PMID- 19644027
OWN - NLM
STAT- MEDLINE
DCOM- 20091224
LR  - 20130926
IS  - 1522-1601 (Electronic)
IS  - 0161-7567 (Linking)
VI  - 107
IP  - 4
DP  - 2009 Oct
TI  - Muscle apoptosis is induced in pressure-induced deep tissue injury.
PG  - 1266-75
LID - 10.1152/japplphysiol.90897.2008 [doi]
AB  - Pressure ulcer is a complex and significant health problem. Although the factors 
      including pressure, shear, and ischemia have been identified in the etiology of 
      pressure ulcer, the cellular and molecular mechanisms that contribute to the 
      development of pressure ulcer are unclear. This study tested the hypothesis that 
      the early-onset molecular regulation of pressure ulcer involves apoptosis in 
      muscle tissue. Adult Sprague-Dawley rats were subjected to an in vivo protocol to 
      mimic pressure-induced deep tissue injury. Static pressure was applied to the 
      tibialis region of the right limb of the rats for 6 h each day on two consecutive 
      days. The compression force was continuously monitored by a three-axial force 
      transducer equipped in the compression indentor. The contralateral uncompressed 
      limb served as intra-animal control. Tissues underneath the compressed region 
      were collected for histological analysis, terminal dUTP nick-end labeling 
      (TUNEL), cell death ELISA, immunocytochemical staining, and real-time RT-PCR gene 
      expression analysis. The compressed muscle tissue generally demonstrated 
      degenerative characteristics. TUNEL/dystrophin labeling showed a significant 
      increase in the apoptotic muscle-related nuclei, and cell death ELISA 
      demonstrated a threefold elevation of apoptotic DNA fragmentation in the 
      compressed muscle tissue relative to control. Positive immunoreactivities of 
      cleaved caspase-3, Bax, and Bcl-2 were evident in compressed muscle. The mRNA 
      contents of Bax, caspase-3, caspase-8, and caspase-9 were found to be higher in 
      the compressed muscle tissue than control. These results demonstrated that 
      apoptosis is activated in muscle tissue following prolonged moderate compression. 
      The data are consistent with the hypothesis that muscle apoptosis is involved in 
      the underlying mechanism of pressure-induced deep tissue injury.
FAU - Siu, Parco M
AU  - Siu PM
AD  - Department of Health Technology and Informatics, The Hong Kong Polytechnic Univ., 
      Hung Hom, Kowloon, Hong Kong, China. htpsiu@inet.polyu.edu.hk
FAU - Tam, Eric W
AU  - Tam EW
FAU - Teng, Bee T
AU  - Teng BT
FAU - Pei, Xiao M
AU  - Pei XM
FAU - Ng, Joann W
AU  - Ng JW
FAU - Benzie, Iris F
AU  - Benzie IF
FAU - Mak, Arthur F
AU  - Mak AF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090730
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (Bax protein, rat)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (RNA, Messenger)
RN  - 0 (bcl-2-Associated X Protein)
RN  - EC 3.4.22.- (Casp3 protein, rat)
RN  - EC 3.4.22.- (Casp8 protein, rat)
RN  - EC 3.4.22.- (Casp9 protein, rat)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspase 8)
RN  - EC 3.4.22.- (Caspase 9)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Caspase 3/metabolism
MH  - Caspase 8/metabolism
MH  - Caspase 9/metabolism
MH  - DNA Fragmentation
MH  - Disease Models, Animal
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Gene Expression Regulation
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Muscle, Skeletal/metabolism/*pathology
MH  - Muscular Diseases/genetics/metabolism/*pathology
MH  - Pressure
MH  - Pressure Ulcer/genetics/metabolism/*pathology
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - bcl-2-Associated X Protein/metabolism
EDAT- 2009/08/01 09:00
MHDA- 2009/12/25 06:00
CRDT- 2009/08/01 09:00
PHST- 2009/08/01 09:00 [entrez]
PHST- 2009/08/01 09:00 [pubmed]
PHST- 2009/12/25 06:00 [medline]
AID - 90897.2008 [pii]
AID - 10.1152/japplphysiol.90897.2008 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2009 Oct;107(4):1266-75. doi: 
      10.1152/japplphysiol.90897.2008. Epub 2009 Jul 30.