Dataset Information

ITRAQ-based quantitative proteomic analysis of the global response to 17β-estradiol in estrogen-degradation strain Pseudomonas putida SJTE-1.

ABSTRACT: Microorganism degradation is efficient to remove the steroid hormones like 17β-estradiol (E2); but their degradation mechanism and metabolic network to these chemicals are still not very clear. Here the global responses of the estrogen-degradation strain Pseudomonas putida SJTE-1 to 17β-estradiol and glucose were analyzed and compared using the iTRAQ (isobaric tags for relative and absolute quantization) strategy combined with LC-MS/MS (liquid chromatography-tandem mass spectrometry). 78 proteins were identified with significant changes in expression; 45 proteins and 33 proteins were up-regulated and down-regulated, respectively. These proteins were mainly involved in the processes of stress response, energy metabolism, transportation, chemotaxis and cell motility, and carbon metabolism, considered probably responding to 17β-estradiol and playing a role in its metabolism. The up-regulated proteins in electron transfer, energy generation and transport systems were thought crucial for efficient uptake, translocation and transformation of 17β-estradiol. The over-expression of carbon metabolism proteins indicated cells may activate related pathway members to utilize 17β-estradiol. Meanwhile, proteins functioning in glucose capture and metabolism were mostly down-regulated. These findings provide important clues to reveal the 17β-estradiol degradation mechanism in P. putida and promote its bioremediation applications.

SUBMITTER: Xu J

PROVIDER: S-EPMC5290480 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature

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iTRAQ-based quantitative proteomic analysis of the global response to 17β-estradiol in estrogen-degradation strain Pseudomonas putida SJTE-1.

Xu Jing J Zhang Lei L Hou Jingli J Wang Xiuli X Liu Huan H Zheng Daning D Liang Rubing R

Scientific reports 20170203

Microorganism degradation is efficient to remove the steroid hormones like 17β-estradiol (E2); but their degradation mechanism and metabolic network to these chemicals are still not very clear. Here the global responses of the estrogen-degradation strain Pseudomonas putida SJTE-1 to 17β-estradiol and glucose were analyzed and compared using the iTRAQ (isobaric tags for relative and absolute quantization) strategy combined with LC-MS/MS (liquid chromatography-tandem mass spectrometry). 78 protein ...[more]

PMID: 28155874

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Project description:Rationale17β-Estradiol (E2) attenuates hypoxic pulmonary vasoconstriction and hypoxic pulmonary hypertension (HPH) through an unknown mechanism that may involve estrogen receptors (ER) or E2 conversion to catecholestradiols and methoxyestradiols with previously unrecognized effects on cardiopulmonary vascular remodeling.ObjectivesTo determine the mechanism by which E2 exerts protective effects in HPH.MethodsMale rats were exposed to hypobaric hypoxia while treated with E2 (75 μg/kg/d) or vehicle. Subgroups were cotreated with pharmacologic ER-antagonist or with inhibitors of E2-metabolite conversion. Complementary studies were performed in rats cotreated with selective ERα- or ERβ-antagonist. Hemodynamic and pulmonary artery (PA) and right ventricular (RV) remodeling parameters, including cell proliferation, cell cycle, and autophagy, were measured in vivo and in cultured primary rat PA endothelial cells.Measurements and main resultsE2 significantly attenuated HPH endpoints. Hypoxia increased ERβ but not ERα lung vascular expression. Co-treatment with nonselective ER inhibitor or ERα-specific antagonist rendered hypoxic animals resistant to the beneficial effects of E2 on cardiopulmonary hemodynamics, whereas ERα- and ERβ-specific antagonists opposed the remodeling effects of E2. In contrast, inhibition of E2-metabolite conversion did not abolish E2 protection. E2-treated hypoxic animals exhibited reduced ERK1/2 activation and increased expression of cell-cycle inhibitor p27(Kip1) in lungs and RV, with up-regulation of lung autophagy. E2-induced signaling was recapitulated in hypoxic but not normoxic endothelial cells, and was associated with decreased vascular endothelial growth factor secretion and cell proliferation.ConclusionsE2 attenuates hemodynamic and remodeling parameters in HPH in an ER-dependent manner, through direct antiproliferative mechanisms on vascular cells, which may provide novel nonhormonal therapeutic targets for HPH.

Dataset Information

ITRAQ-based quantitative proteomic analysis of the global response to 17β-estradiol in estrogen-degradation strain Pseudomonas putida SJTE-1.

Publications

iTRAQ-based quantitative proteomic analysis of the global response to 17β-estradiol in estrogen-degradation strain Pseudomonas putida SJTE-1.

Similar Datasets

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