Expression of fetal isoforms of actin after transplantation injury.
Trauma and injury to transplanted organs in the early post-transplant period are significant factors that affect long-term graft survival. Fetal isoforms of actin are integral members of the immediate early gene family and are expressed in response to free radical injury. We therefore studied actin gene expression in heart transplantation to determine if reperfusion injury activates fetal isoforms of actins. Heterotopic cardiac transplantations were performed in mice. mRNA was extracted from allo- and isografted hearts as well as from normal hearts and spleen. Northern hybridization with actin cDNA to alpha and beta/gamma actin mRNA was performed and analyzed by densitometry. The beta/gamma actin gene expression in the transplanted hearts was found to be significantly elevated within 48 h after transplantation. Analysis of beta/gamma actin gene expression in isografts substantiates the possibility of de novo increase in actin expression. Our studies demonstrate for the first time that fetal isoforms of actin are induced in the allograft heart after transplantation.
Xu
Renkui
R
Department of Surgery, The Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA.
Burdick
James F
JF
Beschorner
William
W
Wilasrusmee
Chumpon
C
Kittur
Dilip S
DS
D000199:Actins / Q000235:genetics*; D000818:Animals; D005786:Gene Expression Regulation; D017781:Genes, Immediate-Early; D005802:Genes, MHC Class II; D016027:Heart Transplantation; D008214:Lymphocytes / Q000473:pathology; D051379:Mice; D009206:Myocardium / Q000378:metabolism; D020033:Protein Isoforms; D012333:RNA, Messenger / Q000032:analysis; D015427:Reperfusion Injury / Q000378:metabolism; D014184:Transplantation, Homologous; D014185:Transplantation, Isogeneic
D000199:Actins; D020033:Protein Isoforms; D012333:RNA, Messenger