Department of Ophthalmology, Fuyang Futian Eye Hospital, Fuyang, Anhui Province, China.
Department of Ophthalmology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, China.
Bioengineered. 2021 Dec;12(1):7213-7222. doi: 10.1080/21655979.2021.1980645.
Cataract is a disease that causes severe visual impairment in patients. Recent studies have found that lens epithelial cell apoptosis caused by oxidative damage is the critical cause of cataract. Moreover, TRIM22 could alleviate the ubiquitination of TRAF6. The expression of TRAF6 could activate the p38/MAPK pathway and aggravate the oxidative stress induced damage of lens epithelial cells. However, whether the TRIM22 could alleviate the oxidative stress induced damage of lens epithelial cells by regulating the expression of TRAF6 and p38/MAPK pathway is unclear. In this study, we stimulated the lens epithelial cells with the HO and established the TRIM22 knockdown cells. Next, proliferation of these cells was determined by CCK-8 and EdU assays. Apoptosis of these cells was detected with the TUNEL assays. Levels of ROS was explored with the DCFH-DA staining. Finally, the expression levels of TRAF6, p-p38 and p-ERK were determined with the western blotting. According to the results, we found that knockdown of TRIM22 suppressed the proliferation and relieved the HO induced DNA double-strand break and apoptosis of these cells. Inhibition of TRIM22 inhibited the production of ROS in these cells. Moreover, restriction of TRIM22 induced the decreased levels of TRAF6, p-p38 and p-ERK in lens epithelial cells. We concluded that inhibition of TRIM22 relieved the apoptosis of lens epithelial cells by suppressing the expression of TRAF6, p-p38 and p-ERK.
白内障是一种导致患者严重视力障碍的疾病。最近的研究发现，氧化损伤引起的晶状体上皮细胞凋亡是白内障的关键原因。此外，TRIM22 可以减轻 TRAF6 的泛素化。TRAF6 的表达可以激活 p38/MAPK 通路，加重晶状体上皮细胞的氧化应激损伤。然而，TRIM22 是否可以通过调节 TRAF6 和 p38/MAPK 通路的表达来减轻氧化应激诱导的晶状体上皮细胞损伤尚不清楚。在这项研究中，我们用 H2O2 刺激晶状体上皮细胞，建立了 TRIM22 敲低细胞。接下来，通过 CCK-8 和 EdU 测定法测定这些细胞的增殖。用 TUNEL 测定法检测这些细胞的凋亡。用 DCFH-DA 染色法检测 ROS 水平。最后，用 Western blot 测定 TRAF6、p-p38 和 p-ERK 的表达水平。结果表明，TRIM22 的敲低抑制了细胞的增殖，并缓解了 H2O2 诱导的这些细胞的 DNA 双链断裂和凋亡。抑制 TRIM22 抑制了这些细胞中 ROS 的产生。此外，限制 TRIM22 诱导了晶状体上皮细胞中 TRAF6、p-p38 和 p-ERK 水平的降低。我们得出结论，抑制 TRIM22 通过抑制 TRAF6、p-p38 和 p-ERK 的表达来缓解晶状体上皮细胞的凋亡。
