title: The human FGF2 level is influenced by genetic predisposition.
abstract: BACKGROUND
  The fibroblast growth factor 2 (FGF2) is involved in various processes possibly leading to the development of complex diseases such as atherosclerosis. In recent studies, its cardioprotective properties, due to its ability to stimulate the proliferation of collateral vessels, could be shown.
  
  
  METHODS
  In this clinical study, the relation between clinical risk markers, a genomic variant of FGF2, namely the c.223C>T polymorphism, and the in vivo FGF2 expression was evaluated. Therefore, 198 clinically well-characterized probands, all of Caucasian origin, were included. The FGF2 mRNA level was determined in monocytes by competitive RT-PCR, whereas the plasma level of circulating FGF2 protein was analysed by ELISA. By considering the angiographically proven stenotic state of the patient, a significant increase in FGF2 mRNA, but not in protein level, could be shown for patients with significant stenosis. Apart from this, no influence on FGF2 expression was found in the case of all of the clinical and biochemical markers investigated. However, in the case of the c.223C>T polymorphism, a significant increase in the individual FGF2 mRNA and protein level in CC-carriers was shown. In multivariate analysis, this relation was independent of all other risk markers investigated.
  
  
  CONCLUSIONS
  Our results suggest that an increase in FGF2 mRNA expression, related to coronary atherosclerosis, may be necessary for the maintenance of the individual FGF2 plasma level. Since the individual FGF2 mRNA and protein level are, to a large extent, triggered off by genetic background, the FGF2 expression cannot be referred to as an independent clinical marker for CAD.
authors.affiliation: Institute of Human Genetics and Medical Biology, University of Halle, Magdeburger Str. 2, D-06097 Halle, Germany.
authors.forename: Susanne
authors.initials: S
authors.lastname: Schulz
authors.forename: Katrin
authors.initials: K
authors.lastname: Köhler
authors.forename: Undraga
authors.initials: U
authors.lastname: Schagdarsurengin
authors.forename: Petra
authors.initials: P
authors.lastname: Greiser
authors.forename: Gerd
authors.initials: G
authors.lastname: Birkenmeier
authors.forename: Ursula
authors.initials: U
authors.lastname: Müller-Werdan
authors.forename: Karl
authors.initials: K
authors.lastname: Werdan
authors.forename: Christiane
authors.initials: C
authors.lastname: Gläser
mesh_terms: D003324:Coronary Artery Disease / Q000097:blood* / Q000235:genetics*; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000235:genetics / Q000378:metabolism*; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012333:RNA, Messenger / Q000378:metabolism; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D012333:RNA, Messenger; D016222:Fibroblast Growth Factor 2