Myometrial Relaxation and Contraction Pathways (Pan troglodytes)

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<Pathway xmlns="http://genmapp.org/GPML/2008a" Name="Myometrial Relaxation and Contraction Pathways" Data-Source="GenMAPP 2.0" Version="20041203" Author="Nathan Salomonis" Email="nsalomonis@gladstone.ucsf.edu" Last-Modified="7/29/2009" Organism="Pan troglodytes">
  <Comment Source="GenMAPP notes">References:                                                   (1) Up-regulation of nitric oxide synthase and modulation of the guanylate cyclase activity by corticotropin-releasing hormone but not urocortin II or urocortin III in cultured human pregnant myometrial cells.
Aggelidou E, Hillhouse EW, Grammatopoulos DK.   PMID: 11854458                                                                             (2) Is up-regulation of phosphodiesterase 4 activity by PGE2 involved in the desensitization of beta-mimetics in late pregnancy human myometrium?

Mehats C, Tanguy G, Dallot E, Cabrol D, Ferre F, Leroy MJ.     PMID: 11701706</Comment>
  <Comment Source="GenMAPP remarks">Right-click here to see references</Comment>
  <Comment Source="WikiPathways-category">Physiological Process</Comment>
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Rozen F, Russo C, Banville D, Zingg HH PMID: 7816817                                              quote: The presence of APREs in the OTR gene promoter suggests that the acute induction of OTR expression at the onset of parturition may be a phenomenon mechanistically similar to the fast induction of acute phase response genes. This notion is strengthened by the observation that the uterus is populated by macrophages and other specific lymphocytes (19,20).  Specifically, at term, nearly half of the decidual cells are of bone marrow origin (20).  IL-1beta released from macrophages stimulates the production and release of IL-6 by uterine stromal cells (21,22).  Moreover, IL- is a central pathophysiological mediator of infection-induced premature delivery (23), and preterm delivery can be prevented by an IL-1 antagonist in mice (24).  We speculate that under physiological as well as phathophysiological conditions, inflammatory cytokines are important inducers of labor and that this mechanism involves the cytokine-induced transcriptional activation of the OTR gene. :end quote

19. Hunt, J.S. (1994) Biol. Reprod. 50, 461-466
20. Vince, G.S., et al. (1990) J. Immunol. Methods 132, 181-189.
21. Tabibzadeh, S. (1991) Endocr. Rev, 12, 272-290.
22. Dudley, D.Jl, et. Al. (1992) J. Clin. Endocrinol. Metab. 74, 884-889
23. Romero, R., et. Al, Am. J. Obstet. Gynecol. 167, 863-872.
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Rozen F, Russo C, Banville D, Zingg HH PMID: 7816817                                              quote: The presence of APREs in the OTR gene promoter suggests that the acute induction of OTR expression at the onset of parturition may be a phenomenon mechanistically similar to the fast induction of acute phase response genes. This notion is strengthened by the observation that the uterus is populated by macrophages and other specific lymphocytes (19,20).  Specifically, at term, nearly half of the decidual cells are of bone marrow origin (20).  IL-1beta released from macrophages stimulates the production and release of IL-6 by uterine stromal cells (21,22).  Moreover, IL- is a central pathophysiological mediator of infection-induced premature delivery (23), and preterm delivery can be prevented by an IL-1 antagonist in mice (24).  We speculate that under physiological as well as phathophysiological conditions, inflammatory cytokines are important inducers of labor and that this mechanism involves the cytokine-induced transcriptional activation of the OTR gene. :end quote

19. Hunt, J.S. (1994) Biol. Reprod. 50, 461-466
20. Vince, G.S., et al. (1990) J. Immunol. Methods 132, 181-189.
21. Tabibzadeh, S. (1991) Endocr. Rev, 12, 272-290.
22. Dudley, D.Jl, et. Al. (1992) J. Clin. Endocrinol. Metab. 74, 884-889
23. Romero, R., et. Al, Am. J. Obstet. Gynecol. 167, 863-872.
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