MolPharm

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


0026-895X/04/6601-122-128$20.00
Mol Pharmacol 66:122-128, 2004

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pae, H.-O.
Right arrow Articles by Chung, H.-T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pae, H.-O.
Right arrow Articles by Chung, H.-T.

Roles of Heme Oxygenase-1 in the Antiproliferative and Antiapoptotic Effects of Nitric Oxide on Jurkat T Cells

Hyun-Ock Pae, Byung-Min Choi, Gi-Su Oh, Myeong-Su Lee, Do-Gon Ryu, Hyun-Yul Rhew, Yung-Myung Kim, and Hun-Taeg Chung

Department of Microbiology and Immunology, Wonkwang University School of Medicine (H.O.P., B.M.C., G.S.O., M.S.L., H.T.C.), and Department of Physiology, Wonkwang University Oriental Medicine (D.G.R.), Iksan, Republic of Korea; Department of Urology, Kosin University Hospital, Busan, Republic of Korea (H.Y.R.); and Department of Molecular and Cellular Biochemistry, Kangwon National University School of Medicine, Chunchon, Republic of Korea (Y.M.K)

Nitric oxide (NO) has been shown to exert antiproliferative and antiapoptotic effects on human T cells. Heme oxygenase-1 (HO-1), which degrades heme into biliverdin, free iron (Fe2+), and carbon monoxide (CO), has also been known to have antiproliferative and antiapoptotic effects. Recent evidence suggests that HO-1 is an important cellular target of NO; whether HO-1 expression contributes to the antiproliferative and/or antiapoptotic effects mediated by NO remains to be investigated. In the present study, we examined the effects of NO on HO-1 expression and possible roles of HO-1 in T cell proliferation and apoptosis. Using human Jurkat T cells, we found that the NO donor sodium nitroprusside (SNP) induced HO-1 expression and that preincubation with SNP suppressed T cell proliferation induced by concanavalin A and apoptosis triggered by anti-Fas antibody. Suppressions of T cell proliferation and apoptosis comparable with SNP were also observed when the T cells were preincubated with the HO-1 inducer cobalt protoporphyrin. A phosphorothioate-linked HO-1 antisense oligonucleotide blocked HO-1 expression, and subsequently abrogated the antiproliferative and antiapoptotic effects of SNP. Overexpression of the HO-1 gene after transfection into Jurkat T cells resulted in significant decreases in T cell proliferation and apoptosis. The CO donor tricarbonyldichlororuthenium (II) dimer mimicked the antiproliferative effect of SNP, and the Fe2+ donor FeSO4 blocked anti-Fas-induced apoptosis. Taken together, our results suggest that NO induces HO-1 expression in T cells and that suppressions of T cell proliferation and apoptosis afforded by NO are associated with an increased expression of HO-1 by NO.


Received January 22, 2004; accepted April 7, 2004

Address correspondence to: Hun-Taeg Chung, Department of Microbiology and Immunology, Wonkwang University Medical School, 344-2 Shinyong-Dong, Iksan, Chonbug 570-749, Republic of Korea. E-mail: htchung{at}wonkwang.ac.kr




This article has been cited by other articles:


Home page
Ann Rheum DisHome page
M L Ferrandiz, N Maicas, I Garcia-Arnandis, M C Terencio, R Motterlini, I Devesa, L A B Joosten, W B van den Berg, and M J Alcaraz
Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis
Ann Rheum Dis, September 1, 2008; 67(9): 1211 - 1217.
[Abstract] [Full Text] [PDF]


Home page
DiabetesHome page
C.-M. Hu, H.-H. Lin, M.-T. Chiang, P.-F. Chang, and L.-Y. Chau
Systemic Expression of Heme Oxygenase-1 Ameliorates Type 1 Diabetes in NOD Mice
Diabetes, May 1, 2007; 56(5): 1240 - 1247.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
P. Chanvorachote, U. Nimmannit, L. Wang, C. Stehlik, B. Lu, N. Azad, and Y. Rojanasakul
Nitric Oxide Negatively Regulates Fas CD95-induced Apoptosis through Inhibition of Ubiquitin-Proteasome-mediated Degradation of FLICE Inhibitory Protein
J. Biol. Chem., December 23, 2005; 280(51): 42044 - 42050.
[Abstract] [Full Text] [PDF]


Home page
FASEB J.Home page
S. B. Blumenthal, A. K. Kiemer, G. Tiegs, S. Seyfried, M. Holtje, B. Brandt, H.-D. Holtje, S. Zahler, and A. M. Vollmar
Metalloporphyrins inactivate caspase-3 and -8
FASEB J, August 1, 2005; 19(10): 1272 - 1279.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
H.-O. Pae, G.-S. Oh, B.-M. Choi, Y.-M. Kim, and H.-T. Chung
A Molecular Cascade Showing Nitric Oxide-Heme Oxygenase-1-Vascular Endothelial Growth Factor-Interleukin-8 Sequence in Human Endothelial Cells
Endocrinology, May 1, 2005; 146(5): 2229 - 2238.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
T. M. Brusko, C. H. Wasserfall, A. Agarwal, M. H. Kapturczak, and M. A. Atkinson
An Integral Role for Heme Oxygenase-1 and Carbon Monoxide in Maintaining Peripheral Tolerance by CD4+CD25+ Regulatory T Cells
J. Immunol., May 1, 2005; 174(9): 5181 - 5186.
[Abstract] [Full Text] [PDF]




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
 Molecular Interventions Drug Metabolism and Disposition

Copyright © 2004 by the American Society for Pharmacology and Experimental Therapeutics