PMID- 17105404
OWN - NLM
STAT- MEDLINE
DCOM- 20070124
LR  - 20171116
IS  - 1547-3287 (Print)
IS  - 1547-3287 (Linking)
VI  - 15
IP  - 5
DP  - 2006 Oct
TI  - Syngenic bone marrow cells restore hepatic function in carbon 
      tetrachloride-induced mouse liver injury.
PG  - 687-95
AB  - Progenitor cells in bone marrow have been explored for the treatment of liver 
      injury. Stem cell homing to the injured tissue is regulated through stromal cell 
      derived factor-1 (SDF-1) and its receptor CXCR4. We hypothesized that syngenic 
      bone marrow cells (BMCs) would restore hepatic function in the injured liver 
      through the regulation by SDF-1/CXCR4 system. After injecting carbon 
      tetrachloride (CCl(4)), the mice were injected with syngenic BMCs or normal 
      saline. Morphological and functional analysis of the liver was performed. Flow 
      cytometry for the stem cell markers and CXCR4 was done with the liver, BM, and 
      spleen cells from each group. Carboxyfluorescein diacetate succinimidyl ester was 
      used to trace the homing of transplanted BMCs. The SDF-1 expression of the liver 
      was assessed by immunohistochemistry. Hepatosplenomegaly and necrosis of the 
      CCl(4)-injected mouse liver were improved after BMCs transplantation The hepatic 
      enzymes were increased after injury and then decreased after BMCs 
      transplantation. The expression of stem cell markers and CXCR4 was exclusively 
      increased in the damaged liver compared to the BM and spleen, and even more 
      elevated after BMCs transplantation. SDF-1 expression in the liver was observed 
      after CCl(4) injection and it was elevated after BMCs transplantation. The 
      intrinsic and extrinsic BMCs migrate specifically to the injured liver rather 
      than BM or spleen, and the transplanted BMCs contribute to the repair of the 
      damaged liver. SDF-1/CXCR-4 interaction plays a role in stem cell homing toward 
      the damaged organ, and transplanted BMCs are involved in the up-regulated SDF-1 
      expression seen in the injured liver.
FAU - Jung, Yun-Jae
AU  - Jung YJ
AD  - Department of Microbiology, Ewha Woman's University College of Medicine, Ewha 
      Medical Research Center, Seoul, Korea.
FAU - Ryu, Kyung-Ha
AU  - Ryu KH
FAU - Cho, Su Jin
AU  - Cho SJ
FAU - Woo, So-Youn
AU  - Woo SY
FAU - Seoh, Ju-Young
AU  - Seoh JY
FAU - Chun, Chung Hyun
AU  - Chun CH
FAU - Yoo, Kwon
AU  - Yoo K
FAU - Moon, Il-Hwan
AU  - Moon IH
FAU - Han, Ho-Seong
AU  - Han HS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Stem Cells Dev
JT  - Stem cells and development
JID - 101197107
RN  - 0 (5-(6)-carboxyfluorescein diacetate succinimidyl ester)
RN  - 0 (Actins)
RN  - 0 (Antigens, CD34)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cxcl12 protein, mouse)
RN  - 0 (Fluoresceins)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Succinimides)
RN  - CL2T97X0V0 (Carbon Tetrachloride)
RN  - EC 3.1.3.48 (Leukocyte Common Antigens)
SB  - IM
MH  - Actins/metabolism
MH  - Animals
MH  - Antigens, CD34/immunology
MH  - Bone Marrow Cells/*cytology
MH  - *Bone Marrow Transplantation
MH  - Carbon Tetrachloride/*toxicity
MH  - *Chemical and Drug Induced Liver Injury
MH  - Chemokine CXCL12
MH  - Chemokines, CXC/metabolism
MH  - Female
MH  - Fluoresceins/metabolism
MH  - Hematopoietic Stem Cells/cytology
MH  - Hepatomegaly/pathology
MH  - Injections, Intraperitoneal
MH  - Leukocyte Common Antigens/immunology
MH  - Liver/*drug effects/enzymology/*physiology
MH  - Liver Diseases/*physiopathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Myocytes, Smooth Muscle/cytology
MH  - Receptors, Chemokine/metabolism
MH  - Splenomegaly/pathology
MH  - Succinimides/metabolism
MH  - Up-Regulation
EDAT- 2006/11/16 09:00
MHDA- 2007/01/25 09:00
CRDT- 2006/11/16 09:00
PHST- 2006/11/16 09:00 [pubmed]
PHST- 2007/01/25 09:00 [medline]
PHST- 2006/11/16 09:00 [entrez]
AID - 10.1089/scd.2006.15.687 [doi]
PST - ppublish
SO  - Stem Cells Dev. 2006 Oct;15(5):687-95. doi: 10.1089/scd.2006.15.687.