Research Paper Volume 13, Issue 19 pp 22649—22665
Effects of periostin deficiency on kidney aging and lipid metabolism
- 1 Department of Internal Medicine, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea
- 2 Department of Applied Chemistry, Institute of Natural Science, Global Center for Pharmaceutical Ingredient Materials, Kyung Hee University, Yongin, Korea
- 3 Department of Biomedical Science and Technology, Kyung Hee Medical Science Research Institute, Kyung Hee University, Seoul, Korea
- 4 Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea
- 5 Department of Internal Medicine, Seoul National University Boramae Medical Center, Seoul, Korea
- 6 Department of Urology, College of Medicine, Chung-Ang University, Seoul, Korea
- 7 Seoul National University Kidney Research Institute, Seoul, Korea
- 8 Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea
- 9 Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea
- 10 Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea
Received: February 27, 2021 Accepted: August 31, 2021 Published: October 3, 2021https://doi.org/10.18632/aging.203580
How to Cite
Copyright: © 2021 An et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Periostin plays a crucial role in fibrosis, which is involved in kidney aging. A few studies have shown that lipid metabolism is involved in kidney aging. We investigated the role of periostin in lipid metabolism during kidney aging. Renal function, fibrosis, and inflammatory markers were studied using urine, blood, and tissue samples from wild-type (WT) C57BL/6 mice and Postn-null mice of 2 and 24 months of age. Lipids were quantitatively profiled using liquid chromatography-tandem mass spectrometry in the multiple reaction monitoring mode. Renal function was worse and tubular atrophy/interstitial fibrosis, periostin expression, and inflammatory and fibrotic markers were more severe in aged WT mice than in young WT mice. In aged Postn-null mice, these changes were mitigated. Thirty-five differentially regulated lipids were identified. Phosphatidylcholines, cholesteryl ester, cholesterol, ceramide-1-phosphate, and CCL5 expression were significantly higher in aged WT mice than in aged Postn-null mice. Particularly, linoleic acid, linolenic acid, arachidonic acid, and docosahexaenoic acid differed strongly between the two groups. Lysophosphatidylcholine acyltransferase 2, which converts lysophosphatidylcholine to phosphatidylcholine, was significantly higher in aged WT mice than in aged Postn-null mice. Periostin expression in the kidneys increased with age, and periostin ablation delayed aging. Changes in lipids and their metabolism were found in Postn-null mice. Further research on the precise mechanisms of and relationships between lipid expression and metabolism, kidney aging, and periostin expression is warranted.