A ROLE OF CYTOKINE IN PROGRESSION OF HEARTFAILRE
| Project/Area Number |
05670592
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Yamagata University School of Medicine |
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Principal Investigator |
YAMAGUCHI Seiji Yamagata Univ.Sch.of Med., Instructor, 医学部, 助手 (30239892)
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| Co-Investigator(Kenkyū-buntansha) |
SHIRAKABE Masanori Yamagata Univ.Sch.of Med., Instructor, 医学部, 助手 (10241697)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1993: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | CONGESTIVE HEART FAILURE / TUMOR NECROSIS FACTOR (TNF) / SOLUBLE TNF RECEPTORS / CYTOKINE / TNFα / soluble TNF receptor / heart failure / cachexia / myocardium |
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| Research Abstract |
Previous investigations have suggested that circulating cytokines (i.e., TNFa) are increased in patients with advanced heart failure (HF). We investigated whether regulatory peptides, two types of naturally occurring soluble TNF receptors (sTNF-RI and sTNF-RII) are increased in patients with HF.These peptides can prevent the adverse pathologic sequela caused by TNF.We assayd plasma from 37 patients with HF (NYHA II 16, III 14, IV 7) and the age-matched control subjects(n=24) with Enzyme-Linked Immunoassay (ELISA). TNFa had no significant difference between heart failure patients and normal subjects (7.7<plus-minus> 1.7 (mean<plus-minus> SEM) vs6.9 <plus-minus> 1.2pg/ml ; ns). However, soluble TNF-RI was significantly higher in patients with heart failure than normal subjects (1629 <plus-minus> 153vs681 <plus-minus> 53pg/ml ; p<0.01) and soluble TNF-RII was also higher in patients with heart failure than control subjects (2124 <plus-minus> 157vs3005 <plus-minus> 196pg/ml ; p<0.01). Further, soluble TNF-RI was increased in relation to the severity of heart failure (normal subjects ; 681 <plus-minus> 53pg/ml, NYHA class II ; 1226 <plus-minus> 115pg/ml, NYHA class III ; 1624 <plus-minus> 207pg/ml, NYHA class IV ; 2789 <plus-minus> 568pg/ml). Similarly, there was an increase in soluble TNF-RII with symptomatic severity in heart failure (normal subjects ; 2124 <plus-minus> 157pg/ml, NYHA class II ; 2555 <plus-minus> 140pg/ml, NYHA class III ; 2909 <plus-minus> 262pg/ml, NYHA class IV ; 4500 <plus-minus> 764pg/ml). The levels of soluble TNF R-1 were related to those of soluble TNF R-II in he
These results suggest that 1) in a variety of tissues in HF patients, the released soluble receptors may inhibit TNF bioactivity by binding the molecule and preventing ligand to the cellular TNF receptors and 2) the levels of soluble TNF receptors may reflect the severity of congestive heart failure.
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Report
(3 results)
Research Products
(16 results)
