| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-81 |
Sentence |
denotes |
FHL2 regulates the resolution of tissue damage in chronic inflammatory arthritis. |
| T1 |
0-81 |
Sentence |
denotes |
FHL2 regulates the resolution of tissue damage in chronic inflammatory arthritis. |
| T2 |
82-92 |
Sentence |
denotes |
OBJECTIVE: |
| T2 |
82-92 |
Sentence |
denotes |
OBJECTIVE: |
| T3 |
93-365 |
Sentence |
denotes |
We analysed the role of the adaptor molecule four-and-a-half Lin11, Isl-1 & Mec-3 (LIM) domain protein 2 (FHL2) in the activation of fibroblast-like synoviocytes in human rheumatoid arthritis (RA) and tumour necrosis factor α (TNFα)-dependent animal models of the disease. |
| T3 |
93-365 |
Sentence |
denotes |
We analysed the role of the adaptor molecule four-and-a-half Lin11, Isl-1 & Mec-3 (LIM) domain protein 2 (FHL2) in the activation of fibroblast-like synoviocytes in human rheumatoid arthritis (RA) and tumour necrosis factor α (TNFα)-dependent animal models of the disease. |
| T4 |
366-374 |
Sentence |
denotes |
METHODS: |
| T4 |
366-374 |
Sentence |
denotes |
METHODS: |
| T5 |
375-566 |
Sentence |
denotes |
Synovial tissues of patients with RA and osteoarthritis (OA) as well as hind paw sections from arthritic human TNFα transgenic (hTNFtg) mice and synovial fibroblasts from these were analysed. |
| T5 |
375-566 |
Sentence |
denotes |
Synovial tissues of patients with RA and osteoarthritis (OA) as well as hind paw sections from arthritic human TNFα transgenic (hTNFtg) mice and synovial fibroblasts from these were analysed. |
| T6 |
567-685 |
Sentence |
denotes |
The effects of cytokines on the expression of FHL2 and disease-relevant matrixmetalloproteases (MMPs) were determined. |
| T6 |
567-685 |
Sentence |
denotes |
The effects of cytokines on the expression of FHL2 and disease-relevant matrixmetalloproteases (MMPs) were determined. |
| T7 |
686-867 |
Sentence |
denotes |
Analyses of human tissue specimens from patients treated with anti-TNFα as well as anti-TNFα treatment of hTNFtg mice were performed to substantiate the TNFα effects on FHL2 levels. |
| T7 |
686-867 |
Sentence |
denotes |
Analyses of human tissue specimens from patients treated with anti-TNFα as well as anti-TNFα treatment of hTNFtg mice were performed to substantiate the TNFα effects on FHL2 levels. |
| T8 |
868-1023 |
Sentence |
denotes |
FHL2(-/-) mice and hTNFtg mice (with constitutive or inducible transgene expression) were crossbred to generate TNFα overexpressing FHL2-deficient animals. |
| T8 |
868-1023 |
Sentence |
denotes |
FHL2(-/-) mice and hTNFtg mice (with constitutive or inducible transgene expression) were crossbred to generate TNFα overexpressing FHL2-deficient animals. |
| T9 |
1024-1143 |
Sentence |
denotes |
Signalling pathways were analysed in cells from these mice and in human cells after knock down of FHL2 by western blot. |
| T9 |
1024-1143 |
Sentence |
denotes |
Signalling pathways were analysed in cells from these mice and in human cells after knock down of FHL2 by western blot. |
| T10 |
1144-1231 |
Sentence |
denotes |
RESULTS: FHL2 levels were higher in RA than in OA and in hTNFtg than in wild-type mice. |
| T10 |
1144-1231 |
Sentence |
denotes |
RESULTS: FHL2 levels were higher in RA than in OA and in hTNFtg than in wild-type mice. |
| T11 |
1232-1332 |
Sentence |
denotes |
Surprisingly, while transforming growth factor (TGF)β-induced FHL2 expression, TNFα suppressed FHL2. |
| T11 |
1232-1332 |
Sentence |
denotes |
Surprisingly, while transforming growth factor (TGF)β-induced FHL2 expression, TNFα suppressed FHL2. |
| T12 |
1333-1424 |
Sentence |
denotes |
In vivo, anti-TNFα treatment led to higher FHL2 levels both in RA patients and hTNFtg mice. |
| T12 |
1333-1424 |
Sentence |
denotes |
In vivo, anti-TNFα treatment led to higher FHL2 levels both in RA patients and hTNFtg mice. |
| T13 |
1425-1527 |
Sentence |
denotes |
The loss of FHL2 increased joint destruction in hTNFtg mice, which was accompanied by elevated MMP-13. |
| T13 |
1425-1527 |
Sentence |
denotes |
The loss of FHL2 increased joint destruction in hTNFtg mice, which was accompanied by elevated MMP-13. |
| T14 |
1528-1683 |
Sentence |
denotes |
In vitro, TNFα-mediated MMP-13 was significantly higher in FHL2(-/-) cells and after knock down of FHL2, which was caused by prolonged p38 MAPK activation. |
| T14 |
1528-1683 |
Sentence |
denotes |
In vitro, TNFα-mediated MMP-13 was significantly higher in FHL2(-/-) cells and after knock down of FHL2, which was caused by prolonged p38 MAPK activation. |
| T15 |
1684-1696 |
Sentence |
denotes |
CONCLUSIONS: |
| T15 |
1684-1696 |
Sentence |
denotes |
CONCLUSIONS: |
| T16 |
1697-1876 |
Sentence |
denotes |
These data suggest that FHL2 serves as a protective factor and that, rather than promoting the pathology, the upregulation of FHL2 in RA occurs in frame of a regenerative attempt. |
| T16 |
1697-1876 |
Sentence |
denotes |
These data suggest that FHL2 serves as a protective factor and that, rather than promoting the pathology, the upregulation of FHL2 in RA occurs in frame of a regenerative attempt. |