title: An immunohistochemical analysis of tissue thrombin expression in the human atria.
abstract: OBJECTIVE
  Thrombin, the final coagulation product of the coagulation cascade, has been demonstrated to have many physiological effects, including pro-fibrotic actions via protease-activated receptor (PAR)-1. Recent investigations have demonstrated that activation of the cardiac local coagulation system was associated with atrial fibrillation. However, the distribution of thrombin in the heart, especially difference between the atria and the ventricle, remains to be clarified. We herein investigated the expression of thrombin and other related proteins, as well as tissue fibrosis, in the human left atria and left ventricle.
  
  
  METHODS
  We examined the expression of thrombin and other related molecules in the autopsied hearts of patients with and without atrial fibrillation. An immunohistochemical analysis was performed in the left atria and the left ventricle.
  
  
  RESULTS
  The thrombin was immunohistologically detected in both the left atria and the left ventricles. Other than in the myocardium, the expression of thrombin was observed in the endocardium and the subendocardium of the left atrium. Thrombin was more highly expressed in the left atrium compared to the left ventricle, which was concomitant with more tissue fibrosis and inflammation, as detected by CD68 expression, in the left atrium. We also confirmed the expression of prothrombin in the left atrium. The expression of PAR-1 was observed in the endocardium, subendocardium and myocardium in the left atrium. In patients with atrial fibrillation, strong thrombin expression was observed in the left atrium.
  
  
  CONCLUSIONS
  The strong expression levels of thrombin, prothrombin and PAR-1 were demonstrated in the atrial tissues of human autopsied hearts.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, Minato-ku, Tokyo, Japan. keke-ito@jikei.ac.jp
authors.forename: Keiichi
authors.initials: K
authors.lastname: Ito
authors.forename: Taro
authors.initials: T
authors.lastname: Date
authors.forename: Masahiro
authors.initials: M
authors.lastname: Ikegami
authors.forename: Kenichi
authors.initials: K
authors.lastname: Hongo
authors.forename: Masami
authors.initials: M
authors.lastname: Fujisaki
authors.forename: Daisuke
authors.initials: D
authors.lastname: Katoh
authors.forename: Takuya
authors.initials: T
authors.lastname: Yoshino
authors.forename: Ryuko
authors.initials: R
authors.lastname: Anzawa
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Nagoshi
authors.forename: Seigo
authors.initials: S
authors.lastname: Yamashita
authors.forename: Keiichi
authors.initials: K
authors.lastname: Inada
authors.forename: Seiichiro
authors.initials: S
authors.lastname: Matsuo
authors.forename: Teiichi
authors.initials: T
authors.lastname: Yamane
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001344:Autopsy; D004699:Endocardium / Q000378:metabolism / Q000473:pathology; D006325:Heart Atria / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008297:Male; D011516:Prothrombin / Q000378:metabolism; D013917:Thrombin / Q000378:metabolism*; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D011516:Prothrombin; D013917:Thrombin; C067980:CD68 antigen, human; D000097382:CD68 Molecule