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10.1161/CIRCULATIONAHA.116.022304 http://scihub22266oqcxt.onion/10.1161/CIRCULATIONAHA.116.022304 C5120587!5120587!27364164     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27364164&cmd=llinks): Failed to open stream: HTTP request failed! 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Leukocyte-Expressed ?2-Adrenergic Receptors are Essential for Survival Following Acute Myocardial Injury |pdf=|usr=}}{{27364164}} gab.com Text Leukocyte-Expressed 2-Adrenergic Receptors are Essential for Survival Following Acute Myocardial Injury JO: Circulation http://www.kidney.de/pget.php?&tw=1&pmid=27364164 #FOAvip Background: Immune cell-mediated inflammation is an essential process for mounting a repair response following myocardial infarction (MI). The sympathetic nervous system is known to regulate immune system function through ?-adrenergic receptors (?AR), however their role in regulating immune cell responses to acute cardiac injury is unknown. Methods: Wild-type (WT) mice were irradiated followed by isoform-specific ?ARKO or WT bone-marrow transplantation (BMT) and after full reconstitution underwent myocardial infarction (MI) surgery. Survival was monitored over time and alterations in immune cell infiltration following MI were examined using immunohistochemistry. Alterations in splenic function were identified through the investigation of altered adhesion receptor expression. Results: ?2ARKO BMT mice displayed 100% mortality resulting from cardiac rupture within 12 days post-MI compared to ~20% mortality in WT BMT mice. ?2ARKO BMT mice displayed severely reduced post-MI cardiac infiltration of leukocytes with reciprocally enhanced splenic retention of the same immune cell populations. Splenic retention of the leukocytes was associated with an increase in VCAM-1 expression, which was itself regulated via ?-arrestin-dependent ?2AR signaling. Further, VCAM-1 expression in both mouse and human macrophages was sensitive to ?2AR activity, and spleens from human tissue donors treated with ?-blocker showed enhanced VCAM1 expression. The impairments in splenic retention and cardiac infiltration of leukocytes following MI were restored to WT levels via lentiviral-mediated re-expression of ?2AR in ?2ARKO BM prior to transplantation, which also resulted in post-MI survival rates comparable to WT BMT mice. Conclusions: Immune cell-expressed ?2AR plays an essential role in regulating the early inflammatory repair response to acute myocardial injury by facilitating cardiac leukocyte infiltration. Twit Text FOAVip Leukocyte-Expressed 2-Adrenergic Receptors are Essential for Survival Following Acute Myocardial Injury ????Circulation http://www.kidney.de/pget.php?&tw=1&pmid=27364164 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27364164 #FOAvip English Wikipedia <ref>{{Cite pmid|27364164}}</ref> Leukocyte-Expressed ?2-Adrenergic Receptors are Essential for Survival Following Acute Myocardial Injury #MMPMID27364164 Grisanti LA; Gumpert AM; Traynham CJ; Gorsky JE; Repas AA; Gao E; Carter RL; Yu D; Calvert JW; García AP; Ibáñez B; Rabinowitz JE; Koch WJ; Tilley DG Circulation 2016[Jul]; 134 (2): 153-67 PMID27364164show ga Background: Immune cell-mediated inflammation is an essential process for mounting a repair response following myocardial infarction (MI). The sympathetic nervous system is known to regulate immune system function through ?-adrenergic receptors (?AR), however their role in regulating immune cell responses to acute cardiac injury is unknown. Methods: Wild-type (WT) mice were irradiated followed by isoform-specific ?ARKO or WT bone-marrow transplantation (BMT) and after full reconstitution underwent myocardial infarction (MI) surgery. Survival was monitored over time and alterations in immune cell infiltration following MI were examined using immunohistochemistry. Alterations in splenic function were identified through the investigation of altered adhesion receptor expression. Results: ?2ARKO BMT mice displayed 100% mortality resulting from cardiac rupture within 12 days post-MI compared to ~20% mortality in WT BMT mice. ?2ARKO BMT mice displayed severely reduced post-MI cardiac infiltration of leukocytes with reciprocally enhanced splenic retention of the same immune cell populations. Splenic retention of the leukocytes was associated with an increase in VCAM-1 expression, which was itself regulated via ?-arrestin-dependent ?2AR signaling. Further, VCAM-1 expression in both mouse and human macrophages was sensitive to ?2AR activity, and spleens from human tissue donors treated with ?-blocker showed enhanced VCAM1 expression. The impairments in splenic retention and cardiac infiltration of leukocytes following MI were restored to WT levels via lentiviral-mediated re-expression of ?2AR in ?2ARKO BM prior to transplantation, which also resulted in post-MI survival rates comparable to WT BMT mice. Conclusions: Immune cell-expressed ?2AR plays an essential role in regulating the early inflammatory repair response to acute myocardial injury by facilitating cardiac leukocyte infiltration. äLeukocyte-Expressed ?2-Adrenergic Receptors are Essential for Survival(epmc).pdf DeepDyve Pubget Overpricing