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Updated: Aug 17, 2026
A Simple and Efficient Method for In Vivo Cardiac-specific Gene Manipulation by Intramyocardial Injection in Mice
Published on: April 16, 2018
Transgenic mouse models for cardiac dysfunction by a specific gene manipulation
Gopal J Babu1, Muthu Periasamy
1Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, USA.
Insights
Altering sarcoplasmic reticulum Ca2+ ATPase (SERCA) levels genetically in mice helps investigate its role in heart function and calcium regulation. This research addresses the cause-effect relationship between SERCA levels and heart failure.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Calcium Signaling
Background:
- Sarcoplasmic reticulum Ca2+ ATPase (SERCA) is crucial for cardiac calcium cycling and heart function.
- Reduced SERCA expression and activity are linked to human and experimental heart failure.
- The role of SERCA levels in cardiac hypertrophy remains controversial.
Purpose of the Study:
- To genetically modify SERCA protein expression in mice.
- To investigate how altered SERCA levels impact cardiac calcium homeostasis.
- To determine if SERCA levels are a cause or effect of cardiac hypertrophy and heart failure.
Main Methods:
- Utilizing transgenic mouse technology to overexpress SERCA isoforms.
- Employing gene-targeted knockout technology to create SERCA2 knockout mice with reduced SERCA levels.
- Developing genetically modified mouse models to study SERCA function in vivo.
Main Results:
- Generation of mouse models with manipulated SERCA protein levels.
- Establishment of tools to study the functional consequences of altered SERCA expression.
- Provides a platform for dissecting the contribution of SERCA to cardiac function and disease.
Conclusions:
- Genetically engineered mouse models are essential for understanding SERCA's role in heart function.
- These models allow direct investigation into the causal relationship between SERCA levels and heart failure.
- The study provides a foundation for future research into SERCA-targeted therapies for heart disease.
Abstract:
The sarcoplasmic reticulum Ca2+ ATPase (SERCA) plays a pivotal role in calcium cycling and the beat-to-beat function of the heart. Recent studies have shown that decreased expression and activity of SERCA are associated with end-stage heart failure in humans and in experimental animal models of heart failure. There has been considerable controversy over whether a decrease in SERCA level is a cause or effect of hypertrophy. To address directly whether alterations in SERCA levels modify calcium homeostasis and heart function, we have chosen to alter the SERCA protein expression genetically using transgenic and gene-targeted knockout mouse technology. This chapter describes the methodology for generation of mouse models that overexpress different SERCA isoforms and a SERCA2 knockout mouse model with decreased SERCA levels.
