Dataset Information

Enhanced estrogen-induced proliferation in obese rat endometrium.

ABSTRACT:

Objective

We tested the hypothesis that the proliferative estrogen effect on the endometrium is enhanced in obese vs lean animals.

Study design

Using Zucker fa/fa obese rats and lean control, we examined endometrial cell proliferation and the expression patterns of certain estrogen-regulated proproliferative and antiproliferative genes after short-term treatment with estradiol.

Results

No significant morphologic/histologic difference was seen between the obese rats and the lean rats. Estrogen-induced proproliferative genes cyclin A and c-Myc messenger RNA expression were significantly higher in the endometrium of obese rats compared with those of the lean control. Expression of the antiproliferative gene p27Kip1 was suppressed by estrogen treatment in both obese and lean rats; however, the decrease was more pronounced in obese rats. Estrogen more strongly induced the antiproliferative genes retinaldehyde dehydrogenases 2 and secreted frizzled-related protein 4 in lean rats but had little or no effect in obese rats.

Conclusion

Enhancement of estrogen-induced endometrial proproliferative gene expression and suppression of antiproliferative gene expression was seen in the endometrium of obese vs lean animals.

SUBMITTER: Zhang Q

PROVIDER: S-EPMC2880878 | biostudies-literature | 2009 Feb

REPOSITORIES: biostudies-literature

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Publications

Enhanced estrogen-induced proliferation in obese rat endometrium.

Zhang Qian Q Shen Qi Q Celestino Joseph J Milam Michael R MR Westin Shannon N SN Lacour Robin A RA Meyer Larissa A LA Shipley Gregory L GL Davies Peter J A PJ Deng Lei L McCampbell Adrienne S AS Broaddus Russell R RR Lu Karen H KH

American journal of obstetrics and gynecology 20090201 2

<h4>Objective</h4>We tested the hypothesis that the proliferative estrogen effect on the endometrium is enhanced in obese vs lean animals.<h4>Study design</h4>Using Zucker fa/fa obese rats and lean control, we examined endometrial cell proliferation and the expression patterns of certain estrogen-regulated proproliferative and antiproliferative genes after short-term treatment with estradiol.<h4>Results</h4>No significant morphologic/histologic difference was seen between the obese rats and the ...[more]

PMID: 19185100

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Project description:Aniline exposure is associated with toxicity to the spleen leading to splenomegaly, hyperplasia, fibrosis and a variety of sarcomas of the spleen on chronic exposure. In earlier studies, we have shown that aniline exposure leads to iron overload, oxidative stress and activation of redox-sensitive transcription factors, which could regulate various genes leading to a tumorigenic response in the spleen. However, molecular mechanisms leading to aniline-induced cellular proliferation in the spleen remain largely unknown. This study was, therefore, undertaken on the regulation of G1 phase cell cycle proteins (cyclins), expression of cyclin-dependent kinases (CDKs), phosphorylation of retinoblastoma protein (pRB) and cell proliferation in the spleen, in an experimental condition preceding a tumorigenic response. Male SD rats were treated with aniline (0.5 mmol/kg/day via drinking water) for 30 days (controls received drinking water only), and splenocyte proliferation, protein expression of G1 phase cyclins, CDKs and pRB were measured. Aniline treatment resulted in significant increases in splenocyte proliferation, based on cell counts, cell proliferation markers including proliferating cell nuclear antigen (PCNA), nuclear Ki67 protein (Ki67) and minichromosome maintenance (MCM), MTT assay and flow cytometric analysis. Western blot analysis of splenocyte proteins from aniline-treated rats showed significantly increased expression of cyclins D1, D2, D3 and E, as compared to the controls. Similarly, real-time PCR analysis showed significantly increased mRNA expression for cyclins D1, D2, D3 and E in the spleens of aniline-treated rats. The overexpression of these cyclins was associated with increases in the expression of CDK4, CDK6, CDK2 as well as phosphorylation of pRB protein. Our data suggest that increased expression of cyclins, CDKs and phosphorylation of pRB protein could be critical in cell proliferation, and may contribute to aniline-induced tumorigenic response in the spleen.

Dataset Information

Enhanced estrogen-induced proliferation in obese rat endometrium.

Objective

Study design

Results

Conclusion

Publications

Enhanced estrogen-induced proliferation in obese rat endometrium.

Similar Datasets

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