Eintrag weiter verarbeiten
Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury
Gespeichert in:
| Zeitschriftentitel: | Anesthesiology |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| In: | Anesthesiology, 116, 2012, 6, S. 1245-1257 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
|
| Schlagwörter: |
| author_facet |
Koeppen, Michael Harter, Patrick N. Bonney, Stephanie Bonney, Megan Reithel, Susan Zachskorn, Cornelia Mittelbronn, Michel Eckle, Tobias Koeppen, Michael Harter, Patrick N. Bonney, Stephanie Bonney, Megan Reithel, Susan Zachskorn, Cornelia Mittelbronn, Michel Eckle, Tobias |
|---|---|
| author |
Koeppen, Michael Harter, Patrick N. Bonney, Stephanie Bonney, Megan Reithel, Susan Zachskorn, Cornelia Mittelbronn, Michel Eckle, Tobias |
| spellingShingle |
Koeppen, Michael Harter, Patrick N. Bonney, Stephanie Bonney, Megan Reithel, Susan Zachskorn, Cornelia Mittelbronn, Michel Eckle, Tobias Anesthesiology Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury Anesthesiology and Pain Medicine |
| author_sort |
koeppen, michael |
| spelling |
Koeppen, Michael Harter, Patrick N. Bonney, Stephanie Bonney, Megan Reithel, Susan Zachskorn, Cornelia Mittelbronn, Michel Eckle, Tobias 0003-3022 Ovid Technologies (Wolters Kluwer Health) Anesthesiology and Pain Medicine http://dx.doi.org/10.1097/aln.0b013e318255793c <jats:sec> <jats:title>Background</jats:title> <jats:p>Cardiac ischemia-reperfusion (I-R) injury represents a major cause of cardiac tissue injury. Adenosine signaling dampens inflammation during cardiac I-R. The authors investigated the role of the adenosine A2b-receptor (Adora2b) on inflammatory cells during cardiac I-R.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>To study Adora2b signaling on inflammatory cells, the authors transplanted wild-type (WT) bone marrow (BM) into Adora2b(-/-) mice or Adora2b(-/-) BM into WT mice. To study the role of polymorphonuclear leukocytes (PMNs), neutrophil-depleted WT mice were treated with an Adora2b agonist. After treatments, mice were exposed to 60 min of myocardial ischemia and 120 min of reperfusion. Infarct sizes and troponin I concentrations were determined by triphenyltetrazolium chloride staining and enzyme-linked immunosorbent assay, respectively.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Transplantation of WT BM into Adora2b(-/-) mice decreased infarct sizes by 19 ± 4% and troponin I by 87.5 ± 25.3 ng/ml (mean ± SD, n = 6). Transplantation of Adora2b(-/-) BM into WT mice increased infarct sizes by 20 ± 3% and troponin I concentrations by 69.7 ± 17.9 ng/ml (mean ± SD, n = 6). Studies on the reperfused myocardium revealed PMNs as the dominant cell type. PMN depletion or Adora2b agonist treatment reduced infarct sizes by 30 ± 11% or 26 ± 13% (mean ± SD, n = 4); however, the combination of both did not produce additional cardioprotection. Cytokine profiling showed significantly higher cardiac tumor necrosis factor α concentrations in Adora2b(-/-) compared with WT mice (39.3 ± 5.3 vs. 7.5 ± 1.0 pg/mg protein, mean ± SD, n = 4). Pharmacologic studies on human-activated PMNs revealed an Adora2b-dependent tumor necrosis factor α release.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion</jats:title> <jats:p>Adora2b signaling on BM-derived cells such as PMNs represents an endogenous cardioprotective mechanism during cardiac I-R. The authors' findings suggest that Adora2b agonist treatment during cardiac I-R reduces tumor necrosis factor α release of PMNs, thereby dampening tissue injury.</jats:p> </jats:sec> Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury Anesthesiology |
| doi_str_mv |
10.1097/aln.0b013e318255793c |
| facet_avail |
Online Free |
| finc_class_facet |
Medizin |
| format |
ElectronicArticle |
| fullrecord |
blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTA5Ny9hbG4uMGIwMTNlMzE4MjU1NzkzYw |
| id |
ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTA5Ny9hbG4uMGIwMTNlMzE4MjU1NzkzYw |
| institution |
DE-Brt1 DE-Zwi2 DE-D161 DE-Gla1 DE-Zi4 DE-15 DE-Pl11 DE-Rs1 DE-105 DE-14 DE-Ch1 DE-L229 DE-D275 DE-Bn3 |
| imprint |
Ovid Technologies (Wolters Kluwer Health), 2012 |
| imprint_str_mv |
Ovid Technologies (Wolters Kluwer Health), 2012 |
| issn |
0003-3022 |
| issn_str_mv |
0003-3022 |
| language |
English |
| mega_collection |
Ovid Technologies (Wolters Kluwer Health) (CrossRef) |
| match_str |
koeppen2012adora2bsignalingonbonemarrowderivedcellsdampensmyocardialischemiareperfusioninjury |
| publishDateSort |
2012 |
| publisher |
Ovid Technologies (Wolters Kluwer Health) |
| recordtype |
ai |
| record_format |
ai |
| series |
Anesthesiology |
| source_id |
49 |
| title |
Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_unstemmed |
Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_full |
Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_fullStr |
Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_full_unstemmed |
Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_short |
Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_sort |
adora2b signaling on bone marrow derived cells dampens myocardial ischemia-reperfusion injury |
| topic |
Anesthesiology and Pain Medicine |
| url |
http://dx.doi.org/10.1097/aln.0b013e318255793c |
| publishDate |
2012 |
| physical |
1245-1257 |
| description |
<jats:sec>
<jats:title>Background</jats:title>
<jats:p>Cardiac ischemia-reperfusion (I-R) injury represents a major cause of cardiac tissue injury. Adenosine signaling dampens inflammation during cardiac I-R. The authors investigated the role of the adenosine A2b-receptor (Adora2b) on inflammatory cells during cardiac I-R.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Methods</jats:title>
<jats:p>To study Adora2b signaling on inflammatory cells, the authors transplanted wild-type (WT) bone marrow (BM) into Adora2b(-/-) mice or Adora2b(-/-) BM into WT mice. To study the role of polymorphonuclear leukocytes (PMNs), neutrophil-depleted WT mice were treated with an Adora2b agonist. After treatments, mice were exposed to 60 min of myocardial ischemia and 120 min of reperfusion. Infarct sizes and troponin I concentrations were determined by triphenyltetrazolium chloride staining and enzyme-linked immunosorbent assay, respectively.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Results</jats:title>
<jats:p>Transplantation of WT BM into Adora2b(-/-) mice decreased infarct sizes by 19 ± 4% and troponin I by 87.5 ± 25.3 ng/ml (mean ± SD, n = 6). Transplantation of Adora2b(-/-) BM into WT mice increased infarct sizes by 20 ± 3% and troponin I concentrations by 69.7 ± 17.9 ng/ml (mean ± SD, n = 6). Studies on the reperfused myocardium revealed PMNs as the dominant cell type. PMN depletion or Adora2b agonist treatment reduced infarct sizes by 30 ± 11% or 26 ± 13% (mean ± SD, n = 4); however, the combination of both did not produce additional cardioprotection. Cytokine profiling showed significantly higher cardiac tumor necrosis factor α concentrations in Adora2b(-/-) compared with WT mice (39.3 ± 5.3 vs. 7.5 ± 1.0 pg/mg protein, mean ± SD, n = 4). Pharmacologic studies on human-activated PMNs revealed an Adora2b-dependent tumor necrosis factor α release.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Conclusion</jats:title>
<jats:p>Adora2b signaling on BM-derived cells such as PMNs represents an endogenous cardioprotective mechanism during cardiac I-R. The authors' findings suggest that Adora2b agonist treatment during cardiac I-R reduces tumor necrosis factor α release of PMNs, thereby dampening tissue injury.</jats:p>
</jats:sec> |
| container_issue |
6 |
| container_start_page |
1245 |
| container_title |
Anesthesiology |
| container_volume |
116 |
| format_de105 |
Article, E-Article |
| format_de14 |
Article, E-Article |
| format_de15 |
Article, E-Article |
| format_de520 |
Article, E-Article |
| format_de540 |
Article, E-Article |
| format_dech1 |
Article, E-Article |
| format_ded117 |
Article, E-Article |
| format_degla1 |
E-Article |
| format_del152 |
Buch |
| format_del189 |
Article, E-Article |
| format_dezi4 |
Article |
| format_dezwi2 |
Article, E-Article |
| format_finc |
Article, E-Article |
| format_nrw |
Article, E-Article |
| _version_ |
1792343625091252230 |
| geogr_code |
not assigned |
| last_indexed |
2024-03-01T16:54:39.212Z |
| geogr_code_person |
not assigned |
| openURL |
url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=Adora2b+Signaling+on+Bone+Marrow+Derived+Cells+Dampens+Myocardial+Ischemia-Reperfusion+Injury&rft.date=2012-06-01&genre=article&issn=0003-3022&volume=116&issue=6&spage=1245&epage=1257&pages=1245-1257&jtitle=Anesthesiology&atitle=Adora2b+Signaling+on+Bone+Marrow+Derived+Cells+Dampens+Myocardial+Ischemia-Reperfusion+Injury&aulast=Eckle&aufirst=Tobias&rft_id=info%3Adoi%2F10.1097%2Faln.0b013e318255793c&rft.language%5B0%5D=eng |
| SOLR | |
| _version_ | 1792343625091252230 |
| author | Koeppen, Michael, Harter, Patrick N., Bonney, Stephanie, Bonney, Megan, Reithel, Susan, Zachskorn, Cornelia, Mittelbronn, Michel, Eckle, Tobias |
| author_facet | Koeppen, Michael, Harter, Patrick N., Bonney, Stephanie, Bonney, Megan, Reithel, Susan, Zachskorn, Cornelia, Mittelbronn, Michel, Eckle, Tobias, Koeppen, Michael, Harter, Patrick N., Bonney, Stephanie, Bonney, Megan, Reithel, Susan, Zachskorn, Cornelia, Mittelbronn, Michel, Eckle, Tobias |
| author_sort | koeppen, michael |
| container_issue | 6 |
| container_start_page | 1245 |
| container_title | Anesthesiology |
| container_volume | 116 |
| description | <jats:sec> <jats:title>Background</jats:title> <jats:p>Cardiac ischemia-reperfusion (I-R) injury represents a major cause of cardiac tissue injury. Adenosine signaling dampens inflammation during cardiac I-R. The authors investigated the role of the adenosine A2b-receptor (Adora2b) on inflammatory cells during cardiac I-R.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>To study Adora2b signaling on inflammatory cells, the authors transplanted wild-type (WT) bone marrow (BM) into Adora2b(-/-) mice or Adora2b(-/-) BM into WT mice. To study the role of polymorphonuclear leukocytes (PMNs), neutrophil-depleted WT mice were treated with an Adora2b agonist. After treatments, mice were exposed to 60 min of myocardial ischemia and 120 min of reperfusion. Infarct sizes and troponin I concentrations were determined by triphenyltetrazolium chloride staining and enzyme-linked immunosorbent assay, respectively.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Transplantation of WT BM into Adora2b(-/-) mice decreased infarct sizes by 19 ± 4% and troponin I by 87.5 ± 25.3 ng/ml (mean ± SD, n = 6). Transplantation of Adora2b(-/-) BM into WT mice increased infarct sizes by 20 ± 3% and troponin I concentrations by 69.7 ± 17.9 ng/ml (mean ± SD, n = 6). Studies on the reperfused myocardium revealed PMNs as the dominant cell type. PMN depletion or Adora2b agonist treatment reduced infarct sizes by 30 ± 11% or 26 ± 13% (mean ± SD, n = 4); however, the combination of both did not produce additional cardioprotection. Cytokine profiling showed significantly higher cardiac tumor necrosis factor α concentrations in Adora2b(-/-) compared with WT mice (39.3 ± 5.3 vs. 7.5 ± 1.0 pg/mg protein, mean ± SD, n = 4). Pharmacologic studies on human-activated PMNs revealed an Adora2b-dependent tumor necrosis factor α release.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion</jats:title> <jats:p>Adora2b signaling on BM-derived cells such as PMNs represents an endogenous cardioprotective mechanism during cardiac I-R. The authors' findings suggest that Adora2b agonist treatment during cardiac I-R reduces tumor necrosis factor α release of PMNs, thereby dampening tissue injury.</jats:p> </jats:sec> |
| doi_str_mv | 10.1097/aln.0b013e318255793c |
| facet_avail | Online, Free |
| finc_class_facet | Medizin |
| format | ElectronicArticle |
| format_de105 | Article, E-Article |
| format_de14 | Article, E-Article |
| format_de15 | Article, E-Article |
| format_de520 | Article, E-Article |
| format_de540 | Article, E-Article |
| format_dech1 | Article, E-Article |
| format_ded117 | Article, E-Article |
| format_degla1 | E-Article |
| format_del152 | Buch |
| format_del189 | Article, E-Article |
| format_dezi4 | Article |
| format_dezwi2 | Article, E-Article |
| format_finc | Article, E-Article |
| format_nrw | Article, E-Article |
| geogr_code | not assigned |
| geogr_code_person | not assigned |
| id | ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTA5Ny9hbG4uMGIwMTNlMzE4MjU1NzkzYw |
| imprint | Ovid Technologies (Wolters Kluwer Health), 2012 |
| imprint_str_mv | Ovid Technologies (Wolters Kluwer Health), 2012 |
| institution | DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3 |
| issn | 0003-3022 |
| issn_str_mv | 0003-3022 |
| language | English |
| last_indexed | 2024-03-01T16:54:39.212Z |
| match_str | koeppen2012adora2bsignalingonbonemarrowderivedcellsdampensmyocardialischemiareperfusioninjury |
| mega_collection | Ovid Technologies (Wolters Kluwer Health) (CrossRef) |
| physical | 1245-1257 |
| publishDate | 2012 |
| publishDateSort | 2012 |
| publisher | Ovid Technologies (Wolters Kluwer Health) |
| record_format | ai |
| recordtype | ai |
| series | Anesthesiology |
| source_id | 49 |
| spelling | Koeppen, Michael Harter, Patrick N. Bonney, Stephanie Bonney, Megan Reithel, Susan Zachskorn, Cornelia Mittelbronn, Michel Eckle, Tobias 0003-3022 Ovid Technologies (Wolters Kluwer Health) Anesthesiology and Pain Medicine http://dx.doi.org/10.1097/aln.0b013e318255793c <jats:sec> <jats:title>Background</jats:title> <jats:p>Cardiac ischemia-reperfusion (I-R) injury represents a major cause of cardiac tissue injury. Adenosine signaling dampens inflammation during cardiac I-R. The authors investigated the role of the adenosine A2b-receptor (Adora2b) on inflammatory cells during cardiac I-R.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>To study Adora2b signaling on inflammatory cells, the authors transplanted wild-type (WT) bone marrow (BM) into Adora2b(-/-) mice or Adora2b(-/-) BM into WT mice. To study the role of polymorphonuclear leukocytes (PMNs), neutrophil-depleted WT mice were treated with an Adora2b agonist. After treatments, mice were exposed to 60 min of myocardial ischemia and 120 min of reperfusion. Infarct sizes and troponin I concentrations were determined by triphenyltetrazolium chloride staining and enzyme-linked immunosorbent assay, respectively.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Transplantation of WT BM into Adora2b(-/-) mice decreased infarct sizes by 19 ± 4% and troponin I by 87.5 ± 25.3 ng/ml (mean ± SD, n = 6). Transplantation of Adora2b(-/-) BM into WT mice increased infarct sizes by 20 ± 3% and troponin I concentrations by 69.7 ± 17.9 ng/ml (mean ± SD, n = 6). Studies on the reperfused myocardium revealed PMNs as the dominant cell type. PMN depletion or Adora2b agonist treatment reduced infarct sizes by 30 ± 11% or 26 ± 13% (mean ± SD, n = 4); however, the combination of both did not produce additional cardioprotection. Cytokine profiling showed significantly higher cardiac tumor necrosis factor α concentrations in Adora2b(-/-) compared with WT mice (39.3 ± 5.3 vs. 7.5 ± 1.0 pg/mg protein, mean ± SD, n = 4). Pharmacologic studies on human-activated PMNs revealed an Adora2b-dependent tumor necrosis factor α release.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion</jats:title> <jats:p>Adora2b signaling on BM-derived cells such as PMNs represents an endogenous cardioprotective mechanism during cardiac I-R. The authors' findings suggest that Adora2b agonist treatment during cardiac I-R reduces tumor necrosis factor α release of PMNs, thereby dampening tissue injury.</jats:p> </jats:sec> Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury Anesthesiology |
| spellingShingle | Koeppen, Michael, Harter, Patrick N., Bonney, Stephanie, Bonney, Megan, Reithel, Susan, Zachskorn, Cornelia, Mittelbronn, Michel, Eckle, Tobias, Anesthesiology, Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury, Anesthesiology and Pain Medicine |
| title | Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_full | Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_fullStr | Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_full_unstemmed | Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_short | Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| title_sort | adora2b signaling on bone marrow derived cells dampens myocardial ischemia-reperfusion injury |
| title_unstemmed | Adora2b Signaling on Bone Marrow Derived Cells Dampens Myocardial Ischemia-Reperfusion Injury |
| topic | Anesthesiology and Pain Medicine |
| url | http://dx.doi.org/10.1097/aln.0b013e318255793c |