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肉鸡腹水综合征肺动脉重构中 mRNA 和 SNP 的表达失调。

Dysregulated expression of mRNA and SNP in pulmonary artery remodeling in ascites syndrome in broilers.

机构信息

Department of Animal Science, Jiangxi Biological Vocational College, Nanchang, Jiangxi 330200, China.

Department of Animal Science, Jiangxi Taihe Lvsejunong Agriculture and Animal Husbandry Food Co., Ltd., Taihe, Jiangxi 343700, China.

出版信息

Poult Sci. 2021 Mar;100(3):100877. doi: 10.1016/j.psj.2020.11.054. Epub 2020 Nov 28.

Abstract

Broiler ascites syndrome (AS), also called pulmonary artery hypertension, is a metabolic disorder that has been observed worldwide in fast-growing broilers. Pulmonary arterial remodeling is a key step in the development of AS. The precise relationship between mRNA and SNP of the pulmonary artery in regulating AS progression remains unclear. In this study, we obtained pulmonary artery tissues from broilers with AS to perform pathologic section and pathologic anatomic observation. SNP, InDel, and mRNA data analysis were carried out using GATK and ANNOVAR software to study the SNP loci of 985 previously reported genes (437 upregulated and 458 downregulated). The pathology results showed that there was a lot of yellow fluid in the abdominal cavity and pericardium, that the ascites cardiac index and hematocrit changed significantly, and that the pulmonary artery had remodeled and become thicker in the disease group. Myocardial sections showed vacuolar degeneration of myocytes and rupture of muscle fibers. In addition, ALDH7A1, IRG1, GGT5, IGSF1, DHX58, USP36, TREML2, SPAG1, CD34, and PLEKHA7 were found to be closely associated with the pathogenesis of pulmonary artery remodeling in AS progression. Taken together, our present study further illuminates the molecular mechanism of pulmonary artery remodeling underlying AS progression.

摘要

肉鸡腹水综合征(AS),又称肺动脉高压,是一种代谢紊乱,在快速生长的肉鸡中已在全球范围内观察到。肺动脉重塑是 AS 发展的关键步骤。肺动脉中 mRNA 和 SNP 调节 AS 进展的确切关系尚不清楚。在这项研究中,我们从患有 AS 的肉鸡中获得肺动脉组织,进行病理切片和病理解剖观察。使用 GATK 和 ANNOVAR 软件对 SNP、InDel 和 mRNA 数据进行分析,以研究 985 个先前报道的基因(437 个上调和 458 个下调)的 SNP 位点。病理结果表明,腹腔和心包中有大量黄色液体,腹水心脏指数和血细胞比容变化明显,疾病组肺动脉发生重塑并变厚。心肌切片显示肌细胞空泡变性和肌纤维破裂。此外,ALDH7A1、IRG1、GGT5、IGSF1、DHX58、USP36、TREML2、SPAG1、CD34 和 PLEKHA7 与 AS 进展中肺动脉重塑的发病机制密切相关。综上所述,我们目前的研究进一步阐明了 AS 进展中肺动脉重塑的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afdd/7936122/01ca4dfc4ab0/gr1.jpg

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