Involvement of the Serotonin 5-HT2B Receptor in Cardiac Hypertrophy Linked to Sympathetic Stimulation Control of Interleukin-6, Interleukin-1 , and Tumor Necrosis Factor- Cytokine Production by Ventricular Fibroblasts

نویسندگان

  • Laurent Monassier
  • Fabrice Jaffré
  • Jacques Callebert
  • Alexandre Sarre
  • Nelly Etienne
  • Canan G. Nebigil
چکیده

Fabrice Jaffré, Jacques Callebert, Alexandre Sarre, Nelly Etienne, Canan G. Nebigil, Jean-Marie Cytokine Production by Ventricular Fibroblasts α Factor, and Tumor Necrosis β Sympathetic Stimulation : Control of Interleukin-6, Interleukin-1 Receptor in Cardiac Hypertrophy Linked to 2B Involvement of the Serotonin 5-HT Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 2004 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation doi: 10.1161/01.CIR.0000139856.20505.57 2004;110:969-974; originally published online August 9, 2004; Circulation. http://circ.ahajournals.org/content/110/8/969 World Wide Web at: The online version of this article, along with updated information and services, is located on the

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Integrative Physiology Serotonin and Angiotensin Receptors in Cardiac Fibroblasts Coregulate Adrenergic-Dependent Cardiac Hypertrophy

By mimicking sympathetic stimulation in vivo, we previously reported that mice globally lacking serotonin 5-HT2B receptors did not develop isoproterenol-induced left ventricular hypertrophy. However, the exact cardiac cell type(s) expressing 5-HT2B receptors (cardiomyocytes versus noncardiomyocytes) involved in pathological heart hypertrophy was never addressed in vivo. We report here that mice...

متن کامل

Serotonin and angiotensin receptors in cardiac fibroblasts coregulate adrenergic-dependent cardiac hypertrophy.

By mimicking sympathetic stimulation in vivo, we previously reported that mice globally lacking serotonin 5-HT(2B) receptors did not develop isoproterenol-induced left ventricular hypertrophy. However, the exact cardiac cell type(s) expressing 5-HT(2B) receptors (cardiomyocytes versus noncardiomyocytes) involved in pathological heart hypertrophy was never addressed in vivo. We report here that ...

متن کامل

The Effect of Human Recombinant Tumor Necrosis Factor Receptor-2 on Reducing Inflammatory of Collagen -Induced Arthritis in Balb/c Mice

Background: The tumor necrosis factor alpha (TNFα) is a cytokine that produced principally by monocyte/macrophages and T lymphocytes, respectively. TNFα is recognized as the primary mediator of immunity in inflammation reaction.  One important application of Tumor Necrosis Factor Receptor 2 (TNFR2) is for the treatment of autoimmune diseases like rheumatoid arthritis (RA).<br /...

متن کامل

Helix-loop-helix protein p8, a transcriptional regulator required for cardiomyocyte hypertrophy and cardiac fibroblast matrix metalloprotease induction.

Cardiomyocyte hypertrophy and extracellular matrix remodeling, primarily mediated by inflammatory cytokine-stimulated cardiac fibroblasts, are critical cellular events in cardiac pathology. The molecular components governing these processes remain nebulous, and few genes have been linked to both hypertrophy and matrix remodeling. Here we show that p8, a small stress-inducible basic helix-loop-h...

متن کامل

Effect of Ganoderma Lucidum on Cytokine Release by Peritoneal Macrophages

Background: The water-soluble extract of Ganoderma lucidum (Reishi) has been used as an immunomodulator to stimulate spleen cells proliferation and cytokine expression. Objective: To investigate the effect of Ganoderma lucidum (G. lucidum) on cytokine production by mice peritoneal macrophages. Methods: Mice peritoneal macrophages were prepared by intra-peritoneal injection of 5 ml cold PBS. Per...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2004