Niacin regulates apolipoprotein M expression via liver X receptor‑α

Yang,Liu; Li,Tie; Zhao,Shuiping; Zhang,Saidan

doi:10.3892/mmr.2019.10557

Niacin regulates apolipoprotein M expression via liver X receptor‑α

Authors:
- Liu Yang
- Tie Li
- Shuiping Zhao
- Saidan Zhang
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Affiliations: International Medical Center, Geriatric Department, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China, Department of Cardiovascular Medicine, Changsha Central Hospital, Changsha, Hunan 410001, P.R. China, Department of Cardiovascular Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China, Department of Cardiovascular Medicine, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China
Published online on: August 6, 2019 https://doi.org/10.3892/mmr.2019.10557
Pages: 3285-3291
Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Niacin is currently the most effective drug that increases HDL‑C levels. Apolipoprotein M (ApoM) in humans is mainly found in plasma high‑density lipoprotein (HDL). Little is known about the role played by niacin in ApoM expression. In this study, the effects of niacin on ApoM expression were assessed as well as the associated mechanism. Human liver cancer cell line HepG2 was treated with niacin alone or with liver X receptor‑α (LXRα) inhibitor at multiple concentrations. The mRNA and protein expression of ApoM were assessed by qRT‑PCR and western blotting. Specific LXRα shRNA was transfected into HepG2 cells to further evaluate the regulatory effects of LXRα on ApoM. An in vivo model was also established to investigate the LXRα inhibitor on the mouse ApoM levels. The comparisons among groups were evaluated using one‑way ANOVA and Student‑Newman‑Keuls test. It was revealed that in HepG2 cells, niacin dose‑dependently increased ApoM gene and protein expression levels. Niacin‑induced upregulation of ApoM was attenuated by an LXRα inhibitor or LXRα shRNA, indicating that LXRα mediated this effect. Moreover, niacin treatment resulted in increased LXRα mRNA levels, in vivo and in vitro; niacin treatment resulted in increased ApoM gene and protein expression levels in mice. In conclusion, niacin upregulates ApoM expression by increasing LXRα expression in vivo and in vitro.

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