title: Time course of gene expression in rat experimental autoimmune myocarditis.
abstract: Genetic responses that characterize experimental autoimmune myocarditis (EAM) have not yet been determined. To investigate gene expression in the myocardium of EAM, absolute copy numbers of 44 mRNA species [calcium-handling proteins, contractile proteins, natriuretic peptides (NPs), cytokines, chemokines, growth factors, renin-angiotensin-aldosterone (RAA) system, endothelins (ETs) and extracellular matrix] in synthesized cDNA from a fixed quantity of total heart RNA were assessed using real-time reverse-transcriptase PCR at days 0, 14, 21 and 28 after immunization. alpha-Cardiac myosin showed a 26.3-fold decrease and beta-cardiac myosin a 3.75-fold increase at day 14. Atrial NP and brain NP increased 47.7- and 6.35-fold at days 21 and 14 respectively. Angiotensin II type 1 receptor, angiotensin-converting enzyme and ET1 increased 22.3-fold at day 21, 6.30-fold at day 21 and 16.8-fold at day 14 respectively. Aldosterone receptor decreased 2.15-fold at day 14, but aldosterone synthetase was detected only at days 14 and 21. Interleukin (IL)-2, IL-10, interferon-gamma and monocyte chemo-attractant protein-1 increased 9.08-fold at day 14, 398-fold at day 21, 43.1-fold at day 14 and 142-fold at day 14 respectively. Collagen type 3, collagen type 1 and fibronectin increased 34.6-, 1.74- and 44.4-fold respectively at day 21. Interestingly, osteopontin showed a 4540-fold increase and it was the highest mRNA of all at day 14. An isoform of cardiac myosin and NP are dramatically changed in EAM. RAA system and ET expressions are changed differently during the EAM time course. Cytokine, chemokine and extracellular matrix greatly increase and, in particular, large numbers of osteopontin mRNA are expressed in early EAM.
authors.affiliation: First Department of Internal Medicine, Niigata University School of Medicine, Asahimachi 1-754, Niigata, 951-8510, Japan. hanawa@med.niigata-u.ac.jp
authors.forename: Haruo
authors.initials: H
authors.lastname: Hanawa
authors.forename: Satoru
authors.initials: S
authors.lastname: Abe
authors.forename: Manabu
authors.initials: M
authors.lastname: Hayashi
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Yoshida
authors.forename: Kaori
authors.initials: K
authors.lastname: Yoshida
authors.forename: Takaaki
authors.initials: T
authors.lastname: Shiono
authors.forename: Koichi
authors.initials: K
authors.lastname: Fuse
authors.forename: Masahiro
authors.initials: M
authors.lastname: Ito
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Tachikawa
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kashimura
authors.forename: Yuji
authors.initials: Y
authors.lastname: Okura
authors.forename: Kiminori
authors.initials: K
authors.lastname: Kato
authors.forename: Makoto
authors.initials: M
authors.lastname: Kodama
authors.forename: Seitaro
authors.initials: S
authors.lastname: Maruyama
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Yoshifusa
authors.initials: Y
authors.lastname: Aizawa
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D018450:Disease Progression; D016326:Extracellular Matrix Proteins / Q000096:biosynthesis / Q000235:genetics; D015870:Gene Expression; D006133:Growth Substances / Q000096:biosynthesis / Q000235:genetics; D009205:Myocarditis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D053495:Osteopontin; D014176:Protein Biosynthesis; D011506:Proteins / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D011917:Rats, Inbred Lew; D012795:Sialoglycoproteins / Q000096:biosynthesis / Q000235:genetics
chemical_list: D016207:Cytokines; D016326:Extracellular Matrix Proteins; D006133:Growth Substances; D011506:Proteins; D012333:RNA, Messenger; D012795:Sialoglycoproteins; C506897:Spp1 protein, rat; D053495:Osteopontin