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The human FGF2 level is influenced by genetic predisposition.
Susanne Schulz1, Katrin Köhler, Undraga Schagdarsurengin
1Institute of Human Genetics and Medical Biology, University of Halle, Magdeburger Str. 2, D-06097 Halle, Germany.
International Journal of Cardiology
|May 11, 2005
Summary
Fibroblast growth factor 2 (FGF2) gene variants influence its expression, impacting coronary artery disease (CAD) risk. FGF2 mRNA increases with stenosis, but its expression is primarily driven by genetics, not an independent CAD marker.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Genetics
Background:
- Fibroblast growth factor 2 (FGF2) plays a role in complex diseases like atherosclerosis.
- Recent studies highlight FGF2's cardioprotective effects via collateral vessel proliferation.
Purpose of the Study:
- To investigate the relationship between clinical risk markers, the FGF2 c.223C>T polymorphism, and in vivo FGF2 expression.
- To assess FGF2's potential as a clinical marker for coronary artery disease (CAD).
Main Methods:
- Clinical study involving 198 Caucasian probands.
- Quantification of FGF2 mRNA in monocytes (RT-PCR) and FGF2 protein in plasma (ELISA).
- Analysis correlated FGF2 expression with clinical risk factors and the c.223C>T polymorphism.
Main Results:
- Significant increase in FGF2 mRNA, but not protein, observed in patients with significant coronary stenosis.
- The FGF2 c.223C>T polymorphism (CC-carriers) showed significantly higher individual FGF2 mRNA and protein levels.
- This genetic influence on FGF2 expression was independent of other investigated risk markers.
Conclusions:
- Increased FGF2 mRNA expression, linked to coronary atherosclerosis, may support individual FGF2 plasma levels.
- FGF2 expression is largely determined by genetic background.
- FGF2 expression is not an independent clinical marker for CAD.