PMID- 19302180
OWN - NLM
STAT- MEDLINE
DCOM- 20090910
LR  - 20181121
IS  - 1478-3231 (Electronic)
IS  - 1478-3223 (Linking)
VI  - 29
IP  - 7
DP  - 2009 Aug
TI  - Impaired liver regeneration with humoral and genetic disturbances in urinary 
      trypsin inhibitor-deficient mice.
PG  - 979-87
LID - 10.1111/j.1478-3231.2009.01990.x [doi]
AB  - BACKGROUND/AIMS: Urinary trypsin inhibitor (UTI) is an innate anti-inflammatory 
      regulator. It can block the release of inflammatory factors, prevent the cascade 
      reaction of cytokines and inhibit excessive activation of leukocytes. Liver 
      regeneration (LR) is a dynamic molecular phenomenon without inflammation. Many 
      cytokines, including tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 
      (IL-6), have been implicated in regulating LR. However, the role of UTI in LR is 
      totally unknown. The aim of this study was to elucidate the role of UTI in LR 
      using genetically UTI-deficient mice. METHODS: We performed 68% hepatectomy, 
      comparing UTI (-/-) and UTI (+/+) mice. Recovery of liver weight was recorded and 
      we calculated labelling indices after 5-bromo-2'-deoxyuridine (BrdU) 
      immunohistochemistry. A DNA microarray was used to examine gene expression 
      followed by real-time polymerase chain reaction. Serum IL-6, IL-10, monocyte 
      chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1beta 
      (MIP-1beta) were measured. RESULTS: LR in UTI (-/-) mice was delayed at 36 h 
      after hepatectomy, at which time the DNA profile was different. One hundred and 
      fourteen genes were upregulated and 100 genes were downregulated in UTI (-/-) 
      mice at 36 h after hepatectomy among the 21, 977 mRNAs examined. Furthermore, 
      serum IL-6, IL-10, MCP-1 and MIP-1beta levels at 36 h after hepatectomy in the 
      UTI (-/-) mice were significantly higher than in the UTI (+/+) mice. CONCLUSION: 
      UTI appears to important cytokine and chemokine regulation in normal liver 
      regeneration.
FAU - Nobuoka, Takayuki
AU  - Nobuoka T
AD  - Department of Surgery I, Sapporo Medical University Hospital, Sapporo Medical 
      University School of Medicine, Sapporo, Japan.
FAU - Mizuguchi, Toru
AU  - Mizuguchi T
FAU - Oshima, Hideki
AU  - Oshima H
FAU - Shibata, Toshihito
AU  - Shibata T
FAU - Kaji, Shinsuke
AU  - Kaji S
FAU - Nagayama, Minoru
AU  - Nagayama M
FAU - Meguro, Makoto
AU  - Meguro M
FAU - Mitaka, Toshihiro
AU  - Mitaka T
FAU - Hirata, Koichi
AU  - Hirata K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090303
PL  - United States
TA  - Liver Int
JT  - Liver international : official journal of the International Association for the 
      Study of the Liver
JID - 101160857
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Ccl4 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Cytokines)
RN  - 0 (Glycoproteins)
RN  - 0 (Interleukin-6)
RN  - 130068-27-8 (Interleukin-10)
RN  - OR3S9IF86U (urinastatin)
SB  - IM
MH  - Animals
MH  - *Antibody Formation/genetics
MH  - *Cell Proliferation
MH  - Cells, Cultured
MH  - Chemokine CCL2/blood
MH  - Chemokine CCL4/blood
MH  - Cytokines/*blood/genetics
MH  - Gene Expression Profiling/methods
MH  - Gene Expression Regulation
MH  - Glycoproteins/*deficiency/genetics
MH  - Hepatectomy
MH  - Immunohistochemistry
MH  - Interleukin-10/blood
MH  - Interleukin-6/blood
MH  - Liver/immunology/metabolism/*pathology/surgery
MH  - *Liver Regeneration/genetics/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Oligonucleotide Array Sequence Analysis
MH  - Organ Size
MH  - Time Factors
EDAT- 2009/03/24 09:00
MHDA- 2009/09/11 06:00
CRDT- 2009/03/24 09:00
PHST- 2009/03/24 09:00 [entrez]
PHST- 2009/03/24 09:00 [pubmed]
PHST- 2009/09/11 06:00 [medline]
AID - LIV1990 [pii]
AID - 10.1111/j.1478-3231.2009.01990.x [doi]
PST - ppublish
SO  - Liver Int. 2009 Aug;29(7):979-87. doi: 10.1111/j.1478-3231.2009.01990.x. Epub 
      2009 Mar 3.