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1,227 results on '"Tsujimoto, Gozoh"'

57. Attenuated stress-induced catecholamine release in mice lacking the vasopressin [V.sub.1b] receptor

Author

Itoh, Shuji, Yamada, Sakiko, Mori, Toyoki, Miwa, Takashi, Tottori, Katsura, Uwahodo, Yasufumi, Yamamura, Yoshitaka, Fukuda, Meiko, Yamamoto, Koji, Tanoue, Akito, and Tsujimoto, Gozoh

Subjects
Vasopressin -- Research, Mice -- Research, Biological sciences
Abstract

Vasopressin [V.sub.1b] receptor is specifically expressed in the pituitary and mediates adreno-corticotropin release, thereby regulating stress responses via its corticotropin releasing factor-like action. In the present study we examined catecholamine release in response to two types of stress in mice lacking the [V.sub.1b] receptor gene ([V.sub.1b][R.sup.-/-] mice) vs. wild-type mice. There were no significant differences in the basal plasma levels of catecholamines between the two genotypes. In response to stress induced by forced swimming, norepinephrine (NE), but not epinephrine (E) or dopamine (DA), was increased in wild-type mice, whereas the increases in NE and DA were not observed in [V.sub.1b][R.sup.-/-] mice. In wild-type mice, E, but not NE or DA, was increased in response to social isolation stress, whereas the increase in E was not observed in [V.sub.1b][R.sup.-/-] mice. These results suggest that the [V.sub.1b] receptor regulates stress-induced catecholamine release. Because it has been suggested that arginine-vasopressin (AVP) is related to the development of depression, we also evaluated immobility time in the forced swimming test, and we found no significant change in [V.sub.1b][R.sup.-/-] mice. Taken together, these findings suggest that, in addition to the previously elucidated effect on the hypothalamic-pituitary-adrenal axis, vasopressin activity via [V.sub.1b] receptors regulates stress-induced catecholamine release. [V.sub.1b] receptor knockout mice; norepinephrine; epinephrine; dopamine; immobility time in the forced swimming test

Published
2006

58. Adrenergic catecholamine trophic activity contributes to flow-mediated arterial remodeling

Author

Erami, Cauveh, Zhang, Hua, Tanoue, Akito, Tsujimoto, Gozoh, Thomas, Steven A., and Faber, James E.

Subjects
Hydroxylases, Dopamine, Carotid artery, Apoptosis, Biological sciences
Abstract

Stimulation of [[alpha].sub.1]-adrenoceptors (ARs) induces proliferation, hypertrophy, and migration of vascular smooth muscle cells and adventitial fibroblasts in cell and organ culture. In vivo studies have confirmed this direct trophic action and found that endogenous catecholamines contribute to neointimal formation and wall hypertrophy induced by mechanical injury. In murine carotid artery, these effects are mediated by [[alpha].sub.1B]-ARs, whereas [[alpha].sub.1D]-ARs mediate contraction and [[alpha].sub.1A]-ARs are not expressed. Herein, we examined whether catecholamines also contribute to arterial wall growth in a noninjury model, i.e., flowmediated remodeling. In wild-type mice or mice deficient in norepinephrine and epinephrine synthesis [dopamine [beta]-hydroxylase knockout (DBH-KO)], all distal branches of the left carotid artery (LC) except the thyroid artery were ligated to reduce flow in the LC and increase flow in the right carotid artery (RC). Twenty-one days later, negative hypertrophic remodeling of the LC [i.e., -20% (decrease) in lumen area, -2% in circumference of the external elastic lamina (CEEL), +98% (increase) in thickness of the intima media, and +71% in thickness for adventitia; P < 0.01 vs. sham ligation] and positive eutrophic remodeling of the RC [+23% in lumen area, + 11% in CEEL; P < 0.01 vs. sham ligation] were inhibited in DBH-KO mice [LC: +10% intima media and +3% adventitia; RC: +9% lumen area and +3% CEEL]. This inhibition was associated with reduced proliferation in the RC and reduced apoptosis and leukocyte accumulation in the RC and LC when examined 5 days after ligation. Carotid remodeling in [[alpha].sub.1D]-AR-knockout mice evidenced little or no inhibition, which suggests dependence on [[alpha].sub.1B]-ARs. These findings suggest that catecholamine-induced trophic activity contributes to both flowmediated negative remodeling and adaptive positive arterial remodeling. dopamine [beta]-hydroxylase; carotid; [alpha]-adrenoceptor; apoptosis; leukocyte accumulation; restenosis

Published
2005

59. Free fatty acids regulate gut incretin glucagon-like peptide-1 secretion through GPR120

Author

Hirasawa, Akira, Tsumaya, Keiko, Awaji, Takeo, Katsuma, Susumu, Adachi, Tetsuya, Yamada, Masateru, Sugimoto, Yukihiko, Miyazaki, Shunichi, and Tsujimoto, Gozoh

Abstract

Author(s): Akira Hirasawa [1, 2, 3]; Keiko Tsumaya [1]; Takeo Awaji [4]; Susumu Katsuma [5]; Tetsuya Adachi [5]; Masateru Yamada [1]; Yukihiko Sugimoto [6]; Shunichi Miyazaki [4]; Gozoh Tsujimoto (corresponding [...]

Published
2005
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61. Gene deletion of dopamine [beta]-hydroxylase and [[alpha].sub.1]-adrenoceptors demonstrates involvement of catecholamines in vascular remodeling

Author

Zhang, Hua, Cotecchia, Susanna, Thomas, Steven A., Tanoue, Akito, Tsujimoto, Gozoh, and Faber, James E.

Subjects
Smooth muscle -- Research, Dopamine -- Research, Biological sciences
Abstract

Gene deletion of dopamine [beta]-hydroxylase and [[alpha].sub.1]-adrenoceptors demonstrates involvement of catecholamines in vascular remodeling. Am J Physiol Heart Circ Physiol 287: H2106-H2114, 2004. First published July 1, 2004; doi:10.1152/ajpheart.00290.2004.--In vitro studies have shown that stimulation of [[alpha].sub.1]-adrenoceptors (ARs) directly induces proliferation, hypertrophy, and migration of arterial smooth muscle cells and adventitial fibroblasts. In vivo studies confirmed these findings and showed that catecholamine trophic activity becomes excessive after experimental balloon injury and contributes to neointimal growth, adventitial thickening, and lumen loss. However, past studies have been limited by selectivity of pharmacological agents. The aim of this study, in which mice devoid of norepinephrine and epinephrine synthesis [dopamine [beta]-hydroxylase (DB[H.sup.-/-])] or deficient in [[alpha].sub.1]-AR subtypes expressed in murine carotid ([[alpha].sub.1B]-[AR.sup.-/-] and [[alpha].sub.1D]-[AR.sup.-/-]) were used, was to test the hypothesis that catecholamines contribute to wall hypertrophy after injury. At 3 wk after injury of wild-type mice, lumen area and carotid circumference increased significantly, and hypertrophy of media and adventitia was in excess of that needed to restore circumferential wall stress to normal. In DB[H.sup.-/-] and [[alpha].sub.1B]-[AR.sup.-/-] mice, increases in lumen area, circumference, and hypertrophy of the media and adventitia were reduced by 50-91%, resulting in restoration of wall tension to nearly normal (DB[H.sup.-/-]) or normal ([[alpha].sub.1B]-[AR.sup.-/-]). In contrast, in [[alpha].sub.1D]-[AR.sup.-/-] mice, increases in lumen area. circumference, and wall hypertrophy were unaffected and wall thickening remained in excess of that required to return tension to normal. When examined 5 days after injury, proliferation and leukocyte infiltration were inhibited in DB[H.sup.-/-] mice. These studies suggest that the trophic effects of catecholamines are mediated primarily by [[alpha].sub.1B]-ARs in mouse carotid and contribute to hypertrophic growth alter vascular injury. adrenergic receptors; knockout; smooth muscle; adventitia; growth; injury

Published
2004

73. Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human

Author

Ichimura, Atsuhiko, Hirasawa, Akira, Poulain-Godefroy, Odile, Bonnefond, Amélie, Hara, Takafumi, Yengo, Loïc, Kimura, Ikuo, Leloire, Audrey, Liu, Ning, Iida, Keiko, Choquet, Hélène, Besnard, Philippe, Lecoeur, Cécile, Vivequin, Sidonie, Ayukawa, Kumiko, Takeuchi, Masato, Ozawa, Kentaro, Tauber, Maithé, Maffeis, Claudio, Morandi, Anita, Buzzetti, Raffaella, Elliott, Paul, Pouta, Anneli, Jarvelin, Marjo-Riitta, Körner, Antje, Kiess, Wieland, Pigeyre, Marie, Caiazzo, Roberto, Van Hul, Wim, Van Gaal, Luc, Horber, Fritz, Balkau, Beverley, Lévy-Marchal, Claire, Rouskas, Konstantinos, Kouvatsi, Anastasia, Hebebrand, Johannes, Hinney, Anke, Scherag, Andre, Pattou, François, Meyre, David, Koshimizu, Taka-aki, Wolowczuk, Isabelle, Tsujimoto, Gozoh, and Froguel, Philippe

Published
2012
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