Zbytek Blazej, Pfeffer Lawrence M, Slominski Andrzej T
Department of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, 930 Madison Avenue #525, Memphis, TN 38163, USA.
Peptides. 2006 Dec;27(12):3276-83. doi: 10.1016/j.peptides.2006.07.017. Epub 2006 Sep 7.
Corticotropin releasing hormone (CRH), a messenger of stress at the central level, is expressed in the epidermis where it operates within local equivalent of hypothalamo-pituitary axis. CRH inhibits NF-kappaB activity in human immortalized epidermal (PIG1) melanocytes. In melanocytes CRH stimulates pro-opiomelanocortin (POMC) mRNA and adrenocorticotropin (ACTH) peptide production. Knockdown of POMC levels by transfecting cells with antisense oligonucleotides blocks the effect of CRH on NF-kappaB signaling indicating that the above inhibition is indirect, e.g. through activation of POMC. We suggest that induction of POMC by CRH serves as a feedback mechanism to self-restrict inflammatory response in the skin.
促肾上腺皮质激素释放激素（CRH）是中枢水平的应激信使，在表皮中表达，在局部相当于下丘脑 - 垂体轴的环境中发挥作用。CRH抑制人永生化表皮（PIG1）黑素细胞中的NF-κB活性。在黑素细胞中，CRH刺激阿黑皮素原（POMC）mRNA和促肾上腺皮质激素（ACTH）肽的产生。用反义寡核苷酸转染细胞降低POMC水平可阻断CRH对NF-κB信号传导的作用，表明上述抑制是间接的，例如通过激活POMC。我们认为CRH诱导POMC作为一种反馈机制来自我限制皮肤中的炎症反应。
