Isoprostanes constrict human radial artery by stimulation of thromboxane receptors, Ca2+ release, and RhoA activation

Mueed, Irem; Tazzeo, Tracy; Liu, Ciaqiong; Pertens, Evi; Zhang, Yongde; Cybulski, Irene; Semelhago, Lloyd; Noora, Joseph; Lamy, André; Teoh, Kevin; Chu, Victor; Janssen, Luke J.

doi:10.1016/j.jtcvs.2007.06.023

Cited by 18 publications

(8 citation statements)

References 28 publications

(35 reference statements)

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“…Thus, we speculated that the mechanism of RA spasm is a calcium‐dependent sensitization mediated by Rho/ROK and plays the major role. Mueed et al 23 reported that isoprostane responses in RA are mediated by prostanoid receptors selective for thromboxane A 2 with activation of Rho‐kinase and release of Ca 2+ , which indicated the role of Rho kinase in RA contraction and can be another piece of evidence to support our conclusion. To confirm our speculation will need further study on the function of RhoA/ROK in the RA.…”

Section: Discussionsupporting

confidence: 76%

RhoA/ROK Pathway Related to the Mechanism of Higher Susceptibility to Spasm in RA Than in IMA

Xia

Wang

Ding³

et al. 2009

Journal of Cardiac Surgery

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Section: Discussionsupporting

confidence: 76%

RhoA/ROK Pathway Related to the Mechanism of Higher Susceptibility to Spasm in RA Than in IMA

Xia

Wang

Ding³

et al. 2009

Journal of Cardiac Surgery

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“…Interestingly, no vasoconstriction was induced in bovine coronary arteries indicating a putative speciesdependent functionality of 8-iso-PGF2α (Kromer and Tippins, 1996). The vasoconstrictor effect of isoprostanes, such as 8-iso-PGF2α and 8-iso-PGE2, is mainly mediated via TP receptors leading to the release of internally sequestered Ca 2+ and activation of the RhoA/Rho kinase 1 and 2 signalling pathway (Kromer and Tippins, 1996;Möbert et al, 1997;Mueed et al, 2008;Sakariassen et al, 2012). On the other hand, bovine aortic ECs possess two distinct binding sites for isoprostanes, indicating that the vasoconstrictor effect of these PG-like compounds may also be mediated by a so far not identified TP receptor-related isoprostane receptor (Yura et al, 1999;van der Sterren and Villamor, 2011).…”

mentioning

confidence: 99%

Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane‐mediated thromboxane A₂ receptor activation

Bauer

Ripperger

Frantz

et al. 2014

British J Pharmacology

139

109

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Isoprostanes are free radical-catalysed PG-like products of unsaturated fatty acids, such as arachidonic acid, which are widely recognized as reliable markers of systemic lipid peroxidation and oxidative stress in vivo. Moreover, activation of enzymes, such as COX-2, may contribute to isoprostane formation. Indeed, formation of isoprostanes is considerably increased in various diseases which have been linked to oxidative stress, such as cardiovascular disease (CVD), and may predict the atherosclerotic burden and the risk of cardiovascular complications in the latter patients. In addition, several isoprostanes may directly contribute to the functional consequences of oxidant stress via activation of the TxA2 prostanoid receptor (TP), for example, by affecting endothelial cell function and regeneration, vascular tone, haemostasis and ischaemia/reperfusion injury. In this context, experimental and clinical data suggest that selected isoprostanes may represent important alternative activators of the TP receptor when endogenous TxA2 levels are low, for example, in aspirin-treated individuals with CVD. In this review, we will summarize the current understanding of isoprostane formation, biochemistry and (patho) physiology in the cardiovascular context. IntroductionOxidative stress in biological systems is defined as an imbalance between the generation of reactive oxygen species (ROS) and antioxidant defence mechanisms (Dalle-Donne et al., 2006;Giustarini et al., 2009). In contrast to the physiological condition, during which ROS are only present at moderate levels and play an important role as messengers in redox signalling, in pathological conditions, when the physiological redox state of cells is disturbed, ROS can severely affect cellular signalling and function. Indeed, ROS which are not neutralized or scavenged by antioxidant molecules, such as GSH or superoxide dismutase, may react with nucleic acids and proteins and thereby alter the biochemical and physical properties of these important cellular components. Moreover, exposure of lipids to free radicals induces a non-enzymatic reaction cascade resulting in an increased formation of bioactive molecules named isoprostanes. Consequently, systemic isoprostane formation is significantly increased in a variety of pathological processes associated with oxidative stress, for example, cancer as well as, cardiovascular, metabolic and neurodegenerative diseases, and isoprostanes are increasingly recognized not only as markers of oxidative stress but also as mediators of disease progression (Praticò et al., 1997;Reilly et al., 1998;Davì et al., 1999;Minuz et al., 2002;Vassalle et al., 2003;Schwedhelm et al., 2004, Xia et al., 2005Montuschi et al., 2007;Schwedhelm et al., 2010; Barocas et al., 2011;Davies and Roberts, 2011; KhademAnsari et al., 2011;Montine et al., 2011;Sbardella et al., 2013). Isoprostanes are PG-like compounds derived from lipid peroxidation of esterified unsaturated fatty acids, for example, arachidonic acid, which are primarily generated in a free rad...

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“…It is noteworthy that lungs and kidneys are among the most affected extrapancreatic tissues in severe acute pancreatitis. In addition, isoprostanes induced vasoconstriction of human radial artery and contraction of vascular smooth muscle from porcine carotid artery via thromboxane A 2 receptors [53], [54], and seem to be involved in angiotensin II-induced vasoconstriction in rabbit aorta or mesentery artery [55]. Furthermore, high isoprostane levels are considered an independent risk factor for coronary heart disease [33].…”

Section: Discussionmentioning

confidence: 99%

Obese Rats Exhibit High Levels of Fat Necrosis and Isoprostanes in Taurocholate-Induced Acute Pancreatitis

et al. 2012

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BackgroundObesity is a prognostic factor for severity in acute pancreatitis in humans. Our aim was to assess the role of oxidative stress and abdominal fat in the increased severity of acute pancreatitis in obese rats.MethodologyTaurocholate-induced acute pancreatitis was performed in lean and obese Zucker rats. Levels of reduced glutathione, oxidized glutathione, L-cysteine, cystine, and S-adenosylmethionine were measured in pancreas as well as the activities of serine/threonine protein phosphatases PP1 and PP2A and tyrosin phosphatases. Isoprostane, malondialdehyde, triglyceride, and free fatty acid levels and lipase activity were measured in plasma and ascites. Lipase activity was measured in white adipose tissue with and without necrosis and confirmed by western blotting.FindingsUnder basal conditions obese rats exhibited lower reduced glutathione levels in pancreas and higher triglyceride and free fatty acid levels in plasma than lean rats. S-adenosyl methionine levels were markedly increased in pancreas of obese rats. Acute pancreatitis in obese rats led to glutathione oxidation and lower reduced glutathione levels in pancreas together with decreased activities of redox-sensitive phosphatases PP1, and PP2A. S-adenosyl methionine levels decreased but cystine levels increased markedly in pancreas upon pancreatitis. Acute pancreatitis triggered an increase in isoprostane levels in plasma and ascites in obese rats. Free fatty acid levels were extremely high in pancreatitis-associated ascitic fluid from obese rats and lipase was bound with great affinity to white adipose tissue, especially to areas of necrosis.ConclusionsOur results show that oxidative stress occurs locally and systemically in obese rats with pancreatitis favouring inactivation of protein phosphatases in pancreas, which would promote up-regulation of pro-inflammatory cytokines, and the increase of isoprostanes which might cause powerful pulmonary and renal vasoconstriction. Future studies are needed to confirm the translational relevance of the present findings obtained in a rat model of taurocholate-induced pancreatic damage and necrosis.

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Isoprostanes constrict human radial artery by stimulation of thromboxane receptors, Ca2+ release, and RhoA activation

Cited by 18 publications

References 28 publications

RhoA/ROK Pathway Related to the Mechanism of Higher Susceptibility to Spasm in RA Than in IMA

RhoA/ROK Pathway Related to the Mechanism of Higher Susceptibility to Spasm in RA Than in IMA

Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane‐mediated thromboxane A₂ receptor activation

Obese Rats Exhibit High Levels of Fat Necrosis and Isoprostanes in Taurocholate-Induced Acute Pancreatitis

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Isoprostanes constrict human radial artery by stimulation of thromboxane receptors, Ca2+ release, and RhoA activation

Cited by 18 publications

References 28 publications

RhoA/ROK Pathway Related to the Mechanism of Higher Susceptibility to Spasm in RA Than in IMA

RhoA/ROK Pathway Related to the Mechanism of Higher Susceptibility to Spasm in RA Than in IMA

Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane‐mediated thromboxane A2 receptor activation

Obese Rats Exhibit High Levels of Fat Necrosis and Isoprostanes in Taurocholate-Induced Acute Pancreatitis

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Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane‐mediated thromboxane A₂ receptor activation