| Expression pattern: |
UP |
| Associated gene: |
NF-jB, JNK/p38 |
| Associated microRNA: |
miR-9 |
| Biological function: |
Silencing cANRIL protects LPS-treated HK-2 cells from inflammatory injury by promoting cell viability and suppressing apoptosis, inflammatory cytokines and ROS generation. |
| Molecular mechanism: |
Silencing cANRIL up-regulates miR-9 and blocks NF-jB and JNK/p38 pathways in LPS-treated HK-2 cells. |
| Biological pathway or process: |
NF-kappaB (promotes); MAPK (promotes); apoptosis (promotes); inflammation (promotes); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Transfection; CCK8; Annexin V/PI Flow Cytometry; Flow Cytometry（Non-apoptosis/cycle）; ELISA; Western Blot |
| Clinical significance: |
These findings might provide a potential molecular therapeutic target for CKD. |
| Description: |
cANRIL is up-regulated in LPS-treated HK-2 cells, an in vitro inflammatory injury model relevant to CKD. Silencing cANRIL alleviates LPS-induced injury by increasing cell viability and reducing apoptosis, IL-1b/IL-6 inflammatory cytokines, and ROS generation. Mechanistically, cANRIL knockdown up-regulates miR-9 and suppresses NF-jB and JNK/p38 pathway activation. |
| Confidence score: |
0.4236 |