PMID- 18219277
OWN - NLM
STAT- MEDLINE
DCOM- 20080624
LR  - 20220408
IS  - 1523-1747 (Electronic)
IS  - 0022-202X (Linking)
VI  - 128
IP  - 7
DP  - 2008 Jul
TI  - The loss of MCP-1 attenuates cutaneous ischemia-reperfusion injury in a mouse 
      model of pressure ulcer.
PG  - 1838-51
LID - 10.1038/sj.jid.5701258 [doi]
AB  - The formation of pressure ulcers is dependent on multiple factors including 
      ischemia-reperfusion (IR). This study assessed the mechanism of a previously 
      reported murine model of cutaneous IR injury. Three cycles of IR (days 1-3) by 
      external application of two magnetic plates were performed to induce pressure 
      ulcer formation. Increased infiltration of neutrophils and macrophages, and 
      augmented expression of proinflammatory cytokines and inducible nitric oxide 
      synthase (iNOS), were observed during IR cycles. In this model, monocyte 
      chemoattractant protein-1 (MCP-1) was remarkably increased at day 1 in the skin 
      followed by inflammatory cell infiltration. Therefore, IR cycles were performed 
      in MCP-1-deficient (MCP-1(-/-)) mice to evaluate the role of this chemokine in 
      pressure ulcer development. MCP-1(-/-) mice showed reduced macrophage 
      infiltration and expression of tumor-necrosis factor-alpha (TNF)-alpha and iNOS 
      during IR cycles leading to attenuated apoptosis and skin injury. Importantly, 
      MCP-1 played a role in apoptosis and injury via inducing iNOS during the 
      reperfusion rather than the ischemic period. These findings indicate that MCP-1 
      may be a critical factor for macrophage recruitment and subsequent skin 
      inflammation and injury during IR cycles. We propose that this is a useful model 
      for investigating the mechanism of pressure ulcer formation using various 
      transgenic mice.
FAU - Saito, Yuki
AU  - Saito Y
AD  - Department of Dermatology, Kanazawa University Graduate School of Medical 
      Science, Kanazawa, Ishikawa, Japan.
FAU - Hasegawa, Minoru
AU  - Hasegawa M
FAU - Fujimoto, Manabu
AU  - Fujimoto M
FAU - Matsushita, Takashi
AU  - Matsushita T
FAU - Horikawa, Mayuka
AU  - Horikawa M
FAU - Takenaka, Motoi
AU  - Takenaka M
FAU - Ogawa, Fumihide
AU  - Ogawa F
FAU - Sugama, Junko
AU  - Sugama J
FAU - Steeber, Douglas A
AU  - Steeber DA
FAU - Sato, Shinichi
AU  - Sato S
FAU - Takehara, Kazuhiko
AU  - Takehara K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080124
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (HSP90 Heat-Shock Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Chemokine CCL2/blood/*physiology
MH  - Female
MH  - HSP90 Heat-Shock Proteins/genetics
MH  - Macrophages/physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neutrophil Infiltration
MH  - Nitric Oxide/biosynthesis
MH  - Nitric Oxide Synthase Type II/genetics
MH  - Pressure Ulcer/*etiology
MH  - RNA, Messenger/analysis
MH  - Reperfusion Injury/pathology/*prevention & control
MH  - Skin/*blood supply/pathology
MH  - Tumor Necrosis Factor-alpha/blood/genetics
MH  - Wound Healing
EDAT- 2008/01/26 09:00
MHDA- 2008/06/25 09:00
CRDT- 2008/01/26 09:00
PHST- 2008/01/26 09:00 [pubmed]
PHST- 2008/06/25 09:00 [medline]
PHST- 2008/01/26 09:00 [entrez]
AID - S0022-202X(15)33930-0 [pii]
AID - 10.1038/sj.jid.5701258 [doi]
PST - ppublish
SO  - J Invest Dermatol. 2008 Jul;128(7):1838-51. doi: 10.1038/sj.jid.5701258. Epub 
      2008 Jan 24.