PMID- 19389872
OWN - NLM
STAT- MEDLINE
DCOM- 20090903
LR  - 20161125
IS  - 1533-1601 (Electronic)
IS  - 0192-6233 (Linking)
VI  - 37
IP  - 4
DP  - 2009 Jun
TI  - Participation of functionally different macrophage populations and monocyte 
      chemoattractant protein-1 in early stages of thioacetamide-induced rat hepatic 
      injury.
PG  - 463-73
LID - 10.1177/0192623309335634 [doi]
AB  - Macrophages are crucial in hepatic fibrogenesis. In acute hepatic necrosis 
      induced in rats by a single injection of 300 mg/kg body weight (BW) of 
      thioacetamide (TAA), macrophage properties were investigated using single or 
      double immunohistochemistry. Macrophages reacting with anti-CD68, anti-CD163, or 
      major histocompatibility complex (anti-MHC) class II antibody appeared in injured 
      centrilobular areas on days 1-5 after injection. Increased expression of CD68 and 
      CD163 reflect phagocytosis and production of pro-inflammatory factors, 
      respectively. There were also macrophages double-positive to CD68/CD163, CD68/MHC 
      class II, or CD163/MHC class II; of these, macrophages double-positive to 
      CD68/MHC class II were most frequent, indicating that macrophages with enhanced 
      phagocytic activity came to express MHC class II. The appearance of these 
      macrophages corresponded to increased expression of mRNAs of monocyte 
      chemoattractant protein-1 (MCP-1), a chemokine, on day 1, and TGF-beta1, a 
      fibrogenic factor, on day 3. Some hepatic stellate cells (HSCs) in injured areas 
      reacted with anti-MCP-1 antibody. To investigate the effects of MCP-1, we added 
      MCP-1 to HS-P, a rat macrophage line. Addition of MCP-1 increased 
      immunoexpression for CD68 and CD163 and up-regulated TGF-beta1 mRNA expression. 
      Collectively, macrophages in acute hepatic necrosis may express different 
      properties such as phagocytosis, MHC class II expression, and TGF-beta1 
      production; such expression may be influenced by MCP-1 produced by HSCs.
FAU - Mori, Yoko
AU  - Mori Y
AD  - Laboratories of Veterinary Pathology and Molecular Science, Life and 
      Environmental Sciences, Osaka Prefecture University, Nakaku, Sakai, Osaka, Japan.
FAU - Izawa, Takeshi
AU  - Izawa T
FAU - Takenaka, Shigeo
AU  - Takenaka S
FAU - Kuwamura, Mitsuru
AU  - Kuwamura M
FAU - Yamate, Jyoji
AU  - Yamate J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090423
PL  - United States
TA  - Toxicol Pathol
JT  - Toxicologic pathology
JID - 7905907
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation)
RN  - 0 (Antigens, Differentiation, Myelomonocytic)
RN  - 0 (CD163 antigen)
RN  - 0 (CD68 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (OX-62 antigen, rat)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 075T165X8M (Thioacetamide)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Antigens, CD/metabolism
MH  - Antigens, Differentiation/metabolism
MH  - Antigens, Differentiation, Myelomonocytic/metabolism
MH  - Cells, Cultured
MH  - *Chemical and Drug Induced Liver Injury
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Gene Expression Regulation
MH  - Hepatic Stellate Cells/metabolism
MH  - Histocompatibility Antigens Class II/metabolism
MH  - Immunohistochemistry
MH  - Liver/metabolism/pathology
MH  - Liver Diseases/metabolism/pathology
MH  - Macrophages/*metabolism
MH  - Male
MH  - Necrosis/chemically induced/metabolism
MH  - Rats
MH  - Rats, Inbred F344
MH  - Receptors, Cell Surface/metabolism
MH  - Thioacetamide/administration & dosage/*toxicity
MH  - Transforming Growth Factor beta1/genetics/metabolism
EDAT- 2009/04/25 09:00
MHDA- 2009/09/04 06:00
CRDT- 2009/04/25 09:00
PHST- 2009/04/25 09:00 [entrez]
PHST- 2009/04/25 09:00 [pubmed]
PHST- 2009/09/04 06:00 [medline]
AID - 0192623309335634 [pii]
AID - 10.1177/0192623309335634 [doi]
PST - ppublish
SO  - Toxicol Pathol. 2009 Jun;37(4):463-73. doi: 10.1177/0192623309335634. Epub 2009 
      Apr 23.