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Titolo:
Resistance of CIN-positive T lymphocytes to etoposide-induced apoptosis mediated by upregulation of Bcl-xL expression in patients with HTLV-I-associated myelopathy
Autore:
Hamasaki, S; Nakamura, T; Furuya, T; Kawakami, A; Ichinose, K; Nakashima, T; Nishiura, Y; Shirabe, S; Eguchi, K;
Indirizzi:
Nagasaki Univ, Sch Med, Dept Internal Med 1, Nagasaki 8528501, Japan Nagasaki Univ Nagasaki Japan 8528501 rnal Med 1, Nagasaki 8528501, Japan Nagasaki Univ, Grad Sch Med Sci, Dept Mol Microbiol & Immunol, Nagasaki 8528501, Japan Nagasaki Univ Nagasaki Japan 8528501 & Immunol, Nagasaki 8528501, Japan Nagasaki Midori Hosp, Div Neurol, Nagasaki, Japan Nagasaki Midori Hosp Nagasaki Japan i Hosp, Div Neurol, Nagasaki, Japan
Titolo Testata:
JOURNAL OF NEUROIMMUNOLOGY
fascicolo: 1-2, volume: 117, anno: 2001,
pagine: 143 - 148
SICI:
0165-5728(20010702)117:1-2<143:ROCTLT>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; CELL-DEATH; INFLAMMATORY CYTOKINES; SPASTIC PARAPARESIS; CYTOCHROME-C; PROVIRAL DNA; ACTIVATION; INDUCTION; MITOCHONDRIA; INHIBITION;
Keywords:
HAM; chronic inflammation; CD4(+) T lymphocyte; Bcl-xL; etoposide; HTLV-I;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Eguchi, K Nagasaki Univ, Sch Med, Dept Internal Med 1, 1-7-1 Sakamoto, Nagasaki 8528501, Japan Nagasaki Univ 1-7-1 Sakamoto Nagasaki Japan 8528501 8501, Japan
Citazione:
S. Hamasaki et al., "Resistance of CIN-positive T lymphocytes to etoposide-induced apoptosis mediated by upregulation of Bcl-xL expression in patients with HTLV-I-associated myelopathy", J NEUROIMM, 117(1-2), 2001, pp. 143-148

Abstract

Human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM) is characterized by chronic inflammation of the spinal cord. The exact mechanisms that enhance the development of chronic myelopathy remain to be determined. One such mechanism could be an altered response of peripheral blood CD4(+) T lymphocytes to apoptotic stimuli. We examined the sensitivity of these cells to apoptosis in HAM patients and control. Apoptosis was induced byetoposide, which induces mitochondria-dependent apoptosis through the release of cytochrome c from the mitochondria. The percentage of apoptotic cells that expressed hypodiploid DNA among etoposide-treated CD4(+) T lymphocytes was significantly lower in HAM patients than in the control. Western blot analysis of cell lysates derived from CD4(+) T lymphocytes demonstrated that the expression level of Bcl-xL protein was significantly higher in HAM patients than in the control. Our results indicate that peripheral blood CD4+ T lymphocytes of HAM patients are resistant to apoptosis triggered through mitochondrial death pathway through upregulation of expression of anti-apoptotic protein, Bcl-xL. This phenomenon might contribute to the prolongation and perpetuation of the chronic inflammatory process in the spinal cordof HAM patients. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/10/20 alle ore 20:14:51