2009
DOI: 10.1016/j.atherosclerosis.2008.05.059
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Enhanced expression of vascular cell adhesion molecule-1 by corticotrophin-releasing hormone contributes to progression of atherosclerosis in LDL receptor-deficient mice

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Cited by 23 publications
(18 citation statements)
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“…Similarly, changes in gene expression of stress-signaling receptors were not observed in the colon of naïve or NMS mice. The current study revealed an overall negative impact of NMS on colorectal sensitivity, both at baseline and following WAS, which is contradictory to previous studies using a 14d-long NMS protocol in either rats (Coutinho et al, 2002; O’Malley et al, 2011; Wu et al, 2009) or mice (Moloney et al, 2012) and suggests that a three-week long NMS protocol in female mice may generate a hypersensitive phenotype that, among the pelvic viscera, is restricted to the urogenital organs (Pierce et al, 2014). This observation highlights the importance of noting the duration of stress and the strain and sex of the animal used across differing NMS protocols.…”
Section: Discussioncontrasting
confidence: 99%
“…Similarly, changes in gene expression of stress-signaling receptors were not observed in the colon of naïve or NMS mice. The current study revealed an overall negative impact of NMS on colorectal sensitivity, both at baseline and following WAS, which is contradictory to previous studies using a 14d-long NMS protocol in either rats (Coutinho et al, 2002; O’Malley et al, 2011; Wu et al, 2009) or mice (Moloney et al, 2012) and suggests that a three-week long NMS protocol in female mice may generate a hypersensitive phenotype that, among the pelvic viscera, is restricted to the urogenital organs (Pierce et al, 2014). This observation highlights the importance of noting the duration of stress and the strain and sex of the animal used across differing NMS protocols.…”
Section: Discussioncontrasting
confidence: 99%
“…IL-8 is a potent neutrophil chemotactic factor that promotes and prolongs the inflammatory response (31). Wu et al identified that NF-κB also induces the production and release of ICAM-1 (32), which dilates blood vessels, causes the migration of inflammatory cells and induces the release of cytokines and chemokines into adherent tissues. A previous study demonstrated that the expression of VCAM-1, ICAM-1 and NF-κB mRNA in cardiac microvascular endothelial cells in reperfusion injury is suppressed by APS (33).…”
Section: Discussionmentioning
confidence: 99%
“…CRFR1 antagonists have also been utilized in the treatment of inflammatory diseases. Our previous data showed that atherosclerotic lesions in LDLR -/-mice were obviously attenuated by the selective CRFR1 antagonist NBI-27914 when given subcutaneously [20]. We also showed that intraperitoneal injection of NBI-27914 could significantly relieve the signs of intensified ischemia in a rat model of thromboangiitis obliterans [21].…”
Section: Crf-bp In Inflammationmentioning
confidence: 84%
“…Our previous data demonstrated that aerosol inhalation of UCN 1 could increase pulmonary vascular permeability via mast cell infiltration and activation [18], and that mast cell activation and degranulation induced by UCN 1 was mediated by increasing intracellular calcium concentration, which could be blocked by a selective CRFR1 antagonist, but not by a CRFR2 antagonist [19]. Furthermore, it was shown by us that the activation of CRFR1 by CRF induced greater expression of VCAM-1, which contributed to the progression of atherosclerosis in LDL-receptor-deficient mice [20]. Our newly published data also showed that the activation of CRFR1 promoted the development of vasculitis in rats, which was due to the up-regulation of COX-2 and ICAM-1 [21].…”
Section: Crfr1 In Inflammationmentioning
confidence: 84%