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Updated: May 20, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca²⁺ Transients and Membrane Currents

Published on: July 3, 2013

Mechanism of macrophage migration inhibitory factor-induced decrease of T-type Ca(2+) channel current in

Fang Rao¹, Chun-Yu Deng, Shu-Lin Wu

¹Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong Academy of Medical Sciences, 96 Dongchuan Road, Guangzhou 510080, PR China.

Experimental Physiology

|August 1, 2012

Summary

Macrophage migration inhibitory factor (MIF) reduces T-type calcium current (I(Ca,T)) in atrial cells, a key factor in atrial fibrillation (AF). This occurs by impairing channel function and activating Src kinases, offering a new therapeutic target for AF.

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Isolation of Atrial Myocytes from Adult Mice

Isolation of Atrial Myocytes from Adult Mice

Published on: July 25, 2019

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Last Updated: May 20, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca²⁺ Transients and Membrane Currents

Published on: July 3, 2013

Isolation of Atrial Myocytes from Adult Mice

Isolation of Atrial Myocytes from Adult Mice

Published on: July 25, 2019

Area of Science:

Cardiology
Molecular Biology
Cell Physiology

Background:

T-type calcium current (I(Ca,T)) is crucial in atrial fibrillation (AF) pathogenesis.
Macrophage migration inhibitory factor (MIF) is a cytokine with a role in various diseases.

Purpose of the Study:

To investigate the role of MIF in regulating T-type calcium channels (TCCs) in atrial myocytes.
To explore the underlying molecular mechanisms of MIF's effect on I(Ca,T) in the context of AF.

Main Methods:

Whole-cell voltage-clamp technique to measure I(Ca,T).
Biochemical assays to study TCC regulation and expression.
Quantitative real-time PCR to assess mRNA levels of TCC subunits (α1G and α1H).
Use of recombinant MIF and Src inhibitors (genistein, PP1).

Main Results:

Decreased gene levels of TCC α1G and α1H subunits in human AF atrial tissue.
Recombinant MIF suppressed I(Ca,T) and downregulated TCC α1G and α1H mRNA in HL-1 cells.
Src inhibitors reversed MIF-induced reduction of I(Ca,T) and TCC mRNA.
TCC α1G was found to associate with Src in atrial myocytes.

Conclusions:

MIF is implicated in AF pathogenesis by reducing atrial I(Ca,T).
MIF impairs TCC function and activates c-Src kinases in atrial myocytes.
This mechanism represents a potential pathogenic pathway in atrial fibrillation.