Nitric Oxide Inhibits Ultraviolet B-induced Murine Keratinocyte Apoptosis by Regulating Apoptotic Signaling Cascades
Nitric Oxide Inhibits Ultraviolet B-induced Murine Keratinocyte Apoptosis by Regulating Apoptotic Signaling Cascades
复制标题
DOI：
10.1080/10715760412331284807
复制
发表时间：
2004-01
影响因子：
3.3
通讯作者：
J. Yamaoka;S. Kawana;Y. Miyachi
中科院分区：
文献类型：
--
作者：
J. Yamaoka;S. Kawana;Y. Miyachi
诱导型一氧化氮合酶（inducible nitric oxide synthase，iNOS）产生的一氧化氮（nitric oxide，NO）的细胞毒性作用被认为是炎症性疾病的主要原因之一。另一方面，NO对毒性损伤诱导的细胞损伤/凋亡的保护作用最近已被证明。紫外线B（UVB）诱导的表皮角质形成细胞凋亡导致皮肤炎症和光老化。然而，尚未阐明NO对UVB诱导的角质形成细胞凋亡有何影响。因此，在本研究中，我们调查了这个问题，并证明NO供体NO抑制UVB诱导的小鼠角质形成细胞凋亡。此外，NO显著抑制caspase 3，caspase 8和caspase 9的活性已被UVB辐射上调。NO还抑制UVB辐射上调的p53表达和上调UVB辐射下调的Bcl-2表达。提示NO可能通过调节p53、Bcl-2、caspase 3、caspase 8和caspase 9等凋亡信号通路抑制UVB诱导的角质形成细胞凋亡。
Cytotoxic effects of nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) are considered to be one of the major causes of inflammatory diseases. On the other hand, protective effects of NO on toxic insults-induced cellular damage/apoptosis have been demonstrated recently. Ultraviolet B (UVB)-induced apoptosis of epidermal keratinocytes leads to skin inflammation and photoageing. However, it has not been elucidated what kind of effects NO has on UVB-induced keratinocyte apoptosis. Thus, in the present study, we investigated the problem and demonstrated that NO from NO donor suppressed UVB-induced apoptosis of murine keratinocytes. In addition, NO significantly suppressed activities of caspase 3, caspase 8 and caspase 9 that had been upregulated by UVB radiation. NO also suppressed p53 expression that had been upregulated by UVB radiation and upregulated Bcl-2 expression that had been downregulated by UVB radiation. These findings suggested that NO might suppress UVB-induced keratinocyte apoptosis by regulating apoptotic signaling cascades in p53, Bcl-2, caspase3, caspase 8 and caspase 9.