一氧化氮
生物学中的钙
化学
肽
钙
生物化学
一氧化氮合酶
细胞内
分子生物学
细胞生物学
生物
有机化学
作者
Soo Kyung Lee,Jung Ok Lee,Ji Hae Kim,Jin Hee Jung,Ga Young You,Sun Hwa Park,Hyeon Soo Kim
出处
期刊:Life Sciences
[Elsevier]
日期:2010-06-01
卷期号:86 (23-24): 863-868
被引量:19
标识
DOI:10.1016/j.lfs.2010.03.022
摘要
C-peptide is a product of pro-insulin cleavage. Numerous studies have demonstrated that C-peptide, although not influencing blood glucose control, may play a role in preventing and potentially reversing some of the chronic complications of type 1 diabetes. The aim of this paper was to present a novel function of C-peptide, focusing on its role in nitric oxide (NO) generation. Murine macrophage Raw264.7 cells and primary peritoneal macrophages were incubated under control conditions, or with C-peptide. Expression level of iNOS and phosphorylation status of JAK2/STAT1 were analyzed by Western blot. Fluorometric NO assay kit was used to assess the concentration of nitrite in culture medium. Intracellular calcium concentration was measured with calcium indicator dyes, such as Fura-2 and Fluo-3 AM. C-peptide increased the level of nitrites in murine macrophage Raw264.7 cells. The nitrites production induced by lipopolysaccharide (LPS) was further enhanced by co-treatment of C-peptide. This up-regulation of nitrites generation also correlated with the induction of inducible nitric oxide synthase (iNOS), a prominent marker of macrophage activation. In addition, C-peptide increased the intracellular concentration of calcium levels. Moreover, C-peptide-induced nitrites generation and increase in calcium was observed in freshly isolated primary peritoneal macrophages. In addition, C-peptide specifically affected the Janus activated kinase (JAK)/signal transducer and activated transcription (STAT) pathway. Finally, C-peptide-mediated nitrites generation and JAK2/STAT1 phosphorylation were not detected in the presence of the intracellular calcium chelator, BAPTA-AM. These results suggest that C-peptide may elicit immune modulatory function via modulation of the calcium/JAK–STAT pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI