Skip to main content
padlock icon - secure page this page is secure

Nitric oxide in bovine corpus luteum: Possible mechanisms of action in luteolysis

Buy Article:

$47.00 + tax (Refund Policy)

ABSTRACT

Although prostaglandin (PG) F is considered as the principal luteolytic factor, its action on the bovine corpus luteum (CL) is mediated by other intraovarian factors. Among them, nitric oxide (NO) seems to play a mandatory role in luteolysis. In this article we review the background and current status of work on possible roles of NO in the CL function, based on available information and our own experimental data. NO is produced in all three main types of bovine CL cells: steroidogenic, endothelial and immune cells. PGF and some luteolytic cytokines (tumor necrosis factor, interferon) increase NO production and stimulate NO synthase expression in the bovine CL. NO inhibits progesterone production, stimulates the secretion of PGF and leukotriene C4, reduces the number of viable luteal cells and, finally, participates in functional luteolysis. NO induces the apoptotic death of CL cells by the modulation of bcl-2 family gene expression and the stimulation of caspase-3 gene expression and activity. However, this simple molecule shows both luteolytic and luteotropic actions during the estrous cycle in ruminants. The aim of this overview is to present and discuss the recent findings crucial for understanding NO role in the process of CL regression in cattle.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Keywords: apoptosis; cattle; corpus luteum; luteolysis; nitric oxide

Document Type: Research Article

Affiliations: 1: Laboratory of Reproductive Immunology, Institute of Animal Reproduction and Food Research, Olsztyn, Poland; and 2: Laboratory of Reproductive Endocrinology, Graduate School of Natural Science and Technology, Okayama University, Okayama, Japan

Publication date: June 1, 2007

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more