2000 Fiscal Year Final Research Report Summary
Role of JAK2 tyrosine kinase in hypertensive vascular hypertrophy
| Project/Area Number |
11670703
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | OSAKA CITY UNIVERSITY MEDICAL SCHOOL |
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Principal Investigator |
NEGORO Nobuo OSAKA CITY UNIVERSITY MEDICAL SCHOOL, RESEARCH ASSOCIATE, 医学部, 助手 (80180701)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMURA Mikio OSAKA CITY UNIVERSITY MEDICAL SCHOOL, ASSISTANT PROFESSOR, 医学部, 講師 (90169144)
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| Project Period (FY) |
1999 – 2000
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| Keywords | hypertension / vascular smooth muscle cells / JAK2 / intracellular signals / hypertrophy |
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| Research Abstract |
Role of JAK2 in hypertrophy of vascular smooth muscle cells in vitro and in vivo.
1) JAK2 inhibitor, AG-490, inhibited hypertophy (cell size, 3H-thimidine uptake and 3H-leucine uptake) in cultured vascular smooth muscle cells induced by angiotensin II (AII).
2) AG-490 inhibited tyrosine phosphorylation of epidermal growth factor (EGF) receptors in AII-induced vascular hypertrophy in cultured vascular smooth muscle cells.
3) AG-490 inhibited vascular hyperophy (weight) of thoracic aortas from 12-week-old spon-taneously hypertensive rats (SHRs) in vivo.
4) AG-490 also inhibited tyrosine phophorylation of EGF receptors from media of thoracic aortas in 15-week-old SHRs. However, AG-490 did not changed blood pressure in the rats.
5) AG-490 inhibited interferon stimulated response element (IRSE), interon gamma-activation site (SAS), and sis-inducible element (SIE), which were detected by the gel shift assays.
These results suggest that JAK2 involves in the vascular hypertrophy of hypertensive rats, possbly through cross-talk of EGF receptors in vitro and in vivo.
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