Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse Model
Tenascin-C (TN-C), an extracellular matrix (ECM) glycoprotein, is specifically induced upon tissue injury and infection and during septic conditions. Carbon monoxide (CO) gas is known to exert various anti-inflammatory effects in various inflammatory diseases. However, the mechanisms underlying the...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/613249 |
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| author | Md. Jamal Uddin Chun-shi Li Yeonsoo Joe Yingqing Chen Qinggao Zhang Stefan W. Ryter Hun Taeg Chung |
| author_facet | Md. Jamal Uddin Chun-shi Li Yeonsoo Joe Yingqing Chen Qinggao Zhang Stefan W. Ryter Hun Taeg Chung |
| author_sort | Md. Jamal Uddin |
| collection | DOAJ |
| description | Tenascin-C (TN-C), an extracellular matrix (ECM) glycoprotein, is specifically induced upon tissue injury and infection and during septic conditions. Carbon monoxide (CO) gas is known to exert various anti-inflammatory effects in various inflammatory diseases. However, the mechanisms underlying the effect of CO on TN-C-mediated inflammation are unknown. In the present study, we found that treatment with LPS significantly enhanced TN-C expression in macrophages. CO gas, or treatment with the CO-donor compound, CORM-2, dramatically reduced LPS-induced expression of TN-C and proinflammatory cytokines while significantly increased the expression of IL-10. Treatment with TN-C siRNA significantly suppressed the effects of LPS on proinflammatory cytokines production. TN-C siRNA did not affect the CORM-2-dependent increase of IL-10 expression. In cells transfected with IL-10 siRNA, CORM-2 had no effect on the LPS-induced expression of TN-C and its downstream cytokines. These data suggest that IL-10 mediates the inhibitory effect of CO on TN-C and the downstream production of proinflammatory cytokines. Additionally, administration of CORM-2 dramatically reduced LPS-induced TN-C and proinflammatory cytokines production while expression of IL-10 was significantly increased. In conclusion, CO regulated IL-10 expression and thus inhibited TN-C-mediated inflammation in vitro and in vivo. |
| format | Article |
| id | doaj-art-39721213b09149fab98202fad7f5ca8b |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-39721213b09149fab98202fad7f5ca8b2025-02-03T01:09:44ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/613249613249Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse ModelMd. Jamal Uddin0Chun-shi Li1Yeonsoo Joe2Yingqing Chen3Qinggao Zhang4Stefan W. Ryter5Hun Taeg Chung6School of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of KoreaDepartment of Pharmacology, Dalian University Medical college, Dalian, Liaoning 133000, ChinaSchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of KoreaSchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of KoreaDepartment of Pharmacology, Dalian University Medical college, Dalian, Liaoning 133000, ChinaJoan and Sanford I. Weill Department of Medicine, New York-Presbyterian Hospital, and Division of Pulmonary and Critical Care Medicine, Weill Cornell Medical Center, New York, NY 10065, USASchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of KoreaTenascin-C (TN-C), an extracellular matrix (ECM) glycoprotein, is specifically induced upon tissue injury and infection and during septic conditions. Carbon monoxide (CO) gas is known to exert various anti-inflammatory effects in various inflammatory diseases. However, the mechanisms underlying the effect of CO on TN-C-mediated inflammation are unknown. In the present study, we found that treatment with LPS significantly enhanced TN-C expression in macrophages. CO gas, or treatment with the CO-donor compound, CORM-2, dramatically reduced LPS-induced expression of TN-C and proinflammatory cytokines while significantly increased the expression of IL-10. Treatment with TN-C siRNA significantly suppressed the effects of LPS on proinflammatory cytokines production. TN-C siRNA did not affect the CORM-2-dependent increase of IL-10 expression. In cells transfected with IL-10 siRNA, CORM-2 had no effect on the LPS-induced expression of TN-C and its downstream cytokines. These data suggest that IL-10 mediates the inhibitory effect of CO on TN-C and the downstream production of proinflammatory cytokines. Additionally, administration of CORM-2 dramatically reduced LPS-induced TN-C and proinflammatory cytokines production while expression of IL-10 was significantly increased. In conclusion, CO regulated IL-10 expression and thus inhibited TN-C-mediated inflammation in vitro and in vivo.http://dx.doi.org/10.1155/2015/613249 |
| spellingShingle | Md. Jamal Uddin Chun-shi Li Yeonsoo Joe Yingqing Chen Qinggao Zhang Stefan W. Ryter Hun Taeg Chung Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse Model Mediators of Inflammation |
| title | Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse Model |
| title_full | Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse Model |
| title_fullStr | Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse Model |
| title_full_unstemmed | Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse Model |
| title_short | Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse Model |
| title_sort | carbon monoxide inhibits tenascin c mediated inflammation via il 10 expression in a septic mouse model |
| url | http://dx.doi.org/10.1155/2015/613249 |
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