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365 results on '"Hitomi, Hirofumi"'

5. The Induction of Parathyroid Cell Differentiation from Human Induced Pluripotent Stem Cells Promoted Via Transforming Growth Factor-α/Epidermal Growth Factor Receptor Signaling

Author

Nakatsuka, Ryusuke, primary, Kato, Tadashi, additional, Zhang, Rong, additional, Uemura, Yasushi, additional, Sasaki, Yuka, additional, Matsuoka, Yoshikazu, additional, Shirouzu, Yasumasa, additional, Fujioka, Tatsuya, additional, Yamashita, Hiromi, additional, Hattori, Fumiyuki, additional, Nozaki, Tadashige, additional, Ogata, Hiroaki, additional, and Hitomi, Hirofumi, additional

Published
2023
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7. Effects of the selective chymase inhibitor TEI‐F00806 on the intrarenal renin–angiotensin system in salt‐treated angiotensin I‐infused hypertensive mice

Author

Tuba M. Ansary, Maki Urushihara, Yoshihide Fujisawa, Sayaka Nagata, Hidenori Urata, Daisuke Nakano, Hitomi Hirofumi, Kazuo Kitamura, Shoji Kagami, and Akira Nishiyama

Subjects
blood pressure, chymase, high salt, intrarenal RAS, Physiology, QP1-981
Abstract

New Findings What is the central question of this study? Can chymase inhibition prevent angiotensin I‐induced hypertension through inhibiting the conversion of angiotensin I to angiotensin II in the kidney? What is the main finding and its importance? Treatment with TEI‐F00806 decreased angiotensin II content of the kidney, renal cortical angiotensinogen protein levels and chymase mRNA expression, and attenuated the development of hypertension. Abstract The effects of the selective chymase inhibitor TEI‐F00806 were examined on angiotensin I (Ang I)‐induced hypertension and intrarenal angiotensin II (Ang II) production in salt‐treated mice. Twelve‐week‐old C57BL male mice were given a high‐salt diet (4% NaCl + saline (0.9% NaCl)), and divided into three groups: (1) sham + vehicle (5% acetic acid in saline), (2) Ang I (1 μg kg−1 min−1, s.c.) + vehicle, and (3) Ang I + TEI‐F00806 (100 mg kg−1 day−1, p.o.) (n = 8–10 per group). Systolic blood pressure was measured weekly using a tail‐cuff method. Kidney Ang II content was measured by radioimmunoassay. Chronic infusion of Ang I resulted in the development of hypertension (P

Published
2018
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9. Efficient protocol for the differentiation of kidney podocytes from induced pluripotent stem cells, involving the inhibition of mTOR

Author

Yasuda, Masahiro, primary, Kato, Tadashi, additional, Okano, Mai, additional, Yamashita, Hiromi, additional, Matsuoka, Yoshikazu, additional, Shirouzu, Yasumasa, additional, Fujioka, Tatsuya, additional, Hattori, Fumiyuki, additional, Tsuji, Shoji, additional, Kaneko, Kazunari, additional, and Hitomi, Hirofumi, additional

Published
2023
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26. Mineralocorticoid receptor blockade and calcium channel blockade have different renoprotective effects on glomerular and interstitial injury in rats

Author

Du, Jun, Fan, Yu-Yan, Hitomi, Hirofumi, Kiyomoto, Hideyasu, Kimura, Shoji, Kong, Chui-Ze, Noma, Takahisa, Kohno, Masakazu, Nishiyama, Akira, and Nakano, Daisuke

Subjects
Mineralocorticoids -- Physiological aspects, Mineralocorticoids -- Research, Hypertension -- Care and treatment, Hypertension -- Research, Hypoxia -- Physiological aspects, Hypoxia -- Research, Kidney failure -- Care and treatment, Kidney failure -- Research, Amlodipine -- Dosage and administration, Amlodipine -- Research, Biological sciences
Abstract

We hypothesized that combination treatment with the mineralocorticoid receptor antagonist eplerenone and the calcium channel blocker amlodipine elicits better renoprotective effects than monotherapy with either drug, via different mechanisms in Dahl salt-sensitive (DS) hypertensive rats. DS rats were fed a high-salt diet (4% NaCl) for 10 wk and were treated with vehicle (n = 12), eplerenone (50 mg x [kg.sup.-1] x [day.sup.-1] x po, n = 12), amlodipine (3 mg x [kg.sup.-1] x [day.sup.-1], po, n = 12), or eplerenone plus amlodipine (n = 12) after 2 wk of salt feeding. Vehicle-treated DS rats developed proteinuria, which was attenuated by eplerenone or amlodipine. Interestingly, eplerenone attenuated the glomemlosclerosis and podocyte injury, but amlodipine did not. Conversely, treatment with amlodipine markedly improved interstitial fibrosis, while the effect of eplerenone was minimal. Combination treatment markedly improved proteinuria, glomerulosclerosis, podocyte injury, and interstitial fibrosis in DS rats. Renal hypoxia estimated by pimonidazole, vascular endothelial growth factor expression, and density of peritubular endothelial cells was exacerbated by salt feeding. Amlodipine, either as monotherapy or in combination, ameliorated the renal hypoxia, whereas eplerenone treatment had no effect. In conclusion, both eplerenone and amlodipine attenuated renal injuries in high salt-fed DS rats, but the targets for renoprotection differed between these two drugs, with eplerenone predominantly acting on glomeruli and amlodipine acting on interstitium. The combination of eplerenone and amlodipine improved renal injury more effectively than either monotherapy in high salt-fed DS rats, presumably by achieving their own renoprotective effects. interstitial fibrosis; hypoxia; salt-sensitive hypertension

Published
2009

27. Role of p38 MAPK and MAPKAPK-2 in angiotensin II-induced Akt activation in vascular smooth muscle cells

Author

Taniyama, Yoshihiro, Ushio-Fukai, Masuko, Hitomi, Hirofumi, Rocic, Petra, Kingsley, Michael J., Pfahnl, Chun, Weber, David S., Alexander, R. Wayne, and Griendling, Kathy K.

Subjects
Angiotensin -- Research, Biological sciences
Abstract

Angiotensin II activates a variety of signaling pathways in vascular smooth muscle cells (VSMCs), including the MAPKs and Akt, both of which are required for hypertrophy. However. little is known about the relationship between these kinases or about the upstream activators of Akt. In this study, we tested the hypothesis that the reactive oxygen species (ROS)-sensitive kinase p38 MAPK and its substrate MAPKAPK-2 mediate Akt activation in VSMCs. In unstimulated VSMCs, Akt and p38 MAPK are constitutively associated and remain so after angiotensin II stimulation. Inhibition of p38 MAPK activity with SB-203580 dose-dependently inhibits Akt phosphorylation on [Ser.sup.473], but not [Thr.sup.308]. Angiotensin II-induced phosphorylation of MAPKAPK-2 is also attenuated by SB-203580, as well as by inhibitors of ROS. In addition, angiotensin II stimulates the association of MAPKAPK-2 with the Akt-p38 MAPK complex, and an in vitro kinase assay shows that MAPKAPK-2 immunoprecipitates of VSMC lysates phosphorylate recombinant Akt in an angiotensin II-inducible manner. Finally, intracellular delivery of a MAPKAPK-2 peptide inhibitor blocks Akt phosphorylation on [Ser.sup.473]. These results suggest that the p38 MAPKMAPKAPK-2 pathway mediates Akt activation by angiotensin II in these cells by recruiting active MAPKAPK-2 to a signaling complex that includes both Akt and p38 MAPK. Through this mechanism, p38 MAPK confers ROS sensitivity to Akt and facilitates downstream signaling. These results provide evidence for a novel signaling complex that may help to spatially organize hypertrophy-related. ROS-sensitive signaling in VSMCs. mitogen-activated protein kinase; reactive oxygen species

Published
2004

49. Effects of the selective chymase inhibitor TEI-F00806 on the intrarenal renin-angiotensin system in salt-treated angiotensin I-infused hypertensive mice

Author

Akira Nishiyama, Yoshihide Fujisawa, Maki Urushihara, Shoji Kagami, Hidenori Urata, Hitomi Hirofumi, Kazuo Kitamura, Daisuke Nakano, Tuba M. Ansary, and Sayaka Nagata

Subjects
0301 basic medicine, Male, medicine.medical_specialty, medicine.medical_treatment, Male mice, Blood Pressure, 030204 cardiovascular system & hematology, Peptidyl-Dipeptidase A, Kidney, Renin-Angiotensin System, 03 medical and health sciences, Mice, 0302 clinical medicine, Chymases, Internal medicine, Renin–angiotensin system, medicine, Animals, Saline, business.industry, Angiotensin II, Chymase, Radioimmunoassay, General Medicine, 030104 developmental biology, Blood pressure, medicine.anatomical_structure, Endocrinology, Hypertension, Angiotensin I, business
Abstract

NEW FINDINGS What is the central question of this study? Can chymase inhibition prevent angiotensin I-induced hypertension through inhibiting the conversion of angiotensin I to angiotensin II in the kidney? What is the main finding and its importance? Treatment with TEI-F00806 decreased angiotensin II content of the kidney, renal cortical angiotensinogen protein levels and chymase mRNA expression, and attenuated the development of hypertension. ABSTRACT The effects of the selective chymase inhibitor TEI-F00806 were examined on angiotensin I (Ang I)-induced hypertension and intrarenal angiotensin II (Ang II) production in salt-treated mice. Twelve-week-old C57BL male mice were given a high-salt diet (4% NaCl + saline (0.9% NaCl)), and divided into three groups: (1) sham + vehicle (5% acetic acid in saline), (2) Ang I (1 μg kg-1 min-1 , s.c.) + vehicle, and (3) Ang I + TEI-F00806 (100 mg kg-1 day-1 , p.o.) (n = 8-10 per group). Systolic blood pressure was measured weekly using a tail-cuff method. Kidney Ang II content was measured by radioimmunoassay. Chronic infusion of Ang I resulted in the development of hypertension (P

Published
2018

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