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Cross-regulation of carbon monoxide and the adenosine A2a receptor in macrophages

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Cross-regulation of carbon monoxide and the adenosine A2a receptor in macrophages. / Haschemi, Arvand; Wagner, Oswald; Marculescu, Rodrig; Wegiel, Barbara; Robson, Simon C; Gagliani, Nicola; Gallo, David; Chen, Jiang-Fan; Bach, Fritz H; Otterbein, Leo E.

in: J IMMUNOL, Jahrgang 178, Nr. 9, 01.05.2007, S. 5921-9.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Haschemi, A, Wagner, O, Marculescu, R, Wegiel, B, Robson, SC, Gagliani, N, Gallo, D, Chen, J-F, Bach, FH & Otterbein, LE 2007, 'Cross-regulation of carbon monoxide and the adenosine A2a receptor in macrophages', J IMMUNOL, Jg. 178, Nr. 9, S. 5921-9.

APA

Haschemi, A., Wagner, O., Marculescu, R., Wegiel, B., Robson, S. C., Gagliani, N., Gallo, D., Chen, J-F., Bach, F. H., & Otterbein, L. E. (2007). Cross-regulation of carbon monoxide and the adenosine A2a receptor in macrophages. J IMMUNOL, 178(9), 5921-9.

Vancouver

Haschemi A, Wagner O, Marculescu R, Wegiel B, Robson SC, Gagliani N et al. Cross-regulation of carbon monoxide and the adenosine A2a receptor in macrophages. J IMMUNOL. 2007 Mai 1;178(9):5921-9.

Bibtex

@article{520bd4389a3c4aacb3da63eb5ad7a7dc,
title = "Cross-regulation of carbon monoxide and the adenosine A2a receptor in macrophages",
abstract = "Adenosine and heme oxygenase-1 (HO-1) exert a wide range of anti-inflammatory and immunomodulatory actions, making them crucial regulatory molecules. Despite the diversity in their modes of action, the similarity of biological effects of adenosine and HO-1 led us to hypothesize a possible interrelationship between them. We assessed a potential role for HO-1 in the ability of adenosine or 5'-N-ethylcarboxamidoadenosine (NECA), a stable adenosine analog, to modify the response of LPS-stimulated macrophages. Adenosine and NECA markedly induced HO-1 and blocked LPS-induced TNF-alpha production via adenosine A2aR-mediated signaling; blocking of HO-1 by RNA interference abrogated the effects of adenosine and NECA on TNF-alpha. HO-1 overexpression or exposure to carbon monoxide (CO), a product of HO-1 enzymatic activity, resulted in augmented A2aR mRNA and protein levels in RAW264.7 cells and primary macrophages. The induction of A2aR expression by HO-1 or CO resulted in an increase in the sensitivity to the anti-inflammatory effects of adenosine and NECA, which was lost in macrophages isolated from A2aR-deficient mice. Moreover, a decrease in cAMP levels upon NECA stimulation of naive macrophages was counterbalanced by CO exposure to up-regulate A2aR levels. This implies adenosine receptor isoform switch as a selective modification in macrophage phenotype. Taken together, these data suggest the existence of a positive feedback loop among adenosine, HO-1, CO, and the A2aR in the chronological resolution of the inflammatory response.",
keywords = "Adenosine, Adenosine-5'-(N-ethylcarboxamide), Animals, Carbon Monoxide, Cells, Cultured, Down-Regulation, Heme Oxygenase-1, Interleukin-10, Interleukin-12, Lipopolysaccharides, Macrophages, Mice, RNA Interference, RNA, Messenger, Receptor, Adenosine A2A, Tumor Necrosis Factor-alpha, Journal Article",
author = "Arvand Haschemi and Oswald Wagner and Rodrig Marculescu and Barbara Wegiel and Robson, {Simon C} and Nicola Gagliani and David Gallo and Jiang-Fan Chen and Bach, {Fritz H} and Otterbein, {Leo E}",
year = "2007",
month = may,
day = "1",
language = "English",
volume = "178",
pages = "5921--9",
journal = "J IMMUNOL",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "9",

}

RIS

TY - JOUR

T1 - Cross-regulation of carbon monoxide and the adenosine A2a receptor in macrophages

AU - Haschemi, Arvand

AU - Wagner, Oswald

AU - Marculescu, Rodrig

AU - Wegiel, Barbara

AU - Robson, Simon C

AU - Gagliani, Nicola

AU - Gallo, David

AU - Chen, Jiang-Fan

AU - Bach, Fritz H

AU - Otterbein, Leo E

PY - 2007/5/1

Y1 - 2007/5/1

N2 - Adenosine and heme oxygenase-1 (HO-1) exert a wide range of anti-inflammatory and immunomodulatory actions, making them crucial regulatory molecules. Despite the diversity in their modes of action, the similarity of biological effects of adenosine and HO-1 led us to hypothesize a possible interrelationship between them. We assessed a potential role for HO-1 in the ability of adenosine or 5'-N-ethylcarboxamidoadenosine (NECA), a stable adenosine analog, to modify the response of LPS-stimulated macrophages. Adenosine and NECA markedly induced HO-1 and blocked LPS-induced TNF-alpha production via adenosine A2aR-mediated signaling; blocking of HO-1 by RNA interference abrogated the effects of adenosine and NECA on TNF-alpha. HO-1 overexpression or exposure to carbon monoxide (CO), a product of HO-1 enzymatic activity, resulted in augmented A2aR mRNA and protein levels in RAW264.7 cells and primary macrophages. The induction of A2aR expression by HO-1 or CO resulted in an increase in the sensitivity to the anti-inflammatory effects of adenosine and NECA, which was lost in macrophages isolated from A2aR-deficient mice. Moreover, a decrease in cAMP levels upon NECA stimulation of naive macrophages was counterbalanced by CO exposure to up-regulate A2aR levels. This implies adenosine receptor isoform switch as a selective modification in macrophage phenotype. Taken together, these data suggest the existence of a positive feedback loop among adenosine, HO-1, CO, and the A2aR in the chronological resolution of the inflammatory response.

AB - Adenosine and heme oxygenase-1 (HO-1) exert a wide range of anti-inflammatory and immunomodulatory actions, making them crucial regulatory molecules. Despite the diversity in their modes of action, the similarity of biological effects of adenosine and HO-1 led us to hypothesize a possible interrelationship between them. We assessed a potential role for HO-1 in the ability of adenosine or 5'-N-ethylcarboxamidoadenosine (NECA), a stable adenosine analog, to modify the response of LPS-stimulated macrophages. Adenosine and NECA markedly induced HO-1 and blocked LPS-induced TNF-alpha production via adenosine A2aR-mediated signaling; blocking of HO-1 by RNA interference abrogated the effects of adenosine and NECA on TNF-alpha. HO-1 overexpression or exposure to carbon monoxide (CO), a product of HO-1 enzymatic activity, resulted in augmented A2aR mRNA and protein levels in RAW264.7 cells and primary macrophages. The induction of A2aR expression by HO-1 or CO resulted in an increase in the sensitivity to the anti-inflammatory effects of adenosine and NECA, which was lost in macrophages isolated from A2aR-deficient mice. Moreover, a decrease in cAMP levels upon NECA stimulation of naive macrophages was counterbalanced by CO exposure to up-regulate A2aR levels. This implies adenosine receptor isoform switch as a selective modification in macrophage phenotype. Taken together, these data suggest the existence of a positive feedback loop among adenosine, HO-1, CO, and the A2aR in the chronological resolution of the inflammatory response.

KW - Adenosine

KW - Adenosine-5'-(N-ethylcarboxamide)

KW - Animals

KW - Carbon Monoxide

KW - Cells, Cultured

KW - Down-Regulation

KW - Heme Oxygenase-1

KW - Interleukin-10

KW - Interleukin-12

KW - Lipopolysaccharides

KW - Macrophages

KW - Mice

KW - RNA Interference

KW - RNA, Messenger

KW - Receptor, Adenosine A2A

KW - Tumor Necrosis Factor-alpha

KW - Journal Article

M3 - SCORING: Journal article

C2 - 17442976

VL - 178

SP - 5921

EP - 5929

JO - J IMMUNOL

JF - J IMMUNOL

SN - 0022-1767

IS - 9

ER -