Id |
Subject |
Object |
Predicate |
Lexical cue |
T1 |
0-103 |
Sentence |
denotes |
Serum Amyloid A Induces Inflammation, Proliferation and Cell Death in Activated Hepatic Stellate Cells. |
T1 |
0-103 |
Sentence |
denotes |
Serum Amyloid A Induces Inflammation, Proliferation and Cell Death in Activated Hepatic Stellate Cells. |
T2 |
104-228 |
Sentence |
denotes |
Serum amyloid A (SAA) is an evolutionary highly conserved acute phase protein that is predominantly secreted by hepatocytes. |
T2 |
104-228 |
Sentence |
denotes |
Serum amyloid A (SAA) is an evolutionary highly conserved acute phase protein that is predominantly secreted by hepatocytes. |
T3 |
229-311 |
Sentence |
denotes |
However, its role in liver injury and fibrogenesis has not been elucidated so far. |
T3 |
229-311 |
Sentence |
denotes |
However, its role in liver injury and fibrogenesis has not been elucidated so far. |
T4 |
312-437 |
Sentence |
denotes |
In this study, we determined the effects of SAA on hepatic stellate cells (HSCs), the main fibrogenic cell type of the liver. |
T4 |
312-437 |
Sentence |
denotes |
In this study, we determined the effects of SAA on hepatic stellate cells (HSCs), the main fibrogenic cell type of the liver. |
T5 |
438-607 |
Sentence |
denotes |
Serum amyloid A potently activated IκB kinase, c-Jun N-terminal kinase (JNK), Erk and Akt and enhanced NF-κB-dependent luciferase activity in primary human and rat HSCs. |
T5 |
438-607 |
Sentence |
denotes |
Serum amyloid A potently activated IκB kinase, c-Jun N-terminal kinase (JNK), Erk and Akt and enhanced NF-κB-dependent luciferase activity in primary human and rat HSCs. |
T6 |
608-714 |
Sentence |
denotes |
Serum amyloid A induced the transcription of MCP-1, RANTES and MMP9 in an NF-κB- and JNK-dependent manner. |
T6 |
608-714 |
Sentence |
denotes |
Serum amyloid A induced the transcription of MCP-1, RANTES and MMP9 in an NF-κB- and JNK-dependent manner. |
T7 |
715-866 |
Sentence |
denotes |
Blockade of NF-κB revealed cytotoxic effects of SAA in primary HSCs with signs of apoptosis such as caspase 3 and PARP cleavage and Annexin V staining. |
T7 |
715-866 |
Sentence |
denotes |
Blockade of NF-κB revealed cytotoxic effects of SAA in primary HSCs with signs of apoptosis such as caspase 3 and PARP cleavage and Annexin V staining. |
T8 |
867-954 |
Sentence |
denotes |
Serum amyloid A induced HSC proliferation, which depended on JNK, Erk and Akt activity. |
T8 |
867-954 |
Sentence |
denotes |
Serum amyloid A induced HSC proliferation, which depended on JNK, Erk and Akt activity. |
T9 |
955-1073 |
Sentence |
denotes |
In primary hepatocytes, SAA also activated MAP kinases, but did not induce relevant cell death after NF-κB inhibition. |
T9 |
955-1073 |
Sentence |
denotes |
In primary hepatocytes, SAA also activated MAP kinases, but did not induce relevant cell death after NF-κB inhibition. |
T10 |
1074-1213 |
Sentence |
denotes |
In two models of hepatic fibrogenesis, CCl4 treatment and bile duct ligation, hepatic mRNA levels of SAA1 and SAA3 were strongly increased. |
T10 |
1074-1213 |
Sentence |
denotes |
In two models of hepatic fibrogenesis, CCl4 treatment and bile duct ligation, hepatic mRNA levels of SAA1 and SAA3 were strongly increased. |
T11 |
1214-1378 |
Sentence |
denotes |
In conclusion, SAA may modulate fibrogenic responses in the liver in a positive and negative fashion by inducing inflammation, proliferation and cell death in HSCs. |
T11 |
1214-1378 |
Sentence |
denotes |
In conclusion, SAA may modulate fibrogenic responses in the liver in a positive and negative fashion by inducing inflammation, proliferation and cell death in HSCs. |