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胆管结扎小鼠模型甲状腺组织转录组谱分析。

Transcriptome Profile of Thyroid Glands in Bile Duct Ligation Mouse Model.

机构信息

Department of Anatomy, Chonnam National University Medical School, Seoyangro 264, Hwasun 58128, Korea.

Biomedical Science Graduate Program (BMSGP), Chonnam National University, Seoyangro 264, Hwasun 58128, Korea.

出版信息

Int J Mol Sci. 2022 Jul 26;23(15):8244. doi: 10.3390/ijms23158244.

DOI:10.3390/ijms23158244
PMID:35897811
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9332885/
Abstract

Thyroid hormone (TH) contributes to multiple cellular mechanisms in the liver, muscle cells, adipose tissue, and brain, etc. In particular, the liver is an important organ in TH metabolism for the conversion of thyronine (T4) into triiodothyronine (T3) by the deiodinase enzyme. TH levels were significantly decreased and thyroid-stimulating hormone (TSH) levels were significantly increased in patients with liver failure compared with normal subjects. Among liver failure diseases, hepatic encephalopathy (HE) deserves more attention because liver damage and neuropathologies occur simultaneously. Although there is numerous evidence of TH dysregulation in the HE model, specific mechanisms and genetic features of the thyroid glands in the HE model are not fully understood. Here, we investigated the significantly different genes in the thyroid glands of a bile duct ligation (BDL) mouse model as the HE model, compared to the thyroid glands of the control mouse using RNA sequencing. We also confirmed the alteration in mRNA levels of thyroid gland function-related genes in the BDL mouse model. Furthermore, we evaluated the increased level of free T4 and TSH in the BDL mouse blood. Thus, we emphasize the potential roles of TH in liver metabolism and suggest that thyroid dysfunction-related genes in the HE model should be highlighted for finding the appropriate solution for an impaired thyroid system in HE.

摘要

甲状腺激素 (TH) 参与肝脏、肌肉细胞、脂肪组织和大脑等多种细胞机制。特别是肝脏是 TH 代谢的重要器官,通过脱碘酶将甲状腺素 (T4) 转化为三碘甲状腺原氨酸 (T3)。与正常受试者相比,肝衰竭患者的 TH 水平显著降低,促甲状腺激素 (TSH) 水平显著升高。在肝衰竭疾病中,肝性脑病 (HE) 更值得关注,因为肝脏损伤和神经病理学同时发生。尽管有大量证据表明 HE 模型中存在 TH 失调,但对 HE 模型中甲状腺的特定机制和遗传特征仍不完全了解。在这里,我们使用 RNA 测序研究了胆管结扎 (BDL) 小鼠模型(作为 HE 模型)甲状腺中的显著差异基因,与对照小鼠的甲状腺进行了比较。我们还证实了 BDL 小鼠模型中甲状腺功能相关基因的 mRNA 水平发生了改变。此外,我们评估了 BDL 小鼠血液中游离 T4 和 TSH 水平的升高。因此,我们强调了 TH 在肝脏代谢中的潜在作用,并建议突出 HE 模型中与甲状腺功能障碍相关的基因,以找到改善 HE 中受损甲状腺系统的适当解决方案。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/eae4b732fa51/ijms-23-08244-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/195945b5a82c/ijms-23-08244-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/df7eb1367043/ijms-23-08244-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/1658653b9b3a/ijms-23-08244-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/36387f71feb9/ijms-23-08244-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/eae4b732fa51/ijms-23-08244-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/195945b5a82c/ijms-23-08244-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/df7eb1367043/ijms-23-08244-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/1658653b9b3a/ijms-23-08244-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/36387f71feb9/ijms-23-08244-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4c0/9332885/eae4b732fa51/ijms-23-08244-g005.jpg

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