title: Reduced presence of tissue-repairing cells in wounds combined with whole-body irradiation injury is associated with both suppression of proliferation and increased apoptosis.
abstract: BACKGROUND
  The goal of our study was to examine the effects of whole body irradiation injury on tissue-repairing cells, so as to elucidate the possible mechanisms of reduced repopulation of tissue-repairing cells.
  
  
  METHODS
  The quantity of tissue-repairing cells in wounds from simple incision injury (WBI) (group S) and combined with WBI injury (group C) was measured histologically. The proliferation and apoptosis of tissue-repairing cells in wounds were determined using immunohistochemical staining for proliferation cell nuclear antigen (PCAN) and by TUNEL assay. Fibroblasts were isolated from the wounds, and their proliferation and apoptosis were detected in vitro. Some key molecules involving in proliferation (cyclin E and cyclin dependent kinase 4) and apoptosis (bcl-2 and bax) were also determined, so as to interpret the mechanisms of the alteration of tissue repairing cells.
  
  
  RESULTS
  The quantity of tissue-repairing cells in group C was significantly less than in group S. The PCNA contents in wounds of group C were significantly less than in group S, whereas the apoptosis of tissue-repairing cells in wounds of group C increased significantly as compared to group S. The expression of the molecules involved in the mediating of proliferation and apoptosis coincided with the proliferation and apoptosis of tissue repairing cells in wounds.
  
  
  CONCLUSIONS
  The quantity of tissue repairing cells in wounds combined with WBI injury is significantly less than in simple incision injury. This is associated with both suppression of proliferation and increased apoptosis.
authors.affiliation: Institute of Combined Injury of PLA, Third Military Medical University, Chongqing, P.R. of China. qujifu@yahoo.com
authors.forename: Jifu
authors.initials: J
authors.lastname: Qu
authors.forename: Tianming
authors.initials: T
authors.lastname: Cheng
authors.forename: Chunmeng
authors.initials: C
authors.lastname: Shi
authors.forename: Yuan
authors.initials: Y
authors.lastname: Lin
authors.forename: Guohe
authors.initials: G
authors.lastname: Yan
authors.forename: Xinze
authors.initials: X
authors.lastname: Ran
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000528:radiation effects*; D002455:Cell Division / Q000528:radiation effects*; D019927:Cyclin E / Q000096:biosynthesis; D051358:Cyclin-Dependent Kinase 4; D018844:Cyclin-Dependent Kinases / Q000096:biosynthesis; D005260:Female; D005347:Fibroblasts / Q000378:metabolism; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014916:Whole-Body Irradiation; D014945:Wound Healing; D051028:bcl-2-Associated X Protein
chemical_list: C494828:Bax protein, rat; D019927:Cyclin E; D018809:Proliferating Cell Nuclear Antigen; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; C495903:Cdk4 protein, rat; D051358:Cyclin-Dependent Kinase 4; D018844:Cyclin-Dependent Kinases