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Sogol Gachkar, Sebastian Nock, Cathleen Geissler, Rebecca Oelkrug, Kornelia Johann, Julia Resch, Awahan Rahman, Anders Arner, Henriette Kirchner and Jens Mittag

to dissect the genomic and non-genomic effects of TH on the aorta, both on the functional level using myography to record the aortic responses to a contractile stimulus as well as on the molecular level studying cytosolic and genomic signalling

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Laura Sabatino, Claudia Kusmic, Giuseppina Nicolini, Rosario Amato, Giovanni Casini, Giorgio Iervasi and Silvana Balzan

signaling has arisen in the infarcted area, it could also reach a more distant vessel, such as the aorta. In particular, the system of the angiopoietins 1/2 (Ang1/2) and tyrosine kinase receptor 2 (Tie2) is essential in angiogenesis and blood vessel

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R. M. Haigh, C. T. Jones and G. Milligan

ABSTRACT

Glucocorticoids are known to influence cardiovascular sensitivity to catecholamines but the molecular mechanisms are undefined. We recently showed that glucocorticoids control the coupling of adrenergic receptors to G protein. Alterations in the amount of G protein is one mechanism by which receptor-G protein coupling may be controlled. Therefore, we set out to measure the levels of G proteins in aorta from normal, adrenalectomized and dexamethasonetreated adrenalectomized rats. G proteins were measured in plasma membrane preparations by immunoblotting and horseradish peroxidase staining. After adrenalectomy there was a 53% (n = 5) decrease in the density of staining for Gi (ANOVA; P<0.05 compared to controls). Conversely, there was a 210% (n = 5) increase in the density of staining for Gs. The levels of Go and the β-subunit of G proteins were not changed by adrenalectomy. Dexamethasone-replacement treatment after adrenalectomy returned Gi and Gs close to control values. Go remained unaltered compared to controls but was 24% (n=3) less than the adrenalectomized values (ANOVA; P<0.05). The levels of β-subunit after dexamethasone replacement were significantly greater (ANOVA; P<0.05) than both the controls and adrenalectomized values. These results show that glucocorticoids can differentially regulate the amounts of G proteins in rat aorta as in other tissues. This may be an important mechanism by which steroids control receptor-G protein coupling and hence transmembrane signalling pathways in vascular smooth muscle.

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Dongxing Zhu, Neil C W Mackenzie, Jose Luis Millan, Colin Farquharson and Vicky E MacRae

genotypes, genomic DNA was isolated from ear clips and analysed using PCR protocols developed by Genetyper (New York, NY, USA). Primary murine VSMC isolation Primary VSMCs were isolated from 5-week-old WT male C57BL/6 mice. Following dissection of the aorta

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Pabitra B Pal, Himangshu Sonowal, Kirtikar Shukla, Satish K Srivastava and Kota V Ramana

. Immunoblotting Treated HUVECs were washed with cold PBS and lysed in RIPA lysis buffer containing 1× phosphatase and protease inhibitor cocktail and centrifuged to obtain cell supernatants. Heart and aorta tissues were homogenized in RIPA buffer containing a

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Huan Zhang, Xiuxia Liu, Shanshan Zhou, Ye Jia, Ying Li, Yuguo Song, Junnan Wang and Hao Wu

600125 was found to activate NRF2 in the aortas of the diabetic mice ( Liu et al . 2014 ), suggesting that JNK may negatively regulate NRF2. However, whether or to what extent NRF2 is required for SP600125’s protective effect was unknown. By using Nrf2

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Yukinori Kazeto, Rie Goto-Kazeto, Peter Thomas and John M Trant

-specific expression of catfish and zebrafish mPRs Total RNA (1 μg) prepared from various tissues (i.e., parts of the brain (telencephalon, cerebellum, diencephalon, hypothalamus and hindbrain), pituitary, gill, ventral aorta, intestine, muscle, heart, spleen

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Mu-Hsin Chang, Wei-Wen Kuo, Ray-Jade Chen, Ming-Chin Lu, Fuu-Jen Tsai, Wu-Hsien Kuo, Ling-Yun Chen, Wen-Jun Wu, Chih-Yang Huang and Chun-Hsien Chu

et al . 2006 ). In our previous study, the upregulation of IGF-II and IGF2R genes were detected in rats made hypertensive by abdominal aorta ligation and H9c2 cardiomyoblast cells treated with ANGII ( Lee et al . 2006 ). Based on these findings, we

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R. M. Haigh and C. T. Jones

ABSTRACT

Glucocorticoids are known to have marked effects on blood pressure regulation, predominantly through altering cardiovascular sensitivity to noradrenaline. However, the molecular mechanisms underlying this action remain unclear. As part of our studies into these we have measured α1-adrenergic receptor binding using the ligand [3H]prazosin in plasma membrane fractions of aortas prepared from control, adrenalectomized and dexamethasone-treated adrenalectomized rats. In controls there were 50±8 (s.e.m.; n=6) fmol α1-adrenergic receptors/mg membrane protein (Bmax) with a dissociation constant (K d) of 0·52±0·10 nm (n=6). Adrenalectomy 8 days before tissue preparation caused a 40% decrease in Bmax and a 60% decrease in K d. Dexamethasone replacement after adrenalectomy returned these values close to those of controls. Noradrenaline competed for the [3H]prazosin-binding sites. Computer analysis by a non-linear curve-fitting program (LIGAND) showed that noradrenaline binding was to a heterogeneous population of high- and low-affinity receptors with K d values of 1·87±0·73 μm and 0·48±0·12 mm (n=5) respectively. Guanosine thiotriphosphate (GTP[S]) caused the conversion of high-affinity to low-affinity binding, consistent with the model of the high-affinity sites being coupled to a G protein. After adrenalectomy, noradrenaline binding was to a homogeneous population of low-affinity receptors; hence, the effect of GTP[S] was no longer apparent, suggesting that under these conditions the α1-adrenergic receptors were unable to couple to a G protein. The two-site model of binding and GTP[S] effect was returned by dexamethasone treatment. These data provide evidence that glucocorticoids not only modulate the number of α1-adrenergic receptors on vascular smooth muscle, but also cause disruptions in receptor—G protein coupling. This may be an important mechanism by which glucocorticoids exert their effect on cardiovascular sensitivity.

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Agua Sobrino, Pilar J Oviedo, Susana Novella, Andrés Laguna-Fernandez, Carlos Bueno, Miguel Angel García-Pérez, Juan J Tarín, Antonio Cano and Carlos Hermenegildo

, including ovine uterine arteries, mesenteric arteries from ovariectomized rats, rat cerebral blood vessels, and aorta from ovariectomized monkeys ( Hermenegildo et al . 2006 ). Regarding cultured endothelial cells, some discrepancies exist. E 2 has been