Histamine 2 receptors in cardiovascular biology: a friend for the heart

Author(s):  
Sherin Saheera ◽  
Ajay Godwin Potnuri ◽  
Ashrith Guha ◽  
Suresh S. Palaniyandi ◽  
Rajarajan A. Thandavarayan
2009 ◽  
Vol 15 (15) ◽  
pp. 1809-1821 ◽  
Author(s):  
Mahinda Abeywardena ◽  
Wayne Leifert ◽  
Kirsty Warnes ◽  
Jose Varghese ◽  
Richard Head

2011 ◽  
Vol 9 ◽  
pp. 151-161 ◽  
Author(s):  
T. HOSODA ◽  
M. ROTA ◽  
J. KAJSTURA ◽  
A. LERI ◽  
P. ANVERSA

2008 ◽  
Vol 114 (12) ◽  
pp. 699-706 ◽  
Author(s):  
Chunxiang Zhang

miRNAs (microRNAs) comprise a novel class of endogenous, small, non-coding RNAs that negatively regulate gene expression via degradation or translational inhibition of their target mRNAs. Recent studies have demonstrated that miRNAs are highly expressed in the cardiovascular system. Although we are currently in the initial stages of understanding how this novel class of gene regulators is involved in cardiovascular biological functions, a growing body of exciting evidence suggests that miRNAs are important regulators of cardiovascular cell differentiation, growth, proliferation and apoptosis. Moreover, miRNAs are key modulators of both cardiovascular development and angiogenesis. Consequently, dysregulation of miRNA function may lead to cardiovascular diseases. Indeed, several recent reports have demonstrated that miRNAs are aberrantly expressed in diseased hearts and vessels. Modulating these aberrantly expressed miRNAs has significant effects on cardiac hypertrophy, vascular neointimal lesion formation and cardiac arrhythmias. Identifying the roles of miRNAs and their target genes and signalling pathways in cardiovascular disease will be critical for future research. miRNAs may represent a new layer of regulators for cardiovascular biology and a novel class of therapeutic targets for cardiovascular diseases.


2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Amy L Wilson-O'Brien ◽  
John Garlick ◽  
Andrew M Wilson

Introduction: Nitric Oxide (NO) is a crucial molecule in cardiovascular biology. Abnormalities in NO are critical in atherosclerosis and impairment of the NO pathway increases risk of cardiovascular disease (CVD). A possible cause of endothelial dysfunction is an elevation (in plasma) of the endogenous inhibitor of NO synthase, asymmetric dimethylarginine (ADMA). ADMA was initially described in renal failure. 80% of ADMA is metabolized by the enzyme dimethylarginine dimethylaminohydrolase (DDAH) in the liver. DDAH-1 is widely distributed and felt to be the major determinant of circulating ADMA levels. Very little data is available regarding the cause and effects of DDAH dysregulation in the liver. Understanding the biology of DDAH represents a target for better understanding of CVD and for novel therapy. Hypothesis: Diabetes and related factors will alter DDAH expression/activity potentially modulating the amount of ADMA. Methods: Liver tissues from control and db/db mice were archival. Human skeletal muscle tissue was obtained from cardiovascular surgical patients. HepG2 cells were used for low/high glucose treatment studies (5mM/25mM). DDAH-1 expression was determined using Western immunoblotting. DDAH activity measurement used a colourimetric assay. Intra/extracellular ADMA were measured in HepG2 cells using an HPLC-MS/MS technique. Results: In skeletal muscle from diabetic cardiac surgery patients DDAH-1 protein expression is increased ( P < 0.05). Further to this, db/db mice livers versus control had a significant increase in DDAH expression and activity. Using HepG2 cells we specifically examined the effect of 25mM glucose on DDAH-1. Treatment increased expression and activity of DDAH-1 ( P <0.05). Elevated glucose appears to have no significant effect on the intra or extracellular concentrations of ADMA. Conclusion: These novel results report an alteration of DDAH-1 expression and activity in hepatic tissues and cells in response to elevated glucose - a result which has not been reported previously. This suggests a possible link between the DDAH/ADMA/NOS pathway, diabetes, and glycaemic dysregulation - key risk factors in CVD.


Author(s):  
John P. Headrick ◽  
Jason N. Peart ◽  
Tina C. Wan ◽  
Wai-Meng Kwok ◽  
John A. Auchampach

2014 ◽  
pp. 245-265 ◽  
Author(s):  
Claudia Cangemi ◽  
Maria Lyck Hansen ◽  
William Scott Argraves ◽  
Lars Melholt Rasmussen

Sign in / Sign up

Export Citation Format

Share Document