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突触素的异常DNA甲基化与肾上腺皮质醇分泌腺瘤有关。

Aberrant DNA methylation of synaptophysin is involved in adrenal cortisol-producing adenoma.

作者信息

Zhong Jia-Yu, Cui Rong-Rong, Lin Xiao, Xu Feng, Zhu Ting, Li Fuxingzi, Wu Feng, Zhou En, Yi Lu, Yuan Ling-Qing

机构信息

Department of Metabolism and Endocrinology, National Clinical Research Center for Metabolic Diseases, The Second Xiang-Ya Hospital, Central South University, Changsha, Hunan, People's Republic of China.

Department of Geriatrics, Institute of Aging and Age-related Disease Research, The Second Xiang-Ya Hospital, Central South University, Changsha, Hunan, People's Republic of China.

出版信息

Aging (Albany NY). 2019 Jul 28;11(14):5232-5245. doi: 10.18632/aging.102119.

DOI:10.18632/aging.102119
PMID:31352437
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6682529/
Abstract

Cortisol-producing adenoma (CPA) is the main cause of Adrenal Cushing syndrome. However, its molecular mechanism is not fully understood. Previous study revealed Synaptophysin () is ubiquitously expressed in adrenocortical tumors, but its function in CPA still need to be discovered. In the present study we determine the molecular mechanism involved in dysregulation in CPA and how affects the secretion of cortisol in CPA. Our results showed that aberrant DNA methylation of is involved in CPA progress. Using a miRNA microarray and qRT-PCR, we found decreased expression of miR-27a-5p in CPA compared with normal adrenal tissue. Moreover, the expression of TET3, the target gene of miR-27a-5p, increased in CPA compared with normal adrenal tissue. Knock-down of TET3 resulted in hypermethylation of SYP which reducing the expression level of SYP in H295R cells. The miR-27a-5p-TET3-SYP signalling pathway may regulate proliferation and cortisol secretion in H295R cells and, thus, play a key role in CPA development.

摘要

产生皮质醇的腺瘤（CPA）是肾上腺库欣综合征的主要病因。然而，其分子机制尚未完全明确。既往研究表明，突触素（）在肾上腺皮质肿瘤中普遍表达，但其在CPA中的功能仍有待探索。在本研究中，我们确定了参与CPA中失调的分子机制以及其如何影响CPA中皮质醇的分泌。我们的结果显示，的异常DNA甲基化参与了CPA的进展。通过miRNA微阵列和qRT-PCR，我们发现与正常肾上腺组织相比，CPA中miR-27a-5p表达降低。此外，与正常肾上腺组织相比，miR-27a-5p的靶基因TET3在CPA中的表达增加。敲低TET3导致SYP的高甲基化，从而降低了H295R细胞中SYP的表达水平。miR-27a-5p-TET3-SYP信号通路可能调节H295R细胞的增殖和皮质醇分泌，因此在CPA的发生发展中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/46bd0cb048ef/aging-11-102119-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/f5724ec6b65c/aging-11-102119-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/db3d564d09bc/aging-11-102119-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/a1a1c2858f6b/aging-11-102119-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/4dc4ceb40599/aging-11-102119-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/46bd0cb048ef/aging-11-102119-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/f5724ec6b65c/aging-11-102119-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/db3d564d09bc/aging-11-102119-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/a1a1c2858f6b/aging-11-102119-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/4dc4ceb40599/aging-11-102119-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e9/6682529/46bd0cb048ef/aging-11-102119-g005.jpg

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