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Protective Effects of Collagen Tripeptides in Human Aortic Endothelial Cells by Restoring ROS-Induced Transcriptional
Hidehito Saito-Takatsuji1, Yasuo Yoshitomi1, Yasuhito Ishigaki2
1Department of Biochemistry, Kanazawa Medical University School of Medicine, 1-1 Daigaku, Uchinada, Kahoku-gun, Ishikawa 920-0293, Japan.
Nutrients
|July 2, 2021
Summary
Collagen tripeptide (CTP) protects human aortic endothelial cells from oxidative stress by restoring gene expression. This suggests CTP may help prevent atherosclerosis by improving endothelial cell function.
Area of Science:
- Biochemistry
- Cell Biology
- Cardiovascular Research
Background:
- Collagen tripeptide (CTP), derived from type I collagen, possesses various biological activities.
- Oxidative endothelial dysfunction is a key factor in the development of atherosclerosis.
- The molecular mechanisms underlying the antiatherosclerotic effects of CTP are not fully understood.
Purpose of the Study:
- To investigate the protective effects of CTP on human aortic endothelial cells (HAECs) under oxidative stress.
- To elucidate the molecular mechanisms by which CTP may prevent atherosclerosis.
Main Methods:
- Primary cultured HAECs were subjected to oxidative stress using reactive oxygen species (ROS).
- DNA microarray and quantitative real-time PCR (RT-qPCR) were used to analyze gene expression changes.
- Interleukin-3 receptor subunit alpha (IL3RA) knockdown was performed to assess its role in cell viability.
- RT-qPCR was used to evaluate the expression of CTP transporters in HAECs.
Main Results:
- CTP treatment reversed ROS-induced downregulation of specific genes, including IL3RA, in HAECs.
- Knockdown of IL3RA significantly reduced HAEC viability, indicating its importance.
- HAECs express peptide transporters (solute carrier 15 family) capable of absorbing CTP.
Conclusions:
- CTP exerts a protective effect on HAECs against oxidative stress.
- This protection is, in part, mediated by CTP's ability to restore gene expression suppressed by ROS.
- CTP may prevent atherosclerosis by preserving endothelial cell function and integrity.
