scholarly journals Downregulation of cyclooxygenase-1 is involved in gastric mucosal apoptosis via death signaling in portal hypertensive rats

Cell Research ◽  
2009 ◽  
Vol 19 (11) ◽  
pp. 1269-1278 ◽  
Author(s):  
Bin Wu ◽  
Lixian Zeng ◽  
Ying Lin ◽  
Zhuofu Wen ◽  
Guihua Chen ◽  
...  
Keyword(s):  
Hypertensive Rats ◽  
Cyclooxygenase 1 ◽  
Mucosal Apoptosis

scholarly journals Exercise-Induced Modulation of Angiotensin II Responses in Femoral Veins From 2-Kidney-1-Clip Hypertensive Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Agnaldo Bruno Chies ◽  
Maria Angélica Spadella ◽  
Priscila Ramos de Oliveira ◽  
Raquel Fantin Domeniconi ◽  
Talita de Mello Santos ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Acute Exercise ◽  
Organ Bath ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Cyclooxygenase 1 ◽  
Single Bout ◽  
Cox 2 ◽  
Exercise Induced ◽  
Cox 1

The present study investigated the angiotensin II (Ang II) responses in rat femoral veins taken from 2-kidney-1clip (2K1C) hypertensive rats at 4 weeks after clipping, as well as the effects of exercise on these responses. In this manner, femoral veins taken from 2K1C rats kept at rest or exposed to acute exercise or to exercise training were challenged with Ang II or endothelin-1 (ET-1) in organ bath. Simultaneously, the presence of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were determined in these preparations by western blotting. In these experiments, femoral veins exhibited subdued Ang II responses. However, after nitric oxide (NO) synthesis blockade, the responses were higher in the femoral veins taken from animals kept at rest [0.137(0.049–0.245); n = 10] than those obtained in trained animals kept at rest [0.008(0.001–0.041); n = 10] or studied after a single bout of exercise [0.001(0.001–0.054); n = 11]. In preparations in which, in addition to NO synthesis, both the local production of prostanoids and the action of ET-1 on type A (ETA) or B (ETB) receptors were inhibited, the differences induced by exercise were no longer observed. In addition, neither ET-1 responses nor the presence of COX-1 and COX-2 in these preparations were modified by the employed exercise protocols. In conclusion, NO maintains Ang II responses reduced in femoral veins of 2K1C animals at rest. However, vasodilator prostanoids as well as other relaxing mechanisms, activated by ETB stimulation, are mobilized by exercise to cooperate with NO in order to maintain controlled Ang II responses in femoral veins.

scholarly journals Enhanced cyclooxygenase-1 expression within the superior mesenteric artery of portal hypertensive rats: Role in the hyperdynamic circulation

Hepatology ◽  
1998 ◽  
Vol 27 (1) ◽  
pp. 20-27 ◽  
Author(s):  
Ming-Chih Hou ◽  
Paul A. Cahill ◽  
Shuangmin Zhang ◽  
Yi-Ning Wang ◽  
Richard J. Hendrickson ◽  
...  
Keyword(s):  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Hypertensive Rats ◽  
Hyperdynamic Circulation ◽  
Cyclooxygenase 1

Differential role of cyclooxygenase-1 and -2 on renal vasoconstriction to α1-adrenoceptor stimulation in normotensive and hypertensive rats

Life Sciences ◽  
2013 ◽  
Vol 93 (16) ◽  
pp. 552-557 ◽  
Author(s):  
Estela D'Abril Ruíz-Leyja ◽  
Rafael Villalobos-Molina ◽  
Juan Javier López-Guerrero ◽  
Itzell Alejandrina Gallardo-Ortíz ◽  
Samuel Enoch Estrada-Soto ◽  
...  
Keyword(s):  
Hypertensive Rats ◽  
Renal Vasoconstriction ◽  
Cyclooxygenase 1

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

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