| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Abstract
Placental blood flow, nitric oxide (NO) levels and eNOS
expression increase during human and ovine pregnancy.
Shear stress stimulates NO production and eNOS expression
in ovine fetoplacental artery endothelial (OFPAE) cells.
Being the rate-limiting enzyme essential for NO synthesis,
both the activity and expression of eNOS are closely
regulated. We investigated signaling mechanisms underlying
pulsatile shear stress-induced increases in eNOS
phosphorylation and protein expression by OFPAE cells.
OFPAE cells were cultured at 3 dynes/cm2 shear
stress, then exposed to 15 dynes/ cm2 shear
stress. Western analysis for phosphorylated ERK1/2, Akt,
p38 MAPK, and eNOS showed that shear stress rapidly
increased phosphorylation of ERK1/2 and Akt, but not p38
MAPK. Phosphorylation of eNOS Ser1177 under shear stress
was elevated by 20 min, a response that was blocked by
PI-3K inhibitors wortmannin and LY294002, but not the MEK
inhibitor UO126. bFGF enhanced eNOS protein levels in
static culture via a MEK-mediated mechanism, but it could
not further augment the elevated eNOS protein levels
otherwise induced by the 15 dynes/ shear stress. Blocking
of neither signaling pathway changed the shear
stress-induced increase in eNOS protein levels. In
conclusion, shear stress-induced rapid eNOS
phosphorylation on Ser1177 in OFPAE cells through a PI-3K
dependent pathway. The bFGF-induced rise in eNOS protein
levels in static culture was much less than those observed
under flow, and was blocked by inhibiting MEK. Prolonged
shear stress-stimulated increases in eNOS protein was not
affected by inhibition of MEK- or PI-3K-mediated pathways.
Key words:
Mechanisms of Hormone Action •
Pregnancy •
Growth factors •
Nitric oxide •
Placenta
This article has been cited by other articles:
|
|
 |
|
  O. Yalcin, P. Ulker, U. Yavuzer, H. J. Meiselman, and O. K. Baskurt Nitric oxide generation by endothelial cells exposed to shear stress in glass tubes perfused with red blood cell suspensions: role of aggregation Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2098 - H2105. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Shirasuna, S. Watanabe, T. Asahi, M. P B Wijayagunawardane, K. Sasahara, C. Jiang, M. Matsui, M. Sasaki, T. Shimizu, J. S Davis, et al. Prostaglandin F2{alpha} increases endothelial nitric oxide synthase in the periphery of the bovine corpus luteum: the possible regulation of blood flow at an early stage of luteolysis Reproduction, April 1, 2008; 135(4): 527 - 539. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Zheng, Y. Wen, Y. Song, K. Wang, D.-B. Chen, and R. R Magness Activation of Multiple Signaling Pathways Is Critical for Fibroblast Growth Factor 2- and Vascular Endothelial Growth Factor-Stimulated Ovine Fetoplacental Endothelial Cell Proliferation Biol Reprod, January 1, 2008; 78(1): 143 - 150. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Zheng, Y. Wen, D.-b. Chen, I. M. Bird, and R. R. Magness Angiotensin II Elevates Nitric Oxide Synthase 3 Expression and Nitric Oxide Production Via a Mitogen-Activated Protein Kinase Cascade in Ovine Fetoplacental Artery Endothelial Cells Biol Reprod, June 1, 2005; 72(6): 1421 - 1428. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Zheng, I. M. Bird, D.-B. Chen, and R. R. Magness Angiotensin II regulation of ovine fetoplacental artery endothelial functions: interactions with nitric oxide J. Physiol., May 15, 2005; 565(1): 59 - 69. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
