| Literature DB >> 34209567 |
Hidehito Saito-Takatsuji1, Yasuo Yoshitomi1, Yasuhito Ishigaki2, Shoko Yamamoto3, Noriaki Numata3, Yasuo Sakai3, Masayoshi Takeuchi4, Naohisa Tomosugi5, Shogo Katsuda6, Hideto Yonekura1, Takayuki Ikeda1.
Abstract
Collagen tripeptide (CTP) is defined as a functional food material derived from collagenase digests of type I collagen and contains a high concentration of tripeptides with a Gly-X-Y sequence. CTP has several biological effects, including the acceleration of fracture healing, ameliorating osteoarthritis, and improving dryness and photoaging of the skin. Recently, an antiatherosclerotic effect of CTP has been reported, although its molecular mechanism is yet to be determined. In this study, we examined the effects of CTP on primary cultured human aortic endothelial cells (HAECs) under oxidative stress, because oxidative endothelial dysfunction is a trigger of atherosclerosis. DNA microarray and RT-qPCR analyses showed that CTP treatment recovered the downregulated expression of several genes, including the interleukin-3 receptor subunit alpha (IL3RA), which were suppressed by reactive oxygen species (ROS) treatment in HAECs. Furthermore, IL3RA knockdown significantly decreased the viability of HAECs compared with control cells. RT-qPCR analysis also showed that solute carrier 15 family peptide transporters, which are involved in CTP absorption into cells, were expressed in HAECs at levels more than comparable to those of a CTP-responsive human osteoblastic cell line. These results indicated that CTP exerts a protective effect for HAECs, at least in part, by regulating the recovery of ROS-induced transcriptional repression.Entities:
Keywords: collagen tripeptide; gene expression; human aortic endothelial cells; oxidative stress
Year: 2021 PMID: 34209567 DOI: 10.3390/nu13072226
Source DB: PubMed Journal: Nutrients ISSN: 2072-6643 Impact factor: 5.717