Eto M, Akishita M, Ishikawa M, Kozaki K, Yoshizumi M, Hashimoto M, Ako J, Sugimoto N, Nagano K, Sudoh N, Toba K, Ouchi Y
Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Biochem Biophys Res Commun. 1998 Aug 19;249(2):339-43. doi: 10.1006/bbrc.1998.9141.
Parathyroid hormone-related peptide (PTHrP) is a potent vasodilatory peptide whose expression has been demonstrated in various tissues. The present study was undertaken to examine the regulation of PTHrP expression in cultured endothelial cells derived from human umbilical vein. Immunoradiometric assay revealed that the amount of PTHrP in the conditioned medium was increased by both tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) in both a time- and a dose-dependent manner. The induction of PTHrP mRNA was also observed, with a peak after 2 hours of incubation with both TNF-alpha and IL-1beta. Angiotensin II, endothelin-1, and arginine vasopressin had no affect on PTHrP production. Our results suggest that PTHrP produced in vascular endothelial cells in response to cytokines may modulate vascular function as a local factor.
甲状旁腺激素相关肽（PTHrP）是一种强效血管舒张肽，其表达已在多种组织中得到证实。本研究旨在检测人脐静脉来源的培养内皮细胞中PTHrP表达的调控情况。免疫放射分析显示，条件培养基中PTHrP的量在肿瘤坏死因子α（TNF-α）和白细胞介素1β（IL-1β）作用下均呈时间和剂量依赖性增加。同时观察到PTHrP mRNA的诱导，在与TNF-α和IL-1β孵育2小时后达到峰值。血管紧张素II、内皮素-1和精氨酸加压素对PTHrP的产生没有影响。我们的结果表明，血管内皮细胞中响应细胞因子产生的PTHrP可能作为一种局部因子调节血管功能。
