| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-158 |
DRI_Background |
denotes |
Delayed Cell Cycle Progression in STHdh(Q111)/Hdh(Q111) Cells, a Cell Model for Huntington's Disease Mediated by microRNA-19a, microRNA-146a and microRNA-432. |
| T2 |
159-305 |
DRI_Challenge |
denotes |
Several indirect evidences are available to indicate that abnormalities in cell cycle may contribute to pathogenesis of Huntington's disease (HD). |
| T3 |
306-474 |
DRI_Outcome |
denotes |
Here, we show that the cell cycle progression in STsdh(Q111)/Hdh(Q111)cells, a cell model of HD, is delayed in S and G2-M phases compared to control STHdhQ7/HdhQ7cells. |
| T4 |
475-564 |
DRI_Background |
denotes |
Expression of 17 genes, like PCNA and CHEK1, was increased in STHdh(Q111)/Hdh(Q111)cells. |
| T5 |
565-783 |
DRI_Background |
denotes |
Increased expressions of PCNA, CHEK1 and CCNA2, and an enhanced phosphorylation of Rb1 were observed in primary cortical neurons expressing mutant N-terminal huntingtin (HTT), R6/2 mice and STHdh(Q111)/Hdh(Q111) cells. |
| T6 |
784-957 |
DRI_Outcome |
denotes |
This increase in the expressions of PCNA, CHEK1 and CCNA2 was found to be the result of decreased expressions of miR-432, miR-146a, and (miR-19a and miR-146a), respectively. |
| T7 |
958-1051 |
DRI_Background |
denotes |
Enhanced apoptosis was observed at late S phase and G2-M phase in STHdh(Q111)/Hdh(Q111)cells. |
| T8 |
1052-1175 |
DRI_Approach |
denotes |
Exogenous expressions of these miRNAs in STHdh(Q111)/Hdh(Q111) cells rescued the abnormalities in cell cycle and apoptosis. |
| T9 |
1176-1271 |
DRI_Outcome |
denotes |
We also observed that inhibitors of cell cycle could decrease cell death in a cell model of HD. |
| T10 |
1272-1482 |
DRI_Approach |
denotes |
Based on these results obtained in cell and animal model of HD, we propose that inhibition of cell cycle either by miRNA expressions or by using inhibitors could be a potential approach for the treatment of HD. |
