β2 adrenergic activation induces the expression of IL-18 binding protein, a potent inhibitor of isoproterenol induced cardiomyocyte hypertrophy in vitro and myocardial hypertrophy in vivo
David R. Murray,Srinivas Mummidi,Anthony J. Valente,Tadashi Yoshida,Naveen K. Somanna,Patrice Delafontaine,Charles A. Dinarello,Bysani Chandrasekar +7 more
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TLDR
It is demonstrated that the β-AR agonist isoproterenol (ISO) increases steady state IL-18BP mRNA and protein levels in adult mouse cardiomyocytes in a β(2)-AR-dependent manner, and that ISO-induced hypertrophy in vitro was dependent on IL- 18 induction as it was blunted byIL-18 neutralizing antibodies and forced expression of IL-17BP.About:
This article is published in Journal of Molecular and Cellular Cardiology.The article was published on 2012-01-01 and is currently open access. It has received 34 citations till now. The article focuses on the topics: CREB & Ccaat-enhancer-binding proteins.read more
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Overview of the IL-1 family in innate inflammation and acquired immunity.
TL;DR: Although the inflammatory properties of the IL‐1 family dominate in innate immunity, IL‐2 family member can play a role in acquired immunity and this overview is a condensed update.
Journal ArticleDOI
Interleukin-18, more than a Th1 cytokine
TL;DR: A role for IL-18 has been implicated in several autoimmune diseases, myocardial function, emphysema, metabolic syndromes, psoriasis, inflammatory bowel disease, macrophage activation syndrome, sepsis and acute kidney injury, although paradoxically, in some models of disease, IL- 18 is protective.
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Induction of M2 regulatory macrophages through the β2-adrenergic receptor with protection during endotoxemia and acute lung injury.
TL;DR: A role for the β2-adrenergic receptor is demonstrated in promoting the M2 macrophage phenotype in mouse models of endotoxemia and LPS-induced acute lung injury, respectively.
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Interleukin-18 as a Therapeutic Target in Acute Myocardial Infarction and Heart Failure
Laura C. O’Brien,Eleonora Mezzaroma,Benjamin W. Van Tassell,Carlo Marchetti,Salvatore Carbone,Antonio Abbate,Stefano Toldo +6 more
TL;DR: The literature regarding the role of IL-18 in AMI and heart failure and the evidence and challenges of usingIL-18BP and blocking IL- 18 antibodies as a therapeutic strategy in patients with heart disease are reviewed.
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PDE1C deficiency antagonizes pathological cardiac remodeling and dysfunction
Walter E. Knight,Si Chen,Yi-shuai Zhang,Masayoshi Oikawa,Mei-ping Wu,Mei-ping Wu,Qian Zhou,Clint L. Miller,Yu-Jun Cai,Deanne Mickelsen,Christine S. Moravec,Eric M. Small,Jun Ichi Abe,Chen Yan +13 more
TL;DR: In vivo, cardiac remodeling and dysfunction induced by transverse aortic constriction, including myocardial hypertrophy, apoptosis, cardiac fibrosis, and loss of contractile function were significantly attenuated in PDE1C-knockout mice relative to wild-type mice.
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Evolving Concepts in G Protein-Coupled Receptor Endocytosis: The Role in Receptor Desensitization and Signaling
TL;DR: The focus of this review is the current and evolving understanding of the contribution of GRKs, beta-arrestins, and endocytosis to GPCR-specific patterns of desensitization and resensitized.
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Switching of the coupling of the beta2-adrenergic receptor to different G proteins by protein kinase A.
TL;DR: A mechanism previously shown to mediate uncoupling of the β2-adrenergic receptor from Gs and thus heterologous desensitization (PKA-mediated receptor phosphorylation), also serves to ‘switch’ coupling of this receptor fromGs to Gi and initiate a new set of signalling events.
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Phosphorylation of NF-κB p65 by PKA Stimulates Transcriptional Activity by Promoting a Novel Bivalent Interaction with the Coactivator CBP/p300
TL;DR: Phosphorylation by PKA both weakens the interaction between the N- and C-terminal regions of p65 and creates an additional site for interaction with CBP/p300, which regulates the transcriptional activity of NF-kappa B by modulating its interaction withCBP/ p300.
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CREB Is a Regulatory Target for the Protein Kinase Akt/PKB
Keyong Du,Marc Montminy +1 more
TL;DR: The results support the notion that Akt/PKB promotes cell survival, at least in part, by stimulating the expression of cellular genes via the CREB/CBP nuclear transduction pathway.
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β-Adrenergic Receptor Blockade in Chronic Heart Failure
TL;DR: This review describes how a treatment that began as a contraindication became an established treatment of chronic heart failure with β-adrenergic blocking agents.