2006 Fiscal Year Final Research Report Summary
Genomic characteristics of pulmonary circulation in high-altitude living animal
Project/Area Number |
16406026
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 海外学術 |
Research Field |
Respiratory organ internal medicine
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Research Institution | University of Fukui |
Principal Investigator |
ISHIZAKI Takeshi University of Fukui, Faculty of Medicine, Professor, 医学部, 教授 (80151364)
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Co-Investigator(Kenkyū-buntansha) |
AMESHIMA Shingo University of Fukui Hospital, Lecturer, 医学部附属病院, 講師 (60262614)
MATSUKAWA Shigeru University of Fukui, Centers for Advanced Research Support, Associate Professor, 助教授 (00092809)
SAKAI Akio Shinshu University, Graduate School of Medicine, Associate Professor, 大学院医学研究科, 助教授 (70020758)
MIZUNO Shirou University of Fukui, Faculty of Medicine, Assistant Professor, 医学部, 助手 (80397281)
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Project Period (FY) |
2004 – 2006
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Keywords | Yak / Pulmonary Circulation / eNOS / DDAH / ADMA / ET-1 |
Research Abstract |
We investigated the pulmonary characteristics of Yak, a high-altitude adapted animal that is resistant to hypoxia-induced pulmonary hypertension, cor pulmonale in terms of hypoxia-responsible genomic products such as eNOS, DDAH (dimethylarginine dimethylaminohydrolase), ADMA (asymmetrically methylated Arginine) and ET-1. Results; 1. The protein expression of eNOS, and protein expression and activity of DDAH in yak's lung tissue were more elevated than that of control cow. However, the degree of protein expression of DDAH in the Kidney was the same in both animals. 2. The plasma level of ADMA was 5-times higher in Yak compared to that of cow. Among cow groups, high-altitude living one has 4-times high ADMA level compared to that of low-altitude living one. 3. The plasma ET-1 level was higher in Yak than in cow. These results suggest that wild yak's lung has augmented eNOS protein and augmented DDAH activity compared to cow. On the contrary, the animal has elevated plasma ADMA and ET-1 suggesting that the balance of vasodilators and vasoconstrictors are up-regulated. Although we did not assess transpulmonary difference of plasma ADMA and ET-1, it appears that Yak's lung preferentially expressed protective NO mechanism(s) which may result the relatively low pulmonary arterial pressure despite of high-altitude. It may induce a good suggestion from the animal study if think about hypoxic-air induced pulmonary hypertension and chronic respiratory failure in clinical medicine in terms of pathogenesis and treatment strategy.
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Research Products
(14 results)
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[Journal Article] Hypoxia-induced proliferation of human pulmonary arterial smooth muscle cell is involved in the suppression of cyclin-dependent kinase inhibitors, P21, P27 andP53.2006
Author(s)
Ishizaki T, Mizuno S, Kadowaki M, Uesaka D, Umeda Y, Morikawa M, Nakanishi M, Demura Y, Ameshima S.
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Journal Title
High Altitude Medicine and Biology Advanc Research Workshop abstract book P12
Description
「研究成果報告書概要(欧文)」より
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