natriuretic-peptide--brain and sodium-bisulfide

natriuretic-peptide--brain has been researched along with sodium-bisulfide* in 1 studies

Other Studies

1 other study(ies) available for natriuretic-peptide--brain and sodium-bisulfide

Article	Year
Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a. Biochemical and biophysical research communications, 2011, Sep-23, Volume: 413, Issue:2 Hydrogen sulphide (H(2)S) has been shown to play a crucial role in cardiovascular physiology and disease. However, there is no information about the possible role of H(2)S in cardiomyocyte hypertrophy (CH). Our results showed that pretreatment with NaHS, an H(2)S donor, significantly reduced [(3)H]-leucine incorporation, cell surface area, mRNA expression of brain natriuretic peptide (BNP), intracellular reactive oxygen species (ROS), miR-21 and increased atrial natriuretic peptide (ANP) and miR-133a expression in hypertrophic cardiomyocytes. Anti-miR133a inhibitor transfection partly reduced the anti-hypertrophic effect of NaHS. In conclusion, H(2)S is a direct inhibitor of CH; it acts by increasing miR-133a and inhibiting the increase in intracellular ROS. Topics: Animals; Cardiomegaly; Cell Line; Hydrogen Sulfide; Hypertrophy; MicroRNAs; Myocytes, Cardiac; Natriuretic Peptide, Brain; Rats; Reactive Oxygen Species; RNA, Messenger; Sulfides; Up-Regulation	2011

Article

Year

Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a.

Biochemical and biophysical research communications, 2011, Sep-23, Volume: 413, Issue:2

Hydrogen sulphide (H(2)S) has been shown to play a crucial role in cardiovascular physiology and disease. However, there is no information about the possible role of H(2)S in cardiomyocyte hypertrophy (CH). Our results showed that pretreatment with NaHS, an H(2)S donor, significantly reduced [(3)H]-leucine incorporation, cell surface area, mRNA expression of brain natriuretic peptide (BNP), intracellular reactive oxygen species (ROS), miR-21 and increased atrial natriuretic peptide (ANP) and miR-133a expression in hypertrophic cardiomyocytes. Anti-miR133a inhibitor transfection partly reduced the anti-hypertrophic effect of NaHS. In conclusion, H(2)S is a direct inhibitor of CH; it acts by increasing miR-133a and inhibiting the increase in intracellular ROS.

Topics: Animals; Cardiomegaly; Cell Line; Hydrogen Sulfide; Hypertrophy; MicroRNAs; Myocytes, Cardiac; Natriuretic Peptide, Brain; Rats; Reactive Oxygen Species; RNA, Messenger; Sulfides; Up-Regulation

2011