title: Reperfusion accelerates the distribution of type I and III collagen messenger RNA expression after acute myocardial infarction: in situ hybridization in experimental infarction in rats.
abstract: BACKGROUND
  The effects of reperfusion on the time-dependent appearance and distribution of type I and III collagen messenger RNA (mRNA) expression had not hitherto been examined.
  
  
  OBJECTIVE
  To compare the sequential changes in the extent of distribution of type I and III collagen mRNA expression in reperfused infarct hearts of rats with those in unreperfused infarct hearts.
  
  
  METHODS
  Using an experimental rat model of infarction, we examined type I and III collagen mRNA expression with specific rat pro alpha 1 (I) and human pro alpha 1 (III) collagen riboprobes by in-situ hybridization. Reperfusion was established after a 2 h coronary ligation that produced complete necrosis of the myocytes.
  
  
  RESULTS
  Positive signals both for alpha 1 (I) and for alpha 1 (III) collagen mRNA appeared in the infarct peripheral zone 12 h after coronary ligation both of the reperfused and of unreperfused hearts. The spread of signal into the infarct central zone occurred 1-2 days earlier for the reperfused hearts than it did for the unreperfused hearts. The difference between the distributions of signals for the reperfused and unreperfused hearts became obscure on day 14. No notable difference between the extents of signal distribution for alpha 1 (I) and alpha 1 (III) collagen mRNA was obtained. We observed intense signals from spindle-shaped mesenchymal cells (myofibroblasts and fibroblasts) located between surviving myocytes in the marginal zone of the infarct. No myocyte exhibited signals both for alpha 1 (I) and for alpha 1 (III) collagen mRNA.
  
  
  CONCLUSIONS
  In the present study, using in-situ hybridization, we demonstrated that reperfusion accelerates the distribution of expression both of alpha 1 (I) and of alpha 1 (III) collagen mRNA in the infarct zone after acute myocardial infarction in rats.
authors.affiliation: First Department of Internal Medicine, Okayama University Medical School, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Moritani
authors.forename: S
authors.initials: S
authors.lastname: Kusachi
authors.forename: K
authors.initials: K
authors.lastname: Takeda
authors.forename: M
authors.initials: M
authors.lastname: Doi
authors.forename: H
authors.initials: H
authors.lastname: Ohnishi
authors.forename: I
authors.initials: I
authors.lastname: Komatsubara
authors.forename: M
authors.initials: M
authors.lastname: Nakahama
authors.forename: T
authors.initials: T
authors.lastname: Higashi
authors.forename: Y
authors.initials: Y
authors.lastname: Ninomiya
authors.forename: T
authors.initials: T
authors.lastname: Tsuji
mesh_terms: D000818:Animals; D003094:Collagen / Q000235:genetics*; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000378:metabolism / Q000473:pathology; D005500:Follow-Up Studies; D017403:In Situ Hybridization; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D015588:Observer Variation; D012333:RNA, Messenger / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D012333:RNA, Messenger; D003094:Collagen