Fibroblast growth factor 2 isoforms and cardiac hypertrophy

Elissavet Kardami¹, Zhi-Sheng Jiang, Sarah K Jimenez

¹Institute of Cardiovascular Sciences 3008, St. Boniface Research Centre and Departments of Human Anatomy and Cell Sciences and Physiology, 351 Tache Ave., University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6. ekardami@sbrc.ca

|July 28, 2004

Summary

Fibroblast growth factor 2 (FGF-2) has two main forms. The 18 kDa FGF-2 aids adaptive cardiac growth, while higher molecular weight forms (hi-FGF-2) promote maladaptive hypertrophy and cell death in heart failure.

Area of Science:

Cardiovascular Biology
Molecular Cell Biology
Biochemistry

Background:

Fibroblast growth factor 2 (FGF-2) is a key regulator of cell growth and differentiation.
FGF-2 exists as 18 kDa (AUG-initiated) and 21-34 kDa (CUG-initiated, hi-FGF-2) isoforms.
FGF-2 is implicated in cardiac hypertrophy, but isoform-specific roles are unclear.

Purpose of the Study:

To differentiate the roles of 18 kDa FGF-2 and hi-FGF-2 in cardiac hypertrophy.
To investigate the impact of sustained intracrine hi-FGF-2 signaling on myocardial cells.
To elucidate the contribution of FGF-2 isoforms to adaptive versus maladaptive cardiac remodeling.

Main Methods:

Analysis of FGF-2 isoform expression and function in cardiac models.
Investigating the effects of exogenous hi-FGF-2 on cardiac cell hypertrophy.
Examining the consequences of sustained intracrine hi-FGF-2 signaling.

Main Results:

Added hi-FGF-2 exhibits a potent pro-hypertrophic effect.
Sustained intracrine hi-FGF-2 signaling demonstrates a pro-apoptotic effect.
The 18 kDa FGF-2 isoform appears to be part of an adaptive trophic response.

Conclusions:

A shift towards hi-FGF-2 accumulation exacerbates cardiac hypertrophy and promotes cell death.
Hi-FGF-2 accumulation drives the myocardium towards a maladaptive phenotype, contributing to heart failure.
Distinguishing FGF-2 isoform activities is crucial for understanding and treating heart failure.

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Fibroblast growth factor 2 isoforms and cardiac hypertrophy

Area of Science:

Background:

Purpose of the Study:

Main Methods:

Main Results:

Conclusions:

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