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Stellate Cell Activation and Imbalanced Expression of TGF-β1/TGF-β3 in Acute Autoimmune Liver Lesions Induced by ConA in Mice.

Abstract Objective. To study the pathogenic feature of liver injury, activation of hepatic stellate cells, and dynamic expression of TGF-β1/TGF-β3 to reveal their role in liver injury induced by ConA. Methods. Mice were randomly divided into control group and ConA treatment group. ConA (20 mg/kg) was injected through vena caudalis in ConA treatment group; the controls received the same volume of saline injection. After injection for 2 h, 8 h, 24 h, and 48 h, animals were terminated. Blood, liver, and spleen were harvested. Liver function and histopathology were studied. α-SMA, vimentin, TGF-β1, and TGF-β3 were detected. Results. After ConA injection, liver damage started to increase. Expression of α-SMA, vimentin, TGF-β1, and TGF-β3 was significantly enhanced; all above indicators reached peak at 8 h; but from 24 h after ConA injection, TGF-β3 expression began to decline, while the TGF-β1/TGF-β3 ratio at 48 h was significantly lower than control. Conclusion. (1) Autoimmune liver injury induced by ConA showed time-based features, in which the most serious liver lesions happened at 8 h after ConA injection. (2) Early activation of HSC and imbalance expression of TGF-β1 and TGF-β3 existed in ConA-induced acute autoimmune liver injury, which may be associated with liver dysfunction and the mechanisms of progression to fibrosis.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28246592
OWN - NLM
STAT- MEDLINE
DA  - 20170301
DCOM- 20170313
LR  - 20170313
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - Stellate Cell Activation and Imbalanced Expression of TGF-beta1/TGF-beta3 in
      Acute Autoimmune Liver Lesions Induced by ConA in Mice.
PG  - 2540540
LID - 10.1155/2017/2540540 [doi]
AB  - Objective. To study the pathogenic feature of liver injury, activation of hepatic
      stellate cells, and dynamic expression of TGF-beta1/TGF-beta3 to reveal their
      role in liver injury induced by ConA. Methods. Mice were randomly divided into
      control group and ConA treatment group. ConA (20 mg/kg) was injected through vena
      caudalis in ConA treatment group; the controls received the same volume of saline
      injection. After injection for 2 h, 8 h, 24 h, and 48 h, animals were terminated.
      Blood, liver, and spleen were harvested. Liver function and histopathology were
      studied. alpha-SMA, vimentin, TGF-beta1, and TGF-beta3 were detected. Results.
      After ConA injection, liver damage started to increase. Expression of alpha-SMA, 
      vimentin, TGF-beta1, and TGF-beta3 was significantly enhanced; all above
      indicators reached peak at 8 h; but from 24 h after ConA injection, TGF-beta3
      expression began to decline, while the TGF-beta1/TGF-beta3 ratio at 48 h was
      significantly lower than control. Conclusion. (1) Autoimmune liver injury induced
      by ConA showed time-based features, in which the most serious liver lesions
      happened at 8 h after ConA injection. (2) Early activation of HSC and imbalance
      expression of TGF-beta1 and TGF-beta3 existed in ConA-induced acute autoimmune
      liver injury, which may be associated with liver dysfunction and the mechanisms
      of progression to fibrosis.
FAU - Wang, Liyun
AU  - Wang L
AUID- ORCID: 0000-0003-1221-7955
AD  - Division of Gastroenterology, Shandong Provincial Qianfoshan Hospital, Jinan,
      Shandong, China; Division of Gastroenterology, Union Hospital, Tongji Medical
      College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
FAU - Tu, Lei
AU  - Tu L
AD  - Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong
      University of Science and Technology, Wuhan, Hubei, China.
FAU - Zhang, Jinping
AU  - Zhang J
AD  - Division of Neurology, Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, 
      China.
FAU - Xu, Keshu
AU  - Xu K
AUID- ORCID: 0000-0003-3979-4840
AD  - Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong
      University of Science and Technology, Wuhan, Hubei, China.
FAU - Qian, Wei
AU  - Qian W
AD  - Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong
      University of Science and Technology, Wuhan, Hubei, China.
LA  - eng
PT  - Journal Article
DEP - 20170129
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 0 (Biomarkers)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (Transforming Growth Factor beta3)
RN  - 0 (Vimentin)
RN  - 11028-71-0 (Concanavalin A)
RN  - EC 2.6.1.- (Transaminases)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Autoimmune Diseases/blood/metabolism/*pathology/physiopathology
MH  - Biomarkers/metabolism
MH  - Concanavalin A
MH  - Female
MH  - Hepatic Stellate Cells/*metabolism/*pathology
MH  - Immunohistochemistry
MH  - Injections, Intravenous
MH  - Liver/enzymology/*pathology/physiopathology
MH  - Liver Function Tests
MH  - Mice
MH  - Spleen/pathology
MH  - Time Factors
MH  - Transaminases/metabolism
MH  - Transforming Growth Factor beta1/blood/*metabolism
MH  - Transforming Growth Factor beta3/blood/*metabolism
MH  - Vimentin/metabolism
PMC - PMC5303577
COI - The authors declare that they have no competing interests.
EDAT- 2017/03/02 06:00
MHDA- 2017/03/14 06:00
CRDT- 2017/03/02 06:00
PHST- 2016/10/23 [received]
PHST- 2016/12/13 [accepted]
AID - 10.1155/2017/2540540 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:2540540. doi: 10.1155/2017/2540540. Epub 2017 Jan 29.

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