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胆碱乙酰转移酶诱导衰老 SAMP1/Kl-/- 小鼠唾液腺的功能再生。

Choline Acetyltransferase Induces the Functional Regeneration of the Salivary Gland in Aging SAMP1/Kl -/- Mice.

机构信息

Department of Pathology, School of Dentistry, Chosun University, Gwangju 61452, Korea.

Department of Biochemistry, School of Oriental Medicine, Dongguk University, Gyeongju 38066, Korea.

出版信息

Int J Mol Sci. 2021 Jan 2;22(1):404. doi: 10.3390/ijms22010404.

DOI:10.3390/ijms22010404
PMID:33401680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7796039/
Abstract

Salivary gland dysfunction induces salivary flow reduction and a dry mouth, and commonly involves oral dysfunction, tooth structure deterioration, and infection through reduced salivation. This study aimed to investigate the impact of aging on the salivary gland by a metabolomics approach in an extensive aging mouse model, SAMP1/Klotho -/- mice. We found that the salivary secretion of SAMP1/Klotho -/- mice was dramatically decreased compared with that of SAMP1/Klotho WT (+/+) mice. Metabolomics profiling analysis showed that the level of acetylcholine was significantly decreased in SAMP1/Klotho -/- mice, although the corresponding levels of acetylcholine precursors, acetyl-CoA and choline, increased. Interestingly, the mRNA and protein expression of choline acetyltransferase (ChAT), which is responsible for catalyzing acetylcholine synthesis, was significantly decreased in SAMP1/Klotho -/- mice. The overexpression of ChAT induced the expression of salivary gland functional markers (α-amylase, ZO-1, and Aqua5) in primary cultured salivary gland cells from SAMP1/Klotho +/+ and -/- mice. In an in vivo study, adeno-associated virus (AAV)-ChAT transduction significantly increased saliva secretion compared with the control in SAMP1/Klotho -/- mice. These results suggest that the dysfunction in acetylcholine biosynthesis induced by ChAT reduction may cause impaired salivary gland function.

摘要

唾液腺功能障碍导致唾液流量减少和口干，并常伴有口腔功能障碍、牙齿结构恶化以及唾液减少导致的感染。本研究旨在通过广泛的衰老小鼠模型 SAMP1/Klotho -/- 小鼠，采用代谢组学方法研究衰老对唾液腺的影响。我们发现，与 SAMP1/Klotho WT (+/+) 小鼠相比，SAMP1/Klotho -/- 小鼠的唾液分泌明显减少。代谢组学分析表明，SAMP1/Klotho -/- 小鼠中的乙酰胆碱水平显著降低，尽管乙酰辅酶 A 和胆碱等乙酰胆碱前体的水平升高。有趣的是，负责催化乙酰胆碱合成的胆碱乙酰转移酶 (ChAT) 的 mRNA 和蛋白表达在 SAMP1/Klotho -/- 小鼠中显著降低。ChAT 的过表达诱导了 SAMP1/Klotho +/+ 和 -/- 小鼠原代唾液腺细胞中唾液腺功能标志物 (α-淀粉酶、ZO-1 和 Aqua5) 的表达。在体内研究中，与对照组相比，腺相关病毒 (AAV)-ChAT 转导显著增加了 SAMP1/Klotho -/- 小鼠的唾液分泌。这些结果表明，ChAT 减少引起的乙酰胆碱生物合成功能障碍可能导致唾液腺功能受损。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1cf/7796039/37bc00c975f6/ijms-22-00404-g006.jpg
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