Protective effects of calbindin‑D28K on the UVB radiation‑induced apoptosis of human lens epithelial cells

Abstract

calbindin-d28K (calb1) may protect human lens epithelial cells (HLEcs) from apoptosis, which is a process resulting in individual cell death. The protective effects of calb1 may be attributed to buffering high concentrations of ca 2+. The present study investigated the mechanisms through which calb1 protects SRA01/04 cells (a human lens epithelial cell line) against apoptosis induced by ultraviolet B (UVB) exposure. cells transfected with a lentivirus overexpressing calb1 and control cells were treated with 40 µW/cm 2 irradiation for 15 min and then cultured for 24 h. The changes in intracellular ca 2+ were detected by colorimetry, and the protein expression levels of Bad, Bcl-2 and caspase-12 were measured by western blot analysis. The intracellular ca 2+ concentration of control HLECs increased significantly following UVB irradiation, whereas in calb1-overexpressing cells, the ca 2+ levels remained steady. In the control cells, the expression of Bad and caspase-12 was upregulated, and that of Bcl-2 was downregulated. Notably, during UVB radiation-induced apoptosis, the overexpression of calb1 inhibited cell death, resulting in the decreased expression of Bad and caspase-12, and in the upregulated expression of Bcl-2. These results suggested that calb1 inhibited the upregulation of genes involved in apoptosis. The siRNA-mediated knockdown of calb1 resulted in increased rates of UVB radiation-induced apoptosis, the increased expression of Bad and caspase-12, and the decreased expression of Bcl-2, further demonstrating that calb1 may mediate UVB radiation-mediated apoptosis by regulating ca 2+. On the whole, the findings of the present study indicate that UVB exposure can lead to an imbalance in the intracellular ca 2+ homeostasis in HLEcs and that calb1 protein exerts a negative effect on the expression of pro-apoptotic genes in HLEcs. calb1 may thus inhibit the UVB radiation-induced apoptosis of HLEcs by regulating ca 2+ .

The Nero Lucano Pig Breed: Recovery and Variability

“…However, when extending the comparison to the most common 171 NL ROH, only four partial ROH overlaps were identified (Table 6). These overlapping regions contain genes whose activities are related to reproduction and production traits such as spermatogenesis (SPATA5) [16], locomotory behavior, meat smell and taste (NOVA1) [14,17], protection from UVB radiation (CALB1) [18], cellular growth and division (DDX10) [19] and lipid composition traits (DECR1) [20]. The inbreeding coefficients based on ROH extension (F ROH ), obtained for the generations 0, 1 and 2, were characterized by the distributions shown in Figure 2 and by mean values of 0.36 ± 0.12, 0.39 ± 0.11 and 0.38 ± 0.13, respectively.…”

Candidate genes identification and RNA-seq based pathway analysis associated with primary angle-closure glaucoma with cataract

“…As reported by Fan Gaskin et al, reactive oxygen species (ROS) produced by NADPH oxidase are important contributors for oxidative stress in glaucoma [ 7 ]. Excessive ROS can lead to apoptosis of human lens epithelial cells (LECs), representing one of the main trigger factors of ARC [ 8 , 9 ]. By analysis the aqueous humor protein profile in PACG patients with cataracts, Adav et al [ 10 ] identified 1,376 different aqueous humor proteins, among which superoxide dismutase, catalase, and peroxiredoxin-2 were significantly increased in PACG patients, indicating a higher level of oxidative stress as compared with patients with cataracts only.…”

Ultraviolet light accelerates the degradation of polyethylene plastics

“…Mostly UVC and UVA spectrum regions are absorbed by ozone, water vapor, oxygen, and carbon dioxide in the atmosphere (Upadhyay, 2020). UVB spectrum region is not filtered as significantly by the atmosphere; as a result, inorganic materials, living things, and the environment are exposed to higher levels of UVB radiation (Ali Karami, Sharif Makhmalzadeh, Pooranian, & Rezai, 2021; Liu et al, 2020). As a result, after a passed long time, UVB radiation breaks plastics' molecular bonds and deteriorates plastics' structure (Asmatulu, Mahmud, Hille, & Misak, 2011).…”