title: [Growth Differentiation Factor 15 Inhibits Elevated Expression of Matrix Metalloproteinase 1 Induced by Pooled Serum in Patients with Coroanry Artery Ectasia].
abstract: OBJECTIVE
  To observe the effects of coroanry artery ectasia (CAE) patients' pooled serum on the main proteinases and extracellular matrix (ECM) synthesis and explore whether the growth differentiation factor 15(GDF 15) can regulate the characteristic changes induced by CAE patients' pooled serum.
  
  
  METHODS
  Serum samples were collected from 32 CAE patients, 30 patients with coronary heart disease (CHD), and 31 subjects with normal coronary arteries (CON) and then mixed in the same volumes by groups. Then human umbilical vein smooth muscle cells were cultured with the media containing 25% pooled serum. After having been disposed, proteinase system and ECM synthesis system were detected in the cell and culture media samples. GDF15 or GDF15 antibodies was added into the 25% pooled serum in each group to observe if GDF 15 could impact the characteristic changes induced by CAE patients' pooled serum.
  
  
  RESULTS
  The expression of matrix metalloproteinases (MMP) 1 mRNA in CAE group was significantly higher than CON group (P=0.002) and CHD group (P=0.000), the secretory MMP1 protein and total MMPs activity in culture media were also upregulated in CAE group (both P<0.01). After adding GDF 15 into the culture media (GDF15+CAE group), the MMP1 mRNA ,secretory MMP1 protein, and total MMPs activity were significantly lower than CAE group (all P<0.01), while in the GDF15 antibody+CAE group, the MMP1 mRNA and total MMPs activities were significantly higher than in GDF15+CAE group (both P<0.01), but the secretory MMP1 protein was not different from GDF 15+CAE group (P>0.05).
  
  
  CONCLUSIONS
  The vascular smooth muscle cells may participate in the CAE process mainly by regulating MMPs system but not the elastase 2 or ECM synthesis system, and GDF15 may be an compensatory factor to prohibit the over-destruction of coronary ECM induced by MMPs.
authors.affiliation: Department of Cardiology,PUMC Hospital,CAMS and PUMC,Beijing 100730,China.
authors.forename: Rui-feng
authors.initials: RF
authors.lastname: Liu
authors.affiliation: Department of Cardiology,PUMC Hospital,CAMS and PUMC,Beijing 100730,China.
authors.forename: Wei
authors.initials: W
authors.lastname: Wu
authors.affiliation: Department of Cardiology,PUMC Hospital,CAMS and PUMC,Beijing 100730,China.
authors.forename: Lian-feng
authors.initials: LF
authors.lastname: Chen
authors.affiliation: Department of Cardiology,PUMC Hospital,CAMS and PUMC,Beijing 100730,China.
authors.forename: Xue-qing
authors.initials: XQ
authors.lastname: Zhu
authors.affiliation: Department of Cardiology,PUMC Hospital,CAMS and PUMC,Beijing 100730,China.
authors.forename: Shu-yang
authors.initials: SY
authors.lastname: Zhang
mesh_terms: D015415:Biomarkers / Q000097:blood; D003324:Coronary Artery Disease; D004108:Dilatation, Pathologic; D055436:Growth Differentiation Factor 15; D006801:Humans; D020781:Matrix Metalloproteinase 1
chemical_list: D015415:Biomarkers; C526140:GDF15 protein, human; D055436:Growth Differentiation Factor 15; C522360:MMP1 protein, human; D020781:Matrix Metalloproteinase 1