iTRAQ-based quantitative proteomic analysis of thoracic aortas from adult rats born to preeclamptic dams.
iTRAQ-based quantitative proteomic analysis of thoracic aortas from adult rats born to preeclamptic dams.
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基于iTRAQ技术对子痫前期母鼠所产成年子代大鼠胸主动脉的定量蛋白质组学分析
DOI:
10.1186/s12014-021-09327-9
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发表时间:
2021-08-21
影响因子:
3.8
通讯作者:
Pan HT
中科院分区:
文献类型:
--
作者:
Yu B;Zhu HD;Shi XL;Chen PP;Sun XM;Xia GY;Fang M;Zhong YX;Tang XL;Zhang T;Pan HT
Preeclampsia and gestational hypertension can cause vascular function impairment in offspring. In our previous work, we described the protein expression profiles of umbilical artery tissues from patients with preeclampsia. To gain insights into the mechanisms of vascular dysfunction in adult rats born to preeclamptic dams, we analyzed thoracic aorta tissues by using iTRAQ isobaric tags and 2D nano LC-MS/MS. By using the iTRAQ method, we analyzed 1825 proteins, of which 106 showed significantly different expression in the thoracic aortic. Ingenuity pathway analysis (IPA) showed that the majority of differentially expressed proteins (DEPs) were associated with cardiovascular function. Further analysis indicated that glucose-6-phosphate dehydrogenase (G6PD), which is inhibited by miR-423-5p and activated by TP53, had the strongest effect on cardiovascular function. The expression of G6PD was upregulated in thoracic aorta tissues, as confirmed by Western blotting. The expression of two other vascular function-related proteins, cysteine- and glycine-rich protein 2 (CSRP2) and tubulin alpha-4 A (TUBA4A), was upregulated, as demonstrated by mass spectrometry (MS). Although the results require further functional validation, these data provide novel findings related to vascular function impairment in the adult offspring of preeclamptic mothers. The online version contains supplementary material available at 10.1186/s12014-021-09327-9.
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DOI:
10.1042/cs20110627
发表时间:
2012-07
期刊:
Clinical science (London, England : 1979)
影响因子:
--
作者:
Davis EF;Newton L;Lewandowski AJ;Lazdam M;Kelly BA;Kyriakou T;Leeson P
通讯作者:
Leeson P
影响因子:
14.9
作者:
Ma J;Chen T;Wu S;Yang C;Bai M;Shu K;Li K;Zhang G;Jin Z;He F;Hermjakob H;Zhu Y
通讯作者:
Zhu Y
影响因子:
8
作者:
Ambartsumian, N;Klingelhöfer, J;Lukanidin, E
通讯作者:
Lukanidin, E
影响因子:
9.8
作者:
Coates, Brian J.;Broderick, Tom L.;Standley, Cynthia A.
通讯作者:
Standley, Cynthia A.
影响因子:
6.2
作者:
Gupta, Sajal;Aziz, Nabil;Agarwal, Ashok
通讯作者:
Agarwal, Ashok