For Libraries For Publication Open Access Downloads About Us Contact Us
Paper Titles
Exercise Induce HO-1 Expression in Skeletal Muscle and Improve Sports Ability of Mice
p.243
Expression of a Fusion Protein of Human Proinsulin with Glutathione-S-Transferase in Escherichia coli
p.248
Foxp3 in Lewis Lung Cancer Cells Enhances the Expression of TGF-β1 and IL-10
p.252
In Situ Imaging of Cancer Cell via Cancer Aptamer and its Fluorescent Clusters
p.256
Inhibition of HIF-1α Signaling in the Ovaries of Sprague-Dawley Rats with Polycystic Ovary Syndrome
p.260
IRE1a Negative Regulates Chondrocyte Differentiation
p.265
Neuroprotection of Saponins from Rhizoma panacis majoris in Cerebral Ischemia/Reperfusion is Related to Nrf2-Mediated Antioxidant Response: Role of Nrf2 and Bcl-2 Family Expressions
p.269
Optimum the Fermentation Condition to Produce the Polysaccharide of Hericium erinaceus with Tofu Whey
p.275
PLK1 Promotes Invasion of Esophageal Squamous Cell Carcinoma Cells through Inducing Epithelial-Mesenchymal Transition
p.279

Inhibition of HIF-1α Signaling in the Ovaries of Sprague-Dawley Rats with Polycystic Ovary Syndrome

Article Preview

Abstract:

Polycystic ovary syndrome (PCOS) is a major public health problem in reproductive-aged women worldwide, but the precise pathogenesis of PCOS remains unclear. Our previous study has clarified that hypoxia-inducible factor-1alpha (HIF-1α) mediated endthlin-2 (ET-2) signaling plays an important role in the ovulatory process in rats. Therefore, the present study used PCOS rat model to test the hypothesis that HIF-1α signaling is inhibited in ovaries during PCOS fromation. By the changed of bodyweight, ovarian histology and ovarian weight, PCOS rat model was further confirmed. And then the present study examined the changes of ET-2 and HIF-1α mRNA levels through real-time PCR finding the significant decrease of ET-2 mRNA level in PCOS rat ovaries was found, while HIF-1α mRNA significantly increased. However, by western blot analysis, the present study found HIF-1α protein expression was significantly decreased, which is consistent with ET-2 protein expression implying HIF-1α-medated ET-2 signaling is vital during PCOS formation. Moreover, the result of HIF prolyl hyodroxylase activity analysis found the decrease of HIF-1α protein may be caused through HIF protein degradation by the increased HIF prolyl hyodroxylase activity. Taken together, these results indicate that HIF-1α signaling is inhibited in PCOS rat model through increase of HIF prolyl hyodroxylase activity suggesting HIF-1α signaling plays an important role in the formation of PCOS. This HIF-1α-mediaged ET-2 expression may be on of the important mechanisms regulating PCOS formation in mammalian ovaries in vivo. Keywords: HIF-1α; ET-2; HIF prolyl hyodroxylase acitvity; polycystic ovary syndrome

You might also be interested in these eBooks
Advances in Applied Sciences, Engineering and Technology II View Preview

Info:

Periodical:

Advanced Materials Research (Volumes 998-999)

Pages:

260-264

DOI:

https://doi.org/10.4028/www.scientific.net/AMR.998-999.260

Citation:

Cite this paper

Online since:

July 2014

Authors:

Fan Wang, Yan Qing Wu, Kai Zhuan Xiao, Zheng Hong Zhang, Qing Wang, Lu Qiang Huang, Zheng Chao Wang*

Keywords:

ET-2, HIF Prolyl Hyodroxylase Acitvity, HIF-1α, Polycystic Ovary Syndrome

Export:

RIS, BibTeX

Price:

Permissions CCC:

Request Permissions

Permissions PLS:

Request Permissions

Сopyright:

© 2014 Trans Tech Publications Ltd. All Rights Reserved

Share:

Citation:

* - Corresponding Author

References

[1] I.F. Stein and M.L. Leventhal: Am. J. Obstet. Gynecol Vol. 29 (1935), pp.181-191.

Google Scholar

[2] R.J. Norman, D. Dewailly, R.S. Legro and T.E. Hickey: Lancet Vol. 370 (2007), pp.685-697.

DOI: 10.1016/s0140-6736(07)61345-2

Google Scholar

[3] S.M. Sirmans and K.A. Pate: Clin. Epidemiol Vol. 6 (2013), pp.1-13.

Google Scholar

[4] R. Homburg: Best. Prac. Res. Clin. Obstet. Gynaecol Vol. 18 (2004), pp.773-788.

Google Scholar

[5] P. Chakraborty, S.K. Goswami, S. Rajani, S. Sharma, S.N. Kabir, B. Chakravarty and K. Jana: PLoS. One Vol. 8 (2013), p.64446.

Google Scholar

[6] J. Zhang, Z. Zhang, Y. Wu, L. Chen, Q. Luo, J. Chen, X. Huang, Y. Cheng and Z. Wang: J. Reprod. Dev Vol. 58 (2012), pp.678-684.

Google Scholar

[7] Z. Wang, Z. Zhang, Y. Wu, L. Chen, Q. Luo, J. Zhang, J. Chen, Z. Luo, X. Huang and Y. Cheng: Exp. Mol. Med Vol. 44 (2012), pp.615-621.

Google Scholar

[8] L. Poretsky, J. Clemons and K. Bogovich. Metabolism Vol. 41 (1992), pp.903-910.

Google Scholar

[9] P. Richard-Fiardo, E. Payen, R. Chèvre, J. Zuber, E. Letrou-Bonneval, Y. Beuzard and B. Pitard: Hum. Gene. Ther Vol. 19 (2008), pp.331-342.

DOI: 10.1089/hum.2006.0101

Google Scholar

[10] Z. Wang, Q. Zhu, M. Xia, P.L. Li, S.J. Hinton and N. Li: Hypertension Vol. 55 (2010), pp.1129-1136.

Google Scholar

[11] C. Ko, M.C. Gieske, L. Al-Alem, Y. Hahn, W. Su, M.C. Gong, M. Iglarz and Y Koo: Endocrinology Vol. 147 (2006), pp.1770-1779.

DOI: 10.1210/en.2005-1228

Google Scholar

[12] L. Al-Alem, P.J. Bridges, W. Su, M.C. Gong, M. Iglarz and C. Ko: J. Endocrinol Vol. 193 (2007), pp.383-391.

Google Scholar

[13] G. Na, P.J. Bridges, Y. Koo, C. Ko: Can. J. Physiol. Pharmacol Vol. 86 (2008), pp.310-319.

Google Scholar

[14] J. Kim, I.C. Bagchi and M.K. Bagchi: Endocrinology Vol. 150 (2009), pp.3392-3400.

Google Scholar

[15] Z. Wang, L. Tang, Q. Zhu, F. Yi, F. Zhang, P.L. Li and N. Li: Kidney. Int Vol. 79 (2011), pp.300-310.

Google Scholar

[16] Z. Zhang, D. Yin and Z. Wang: Anim. Sci. J Vol. 82 (2011), pp.244-250.

Google Scholar

[17] Z. Zhang, D. Yu, D. Yin and Z. Wang: Anim. Reprod. Sci Vol. 125 (2011), pp.42-48.

Google Scholar

[18] A.A. Kazi, J.M. Jones and R.D. Koos: Mol Endocrinol Vol. 19 (2005), p.2006-(2019).

Google Scholar

[19] A.A. Kazi and R.D. Koos: Endocrinology Vol. 148 (2007), pp.2363-2374.

Google Scholar

[20] K.H. Molitoris, A.A. Kazi and R.D. Koos: Endocrinology Vol. 150 (2009), pp.5405-5414.

Google Scholar

[21] R.K. Bruick and S.L. McKnight: Science Vol. 294 (2001), pp.1337-1340.

Google Scholar

[22] M. Ivan, K. Kondo, H. Yang, W. Kim, J. Valiando, M. Ohh, A. Salic, J.M. Asara, W.S. Lane and W.G. Kaelin: Science Vol. 292 (2001), pp.464-468.

DOI: 10.1126/science.1059817

Google Scholar

[23] P. Jaakkola, D.R. Mole, Y.M. Tian, M.I. Wilson, J. Gielbert, S.J. Gaskell, A. Kriegsheim, H.F. Hebestreit, M. Mukherji, C.J. Schofield, P.H. Maxwell, C.W. Pugh and P.J. Ratcliffe: Science Vol. 292 (2001), pp.468-472.

DOI: 10.1126/science.1059796

Google Scholar

[24] L.M. Seeber, N. Horree, M.A. Vooijs, A.P. Heintz, E. van der Wall, R.H. Verheijen and P.J. van Diest: Crit. Rev. Oncol. Hematol Vol. 78 (2011), pp.173-184.

DOI: 10.1016/j.critrevonc.2010.05.003

Google Scholar

[25] A. Galanis, A. Pappa, A. Giannakakis, E. Lanitis, D. Dangaj and R. Sandaltzopoulos: Cancer. Lett Vol. 266 (2008), pp.12-20.

DOI: 10.1016/j.canlet.2008.02.028

Google Scholar

[26] M. Miyazawa, M. Yasuda, M. Fujita, T. Hirasawa, H. Kajiwara, K. Hirabayashi, N. Ogane, M. Shimizu, H. Asanuma, M. Murakami, S. Takekoshi, M. Mikami, R.Y. Osamura: Arch. Gynecol. Obstet Vol. 279 (2009), pp.789-796.

DOI: 10.1007/s00404-008-0816-z

Google Scholar

© 2025 Trans Tech Publications Ltd. All rights are reserved, including those for text and data mining, AI training, and similar technologies. For open access content, terms of the Creative Commons licensing CC-BY are applied.
Scientific.Net is a registered trademark of Trans Tech Publications Ltd.