title: Expression of Dishevelled-1 in wound healing after acute myocardial infarction: possible involvement in myofibroblast proliferation and migration.
abstract: One of our previous studies indicated that the expression of beta-catenin, which is the key factor of wnt-frizzled pathway, increased significantly in the ischemic area of the rat heart 7 days after myocardial infarction (MI). Together with the results of other recent studies, we made an assumption that wnt-frizzled pathway may be involved in the controlled cell proliferation and migration during repair processes after MI. To verify this assumption we tried to investigate the expression of another signal transduction molecule called Dishevelled in wnt-frizzled pathway during the wound healing process after MI. The left descending coronary arteries of rats were ligated to induce MI. Immunohistochemistry SABC method and in situ hybridization were performed to detect the expression of Dishevelled-1. The results showed, that one day after MI, Dishevelled-1 mRNA but not protein expression was detected in the cells at the border zone of the infarction area; 4 days after MI the expression of Dishevelled-1 increased exclusively and cytoplasmic Dishevelled-1 was observed not only at the border zone but also in the infarct area; 7 days after MI, it seems that the expression reached its peak, the positive staining even spread into the endothelial and smooth muscle cells of the newly formed and pre-existing blood vessels in the infarction area; after that the Dishevelled-1 expression decreased abruptly and could hardly be detected 28 days after MI. Thus cytoplasmic Dishevelled-1 may be involved in the controlled proliferation and migration of myofibroblasts and vascular endothelial cells, hence play a role during the wound healing process after MI.
authors.affiliation: Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
authors.forename: Lijun
authors.initials: L
authors.lastname: Chen
authors.forename: Qingfeng
authors.initials: Q
authors.lastname: Wu
authors.forename: Feng
authors.initials: F
authors.lastname: Guo
authors.forename: Beili
authors.initials: B
authors.lastname: Xia
authors.forename: Ji
authors.initials: J
authors.lastname: Zuo
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D002465:Cell Movement; D049109:Cell Proliferation; D000072261:Dishevelled Proteins; D005347:Fibroblasts / Q000166:cytology*; D005786:Gene Expression Regulation; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D008297:Male; D009203:Myocardial Infarction / Q000235:genetics* / Q000473:pathology; D009206:Myocardium / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D010750:Phosphoproteins; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014945:Wound Healing / Q000235:genetics*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D000072261:Dishevelled Proteins; C000606580:Dvl1 protein, rat; D047908:Intracellular Signaling Peptides and Proteins; D010750:Phosphoproteins; D012333:RNA, Messenger