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Disease
Symptom
Drug
Enzyme
Compound
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Gene/Protein
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Target Concepts:
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Query: UNIPROT:P05231 (
interleukin-6
)
23,907
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The aim of this study was to investigate the role of Mesenchymal Stem Cell (MSC) conditioned medium (CM(MSC)) on apoptosis of cultured mouse primary hepatocytes after in vivo carbon tetrachloride (CCl4)-induced acute liver injury. The acute liver injury was induced by injecting CCl4 intraperitoneally in C57/BL6 mice. Hepatocytes were isolated by liver perfusion, cultured in a defined medium to maintain their differentiation and characterized by reverse transcriptase polymerase chain reaction (RT-PCR) using the hepatic cell specific genes albumin, hepatocyte nuclear factor 4 (HNF4) and cytokeratin 18 (CK18). CM(MSC) was generated from cultured bone marrow-derived MSCs (BM-MSCs). BM-MSCs were positive for CD73, CD90, CD44 by flow cytometry and able to differentiate into chondrocytes, adipocytes and osteocytes. Apoptosis was evaluated by both annexin V. CM(MSC) were examined by flow cytometry to detect MSC-derived annexin V- and CD54/CD44-positive microparticles (MPs). In the CCl4-CM(MSC) treated hepatocytes,
interleukin-6
(
IL-6
) was increased on the first day of culture compared to control and CCl4 and was followed by upregulation of fibroblast-like-protein (
FGL1
) expression after 48 hrs. This was associated with a significant decrease of annexin V positive CCl4-CM(MSC) treated hepatocytes at day 3 post plating. Recombinant
IL-6
was induced
FGL1
expression in hepatocytes derived from CCl4-treated mice suggesting that CM(MSC), which is enriched also in microparticles, attenuates CCl4-induced early apoptosis in hepatocytes through activation of
FGL1
.
...
PMID:Protective effect of mesenchymal stem cell-conditioned medium on hepatic cell apoptosis after acute liver injury. 2363 14
Hepassocin
(
HPS
) is a hepatokine that regulates hepatocyte proliferation. It is known that
HPS
plays an important role in the development of nonalcoholic fatty liver diseases (NAFLD). Fatty acids, such as oleic acid (OLA), exhibit the ability to activate the signal transducer and activator of transcription-3 (STAT3), and the binding site of STAT3 is found in the promoter region of
HPS
. However, the regulation of
HPS
by fatty acids is still obscure. To clarify the regulation of
HPS
, we detected the expression of
HPS
by western blots. In addition, a hepatic steatosis cell culture model was established by treatment of different fatty acids, including linoleic acid (LNA), oleic acid, palmitic acid, and stearic acid. The intracellular lipid accumulation was confirmed by oil red O staining. Blocking of STAT3 activity was achieved by the pretreatment of the STAT3 inhibitor, stattic. We found that activation of STAT3 by
interleukin-6
(
IL-6
) was mediated in the regulation of
HPS
expression. Treatment of unsaturated fatty acids significantly induced intracellular lipid accumulation in HepG2 cells. Moreover, the expressions of
HPS
were increased in unsaturated fatty acid-treated HepG2 cells, as compared with saturated fatty acid-treated groups. Also, the expression of
HPS
induced by OLA was blocked by the inhibition of STAT3 activity. Furthermore, we found that deletion of
HPS
by small interfering ribonucleic acid transfection decreased the protective effect of OLA on cell viability. Taken together, we provided evidence that STAT3 plays an important role in the regulation of OLA-induced
HPS
expression and the increased
HPS
may further participate in the development of NAFLD. In addition, the increase of
HPS
might be involved in the protective effect of OLA on cell viability.
...
PMID:Unsaturated Fatty Acids Increase the Expression of Hepassocin through a Signal Transducer and Activator of Transcription 3-Dependent Pathway in HepG2 Cells. 3046 Jun 99
