title: Soluble elastin decreases in the progress of atheroma formation in human aorta.
abstract: BACKGROUND
  The serum levels of soluble elastin increase in patients with aortic dissection, but its distribution and characteristics are unclear.
  
  
  RESULTS
  The 173 aortic specimens were categorized into 4 groups under microscopy (non-atherosclerotic aorta, n=13; fiber-rich plaque, n=77; lipid-rich plaque, n=66; ruptured plaque, n=17). Soluble elastin was abundant within the intima of both the non-atherosclerotic aorta and fiber-rich plaque, rather than in the media, and was decreased within the intima of lipid-rich and ruptured plaques. Soluble elastin levels decreased with progress of atherosclerosis (6.0 +/-0.3 microg/mg protein in non-atherosclerotic aorta; 5.8 +/-0.2 microg/mg protein in fiber-rich plaque; 4.9 +/-0.2 microg/mg protein in lipid-rich plaque; 2.8 +/-0.4 microg/mg protein in ruptured plaque, P<0.05). As well, both matrix metalloprotease-9 activity and elastin mRNA expression showed inverse distribution against soluble elastin (r=0.437, P<0.0001; r=0.186, P<0.05, respectively). Multivariable analysis revealed a decrease in the level of soluble elastin in ruptured plaque (2.8 +/-0.4 microg/mg protein in ruptured plaque, n=18; 5.5 +/-0.2 microg/mg protein in non-ruptured plaque, n=155, P<0.01). Furthermore, western blot showed soluble elastin consists of heterogeneous molecular pattern proteins.
  
  
  CONCLUSIONS
  Both the synthesis and degradation of elastin may be enhanced in active atherosclerotic lesions.
authors.affiliation: Department of Pathology and Laboratory Medicine, National Defense Medical College, Tokorozawa, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Akima
authors.forename: Kuniaki
authors.initials: K
authors.lastname: Nakanishi
authors.forename: Kimihiro
authors.initials: K
authors.lastname: Suzuki
authors.forename: Masahiko
authors.initials: M
authors.lastname: Katayama
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Ohsuzu
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Kawai
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001011:Aorta / Q000378:metabolism* / Q000473:pathology; D050197:Atherosclerosis / Q000209:etiology* / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D001483:Base Sequence; D015153:Blotting, Western; D017931:DNA Primers / Q000235:genetics; D004549:Elastin / Q000235:genetics / Q000378:metabolism*; D005260:Female; D006801:Humans; D017403:In Situ Hybridization; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012995:Solubility; D014018:Tissue Distribution
chemical_list: D017931:DNA Primers; D012333:RNA, Messenger; D004549:Elastin; D020780:Matrix Metalloproteinase 9