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Thioredoxin-1 ameliorates myosin-induced autoimmune myocarditis by suppressing chemokine expressions and leukocyte chemotaxis in mice.
Circulation. 2004 Sep 07; 110(10):1276-83.Circ

Abstract

BACKGROUND

Cardiac myosin-induced myocarditis is an experimental autoimmune myocarditis (EAM) model used to investigate autoimmunological mechanisms in inflammatory heart diseases and resembles fulminant myocarditis in humans. We investigated the therapeutic role of thioredoxin-1 (TRX-1), a redox-regulatory protein with antioxidant and antiinflammatory effects, in murine EAM.

METHODS AND RESULTS

EAM was generated in 5-week-old male BALB/c mice by immunization with porcine cardiac myosin at days 0 and 7. Recombinant human TRX-1 (rhTRX-1), C32S/C35S mutant rhTRX-1, or saline was administered intraperitoneally every second day from day 0 to 20. In addition, rabbit anti-mouse TRX-1 serum or normal rabbit serum was administered intraperitoneally on days -1, 2, and 6. Animals were euthanized on day 21. Histological analysis of the heart showed that TRX-1 significantly reduced the severity of EAM, whereas mutant TRX-1 failed to have such an effect, and anti-TRX-1 antibody enhanced the disease markedly. Immunohistochemical analysis showed that TRX-1 significantly suppressed cardiac macrophage inflammatory protein (MIP)-1alpha, MIP-2, and 8-hydroxydeoxyguanosine expression and macrophage infiltration into the heart in EAM. Although serum levels of MIP-1alpha were not suppressed by TRX-1 until day 21, both an in vitro chemotaxis chamber assay and an in vivo air pouch model showed that TRX-1 significantly suppressed MIP-1alpha- or MIP-2-induced leukocyte chemotaxis. However, real-time reverse transcription-polymerase chain reaction showed that TRX-1 failed to decrease chemokine receptor expression increased in the bone marrow cells of EAM mice.

CONCLUSIONS

TRX-1 attenuates EAM by suppressing chemokine expressions and leukocyte chemotaxis in mice.

Authors+Show Affiliations

Department of Biological Responses, Institute for Virus Research, Kyoto University, Kyoto, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15337697

Citation

Liu, Wenrui, et al. "Thioredoxin-1 Ameliorates Myosin-induced Autoimmune Myocarditis By Suppressing Chemokine Expressions and Leukocyte Chemotaxis in Mice." Circulation, vol. 110, no. 10, 2004, pp. 1276-83.
Liu W, Nakamura H, Shioji K, et al. Thioredoxin-1 ameliorates myosin-induced autoimmune myocarditis by suppressing chemokine expressions and leukocyte chemotaxis in mice. Circulation. 2004;110(10):1276-83.
Liu, W., Nakamura, H., Shioji, K., Tanito, M., Oka, S., Ahsan, M. K., Son, A., Ishii, Y., Kishimoto, C., & Yodoi, J. (2004). Thioredoxin-1 ameliorates myosin-induced autoimmune myocarditis by suppressing chemokine expressions and leukocyte chemotaxis in mice. Circulation, 110(10), 1276-83.
Liu W, et al. Thioredoxin-1 Ameliorates Myosin-induced Autoimmune Myocarditis By Suppressing Chemokine Expressions and Leukocyte Chemotaxis in Mice. Circulation. 2004 Sep 7;110(10):1276-83. PubMed PMID: 15337697.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Thioredoxin-1 ameliorates myosin-induced autoimmune myocarditis by suppressing chemokine expressions and leukocyte chemotaxis in mice. AU - Liu,Wenrui, AU - Nakamura,Hajime, AU - Shioji,Keisuke, AU - Tanito,Masaki, AU - Oka,Shin-ichi, AU - Ahsan,M Kaimul, AU - Son,Aoi, AU - Ishii,Yasuyuki, AU - Kishimoto,Chiharu, AU - Yodoi,Junji, Y1 - 2004/08/30/ PY - 2004/9/1/pubmed PY - 2006/4/8/medline PY - 2004/9/1/entrez SP - 1276 EP - 83 JF - Circulation JO - Circulation VL - 110 IS - 10 N2 - BACKGROUND: Cardiac myosin-induced myocarditis is an experimental autoimmune myocarditis (EAM) model used to investigate autoimmunological mechanisms in inflammatory heart diseases and resembles fulminant myocarditis in humans. We investigated the therapeutic role of thioredoxin-1 (TRX-1), a redox-regulatory protein with antioxidant and antiinflammatory effects, in murine EAM. METHODS AND RESULTS: EAM was generated in 5-week-old male BALB/c mice by immunization with porcine cardiac myosin at days 0 and 7. Recombinant human TRX-1 (rhTRX-1), C32S/C35S mutant rhTRX-1, or saline was administered intraperitoneally every second day from day 0 to 20. In addition, rabbit anti-mouse TRX-1 serum or normal rabbit serum was administered intraperitoneally on days -1, 2, and 6. Animals were euthanized on day 21. Histological analysis of the heart showed that TRX-1 significantly reduced the severity of EAM, whereas mutant TRX-1 failed to have such an effect, and anti-TRX-1 antibody enhanced the disease markedly. Immunohistochemical analysis showed that TRX-1 significantly suppressed cardiac macrophage inflammatory protein (MIP)-1alpha, MIP-2, and 8-hydroxydeoxyguanosine expression and macrophage infiltration into the heart in EAM. Although serum levels of MIP-1alpha were not suppressed by TRX-1 until day 21, both an in vitro chemotaxis chamber assay and an in vivo air pouch model showed that TRX-1 significantly suppressed MIP-1alpha- or MIP-2-induced leukocyte chemotaxis. However, real-time reverse transcription-polymerase chain reaction showed that TRX-1 failed to decrease chemokine receptor expression increased in the bone marrow cells of EAM mice. CONCLUSIONS: TRX-1 attenuates EAM by suppressing chemokine expressions and leukocyte chemotaxis in mice. SN - 1524-4539 UR - https://www.unboundmedicine.com/medline/citation/15337697/Thioredoxin_1_ameliorates_myosin_induced_autoimmune_myocarditis_by_suppressing_chemokine_expressions_and_leukocyte_chemotaxis_in_mice_ L2 - http://www.ahajournals.org/doi/full/10.1161/01.CIR.0000141803.41217.B6?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -