Human Reproduction, Vol. 19, No. 1, 30-40,
January 2004
© 2004 European Society of Human Reproduction and Embryology
Expression of nitric oxide synthase and effect of substrate manipulation of the nitric oxide pathway in mouse ovarian follicles
Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, UK
1 Present address: Bourn Hall, Bourn, Cambridge CB3 7TR, UK
2 To whom correspondence should be addressed. e-mail: geraldine.hartshorne{at}warwick.ac.uk
BACKGROUND: Nitric oxide (NO) is a cell messenger with multiple actions in different biological systems, implicated in the control of follicle and oocyte function. NO is formed from L-arginine by isoforms of nitric oxide synthase (NOS) via NG-hydroxy-L-arginine, with L-citrulline as a byproduct. This study aimed to show how modulation of NO by manipulating NOS substrates would affect mouse follicle growth and ovulation in vitro, where vascular effects of NO are attenuated. METHODS: Immunohistochemistry [endothelial (eNOS) and inducible (iNOS)] and in situ hybridization (iNOS) were applied on mouse ovaries. Cultured follicles were also stained for iNOS by immunohistochemistry. For follicles cultured in the presence or absence of L-arginine, the ability of L-citrulline or NG-hydroxy-L-arginine to substitute for L-arginine was assessed in terms of follicle growth and ovulation. RESULTS: iNOS and eNOS were localized in oocytes and theca, with some staining in granulosa. iNOS mRNA occurred predominantly in granulosa and oocyte. Omission of L-arginine significantly reduced follicle survival and ovulation. Partial compensation for L-arginine withdrawal was achieved with L-citrulline and NG-hydroxy-L- arginine. Specific abnormalities of follicle growth were noted. CONCLUSIONS: NOS is present in mouse follicles, and its action is necessary at a local level for normal follicle development in vitro. Reduced growth, persistent basement membranes and reduced ovulation were associated with in vitro disruption of NO.
Key words: mouse follicles/nitric oxide/nitric oxide synthase/oocytes/ovulation
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  A. T Grazul-Bilska, C. Navanukraw, M. L. Johnson, D. A Arnold, L. P Reynolds, and D. A Redmer Expression of endothelial nitric oxide synthase in the ovine ovary throughout the estrous cycle. Reproduction, October 1, 2006; 132(4): 579 - 587. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K.R. Barnett, C. Schilling, C.R. Greenfeld, D. Tomic, and J.A. Flaws Ovarian follicle development and transgenic mouse models Hum. Reprod. Update, September 1, 2006; 12(5): 537 - 555. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Vaisanen-Tommiska, R. Butzow, O. Ylikorkala, and T. S. Mikkola Mifepristone-induced nitric oxide release and expression of nitric oxide synthases in the human cervix during early pregnancy Hum. Reprod., August 1, 2006; 21(8): 2180 - 2184. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L.-J. Huo, C.-G. Liang, L.-Z. Yu, Z.-S. Zhong, Z.-M. Yang, H.-Y. Fan, D.-Y. Chen, and Q.-Y. Sun Inducible nitric oxide synthase-derived nitric oxide regulates germinal vesicle breakdown and first polar body emission in the mouse oocyte Reproduction, April 1, 2005; 129(4): 403 - 409. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-F. Huang, B. Wang, X.-F. Yang, Q. Luo, and J.-Z. Sheng Nitric Oxide Mediates Inhibitory Effect of Leptin on Insulin-Like Growth Factor I Augmentation of 17{beta}-Estradiol Production in Human Granulosa Cells Biol Reprod, January 1, 2005; 72(1): 102 - 106. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. M. Mitchell, C.R. Kennedy, and G. M. Hartshorne Pharmacological manipulation of nitric oxide levels in mouse follicle cultures demonstrates key role of extrafollicular control of ovulation Hum. Reprod., August 1, 2004; 19(8): 1705 - 1712. [Abstract] [Full Text] [PDF]
|
|