{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,29]],"date-time":"2025-09-29T11:57:46Z","timestamp":1759147066816},"reference-count":37,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2003,4,22]],"date-time":"2003-04-22T00:00:00Z","timestamp":1050969600000},"content-version":"vor","delay-in-days":111,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Biochem &amp; Molecular Tox"],"published-print":{"date-parts":[[2003,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Exposure to ultraviolet radiation (UVR) is a known risk factor for cataract, but the molecular mechanisms involved have not been elucidated. We hypothesized that exposure to UVR would modulate the activation of nuclear factor kappa\u2010B (NF\u2010\u03baB) within the human lens epithelium, since NF\u2010\u03baB is a key regulator of cellular responses to UVR stress in other cell types. Human lens epithelial (HLE) cells were exposed to acute physiological doses of ultraviolet A (UVAR), B (UVBR), C (UVCR) radiation, or interleukin\u20101\u03b2 (IL\u20101\u03b2) and NF\u2010\u03baB activation was measured by electrophoretic shift assay (EMSA). Phosphorylation of I\u03baB in response to UVAR was measured by Western blotting. Irradiation of HLE cells with UVAR (0\u20131100 J\/m<jats:sup>2<\/jats:sup>) did not reduce cell survival, while UVBR (400\u20131600 J\/m<jats:sup>2<\/jats:sup>) and UVCR (300\u2013900 J\/m<jats:sup>2<\/jats:sup>) significantly reduced HLE cell survival. EMSA analysis of HLE nuclear proteins indicated activation of NF\u2010\u03baB, but not activator protein\u20101 (AP\u20101), by UVAR. The effects of UVBR and UVCR were less pronounced. Exposure of HLE cells to UVAR (0\u2013900 J\/m<jats:sup>2<\/jats:sup>) followed by a 30\u2010min incubation resulted in a dose\u2010dependent activation of NF\u2010\u03baB. UVAR\u2010induced NF\u2010\u03baB activation in HLE cells was evident 10 min postirradiation, maximal at 60 min and returned to control levels by 120 min. Western blot analysis of phosphorylation of the NF\u2010\u03baB inhibitory protein, I\u03baB, revealed that UVAR activates NF\u2010\u03baB via a mechanism involving the phosphorylation of I\u03baB\u2010\u03b1; this effect was dose\u2010dependent. Supershift analysis demonstrated that UVAR and IL\u20101\u03b2 activate the transcriptionally active p65\/p50 NF\u2010\u03baB dimer. These studies demonstrate that UVAR activates NF\u2010\u03baB in HLE cells in a time\u2010 and dose\u2010dependent manner via signaling through I\u03baB\u2010\u03b1. The activation of NF\u2010\u03baB in HLE cells by UVAR may have implications for the development and progression of cataract and other related ocular disorders.\u00a9 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:108\u2013113, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). 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