@Article{biocell.2024.050219,
AUTHOR = {LITING WEN, XIAOXIA ZENG, PEIXIONG CHEN, DAPENG ZHAO, YANGYANG LI, XIANHAI ZENG},
TITLE = {<i>Bhlhe40</i> protects cochlear hair cell-like HEI-OC1 cells against HO‑triggered oxidative injury},
JOURNAL = {BIOCELL},
VOLUME = {48},
YEAR = {2024},
NUMBER = {6},
PAGES = {991--999},
URL = {http://www.techscience.com/biocell/v48n6/57034},
ISSN = {1667-5746},
ABSTRACT = { <b>Background:</b> Cochlear hair cell injury is a common pathological feature of hearing loss. The basic helix-loop-helix family, member e40 (<i>Bhlhe40</i>), a gene belonging to the basic helix-loop-helix (bHLH) family, exhibits strong transcriptional repression activity. <b>Methods:</b> Oxidative damage, in House Ear Institute-Organ of Corti 1 (HEI‑OC1) cells, was caused using hydrogen peroxide (HO). The Ad-<i>Bhlhe40</i> particles were constructed to overexpress <i>Bhlhe40</i> in HEI-OC1 cells. Various assays including cell counting kit-8 (CCK-8), terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay (TUNEL), flow cytometry, immunofluorescence, and corresponding commercial kits were employed to investigate the impacts of <i>Bhlhe40</i> on cell viability, apoptosis, oxidative stress levels, mitochondrial membrane potential and cellular senescence. Additionally, a dual-luciferase reporter assay was performed to confirm the targeting of the histone deacetylases 2 (<i>Hdac2</i>) by <i>Bhlhe40</i>. <b>Results:</b> The results revealed that <i>Bhlhe40</i> was downregulated in HO‑treated HEI‑OC1 cells, but its overexpression improved cell viability and mitigated HO‑induced oxidative injury in HEI‑OC1 cells with increase of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities and decrease of reactive oxygen species (ROS) levels. Besides, overexpression of <i>Bhlhe40</i> suppressed HO‑triggered cell senescence, as evidenced by the fact that the upregulation of P53, P21, and P16 in HEI-OC1 cells treated with HO were all alleviated by <i>Bhlhe40</i> overexpression. And we further verified that overexpression of <i>Bhlhe40</i> could inhibit the expression of <i>Hdac2</i>, which may be related to the repression of <i>Hdac2</i> transcription. <b>Conclusion:</b> This study suggests that <i>Bhlhe40</i> plays a protective role against senescence and oxidative damage in cochlear hair cells exposed to HO.},
DOI = {10.32604/biocell.2024.050219}
}