PMID- 19439323
OWN - NLM
STAT- MEDLINE
DCOM- 20100913
LR  - 20220317
IS  - 1095-8673 (Electronic)
IS  - 0022-4804 (Linking)
VI  - 162
IP  - 2
DP  - 2010 Aug
TI  - Apoptosis is differentially regulated by burn severity and dermal location.
PG  - 258-63
LID - 10.1016/j.jss.2009.01.038 [doi]
AB  - BACKGROUND: The cellular processes that contribute to cell death in burns are 
      poorly understood. This study evaluated the distribution and extent of apoptosis 
      in an established rat model of acute dermal burn injury. MATERIALS AND METHODS: A 
      branding iron (100 degrees C) was applied to the depilated dorsum of seven rats, 
      creating burn contact times of 1-8, 10, 12, and 14 s. Biopsies were collected and 
      immunohistochemistry performed for apoptosis and cell injury/necrosis by 
      detection of terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL) and high-mobility group box 1 (HMGB1), respectively. The slides 
      were scored by evaluating staining in superficial, middle, and deep dermal 
      fields. Within these, basal keratinocytes of the epidermis, mesenchymal cells, 
      adnexal epithelia, and vasculature wall cells were morphometrically analyzed for 
      stain detection of selected markers. RESULTS: TUNEL staining had an inverse 
      relationship with contact time in most fields except in deep dermal mesenchymal 
      cells where it was increased. HMGB1 nuclear staining was significantly decreased 
      with progressive contact time consistent with transition to cell injury/necrosis. 
      CONCLUSIONS: This study is the first to demonstrate that apoptosis rate is 
      dependent on dermal location, cell type, and severity of thermal injury. 
      Furthermore, this work suggests that for most dermal locations increased thermal 
      injury corresponds with decreased apoptosis and increased cell injury/necrosis. 
      Together, these findings indicate that many parameters can regulate apoptosis in 
      burn wounds, and these results will be critical to understanding burn 
      pathogenesis and assessing future therapies.
CI  - Copyright 2010 Elsevier Inc. All rights reserved.
FAU - McNamara, Andrew R
AU  - McNamara AR
AD  - Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA.
FAU - Zamba, Kokou D
AU  - Zamba KD
FAU - Sokolich, Julio C
AU  - Sokolich JC
FAU - Jaskille, Amin D
AU  - Jaskille AD
FAU - Light, Timothy D
AU  - Light TD
FAU - Griffin, Michelle A
AU  - Griffin MA
FAU - Meyerholz, David K
AU  - Meyerholz DK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090224
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (HMGB1 Protein)
RN  - 0 (Hbp1 protein, rat)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/metabolism
MH  - Animals
MH  - *Apoptosis
MH  - Biopsy
MH  - Burns/*pathology
MH  - Femoral Artery/pathology
MH  - HMGB1 Protein/metabolism
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Necrosis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Resuscitation
MH  - Skin/*pathology
MH  - Wounds and Injuries/pathology
EDAT- 2009/05/15 09:00
MHDA- 2010/09/14 06:00
CRDT- 2009/05/15 09:00
PHST- 2008/11/25 00:00 [received]
PHST- 2008/12/29 00:00 [revised]
PHST- 2009/01/28 00:00 [accepted]
PHST- 2009/05/15 09:00 [entrez]
PHST- 2009/05/15 09:00 [pubmed]
PHST- 2010/09/14 06:00 [medline]
AID - S0022-4804(09)00047-X [pii]
AID - 10.1016/j.jss.2009.01.038 [doi]
PST - ppublish
SO  - J Surg Res. 2010 Aug;162(2):258-63. doi: 10.1016/j.jss.2009.01.038. Epub 2009 Feb 
      24.