@Article{biocell.2023.023585,
AUTHOR = {CHAO WANG, JUNWEI WANG, FANQIAN SONG, HANRUO LIU, LIYAO SUN, XI WEI, TAO ZHENG, HUA QIAN, XIAOGUANG LI, WEIHUA ZHANG, XIANLING TANG, PING LIU},
TITLE = {Upregulation of histone H3 caused by CRYAA may contribute to the development of age-related cataract},
JOURNAL = {BIOCELL},
VOLUME = {47},
YEAR = {2023},
NUMBER = {1},
PAGES = {143--154},
URL = {http://www.techscience.com/biocell/v47n1/49931},
ISSN = {1667-5746},
ABSTRACT = {<b>Objective:</b> Age-relate cataract (ARC) is a disease of the eyes with no effective drugs to prevent or treat patients.
The aim of the present study is to determine whether histone H3, αA-crystallin (CRYAA), β-galactosidase (GLB1), and
p53 are involved in the pathogenesis of ARC. <b>Methods: </b>A total of 99 anterior lens capsules (ALCs) of patients with ARC
of various nuclear grades, ultraviolet models of ALCs, and two human lens epithelial cell lines (FHL-124 and SRA01/04)
were used, and the expression of histone H3, CRYAA, GLB1, and p53 were detected by immunoblotting and reverse
transcription and real time-quantitative polymerase chain reaction. The association between CRYAA with histone H3,
GLB1, and p53 was assessed in FHL-124 and SRA01/04 cells following CRYAA overexpression. <b>Results:</b> Histone H3
and p53 in ALCs of patients with ARC were up-regulated in a grade-dependent manner, and the expression of
CRYAA showed a positive association with histone H3, p53, and GLB1. In UV models of ALCs and human lens
epithelial cell lines, the expression levels of histone H3, cell apoptosis factors (Bax/Bcl-2, cleaved caspase-3), and
inflammation factors (interleukin-6, tumor necrosis factor-α) were all up-regulated. Furthermore, transfection of
CRYAA in FHL-124 cells induced overexpression of histone H3. <b>Conclusion:</b> CRYAA-mediated upregulation of
histone H3 may be involved in the pathogenesis of ARC. p53 may also have a role in ARC development, but not via
the CRYAA-histone H3 axis. The results of the present study may assist in improving our understanding of the
pathogenesis of ARC and in identifying potential targets for treatment.},
DOI = {10.32604/biocell.2023.023585}
}