哈卡特
TRPV1型
瞬时受体电位通道
化学
卡普萨平
细胞生物学
辣椒素
转染
基质金属蛋白酶
蛋白激酶C
细胞培养
角质形成细胞
分子生物学
受体
信号转导
生物化学
生物
体外
基因
遗传学
作者
Young Mee Lee,Yeon Kyung Kim,Kyu Han Kim,Su Jung Park,Sung Joon Kim,Jin Ho Chung
摘要
Abstract Transient receptor potential vanilloid type 1 (TRPV1) is a molecular sensor for detecting adverse stimuli, such as capsaicin, heat, and acid. TRPV1 has been localized in keratinocytes and is suggested to be a mediator of heat‐induced matrix metalloproteinase‐1 (MMP‐1). With regard to the multimodal activation of TRPV1, we hypothesize that TRPV1 might also mediate UV‐induced MMP‐1 in keratinocytes. In HaCaT, a human keratinocyte cell line, we initially confirmed capsaicin‐induced membrane current and Ca 2+ influx. UV irradiation induced slow and persistent calcium influx and increased membrane current, which was inhibited by TRPV1 inhibitors (capsazepine and ruthenium red). The UV‐induced MMP‐1 expression in HaCaT was also decreased by TRPV1 inhibitors and was facilitated by capsaicin. Knock‐down of TRPV1 using siRNA transfection also decreased MMP‐1 expression, as well as UV‐induced Ca 2+ influx in HaCaT. UV failed to induce MMP‐1 expression in HaCaT cells cultured in Ca 2+ ‐free media. Both the UV‐induced increase in [Ca 2+ ] i and MMP‐1 were suppressed by Gö6976 (a calcium‐dependent PKC inhibitor), but not by rottlerin (a calcium‐independent PKC inhibitor). In addition to a plausible role of TRPV1 in UV‐induced MMP‐1 expression, we showed that UV increased TRPV1 expression in both HaCaT cells and human skin in vivo. From these results, we suggest that UV‐induced MMP‐1 expression might be mediated in part by PKC‐dependent activation of TRPV1 and subsequent Ca 2+ ‐influx in human keratinocytes. J. Cell. Physiol. 219: 766–775, 2009. © 2009 Wiley‐Liss, Inc.
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