用。与年龄相关的 Tpm1 失调或缺乏可能会导致白内障形成。