Related Experiment Video

Updated: Aug 29, 2026

Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes
07:32

Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes

Published on: May 25, 2022

Cyclic GMP protein kinase activity is reduced in thyroxine-induced hypertrophic cardiac myocytes

Lin Yan1, Qihang Zhang, Peter M Scholz

  • 1Heart and Brain Circulation Laboratory, Departments of Physiology & Biophysics and Surgery, University of Medicine and Dentistry of New Jersey - Robert Wood Johnson Medical School, Piscataway, New Jersey 08854-5635, USA.

Clinical and Experimental Pharmacology & Physiology
|December 18, 2003
PubMed

Insights

The cGMP-dependent protein kinase negatively impacts cardiac myocyte function, but this effect is reduced in thyroxine-induced hypertrophic myocytes. This suggests a diminished role for the cGMP pathway in T4-treated cardiac cells.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Physiology

Background:

  • The cGMP-dependent protein kinase (PKG) pathway plays a role in cardiac myocyte function.
  • Thyroxine (T4) treatment induces cardiac hypertrophy, potentially altering cellular signaling pathways.

Purpose of the Study:

  • To investigate the functional effects of PKG in cardiac myocytes.
  • To determine if the importance of the PKG pathway is reduced in T4-induced hypertrophic myocytes.

Main Methods:

  • Isolated ventricular myocytes from control and T4-treated rabbits were used.
  • Myocyte shortening, oxygen consumption, and protein phosphorylation were measured.
  • Cells were treated with cGMP analogs (PCPT, SP) and cAMP (8-bromo-cAMP).

Main Results:

  • PKG activation by SP and PCPT significantly decreased myocyte shortening and contraction rate in control cells.
  • These negative effects were significantly reduced in T4-hypertrophic myocytes.
  • cAMP increased myocyte shortening and contraction rate similarly in both groups.
  • PKG activation after cAMP stimulation had less impact in control cells and no altered impact in T4 myocytes.
  • PKG and cAMP phosphorylated the same proteins, but to a lesser extent in T4 myocytes.

Conclusions:

  • PKG exerts significant negative functional effects on normal cardiac myocytes.
  • The functional importance of the PKG pathway is diminished in T4-induced hypertrophic myocytes.
  • The interaction between cAMP and PKG signaling is altered in T4-hypertrophic cardiac myocytes.

More Related Videos

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling08:29

Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling

Published on: August 1, 2016

Related Concept Videos

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Cellular Adaptation II: Hypertrophy01:26

Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...