Add like
Add dislike
Add to saved papers

Long non-coding RNA PVT1 promote LPS-induced septic acute kidney injury by regulating TNFα and JNK/NF-κB pathways in HK-2 cells.

This study aimed to investigate the effect and underlying mechanism of long non-coding RNA plasmacytoma variant translocation 1 (PVT1) in lipopolysaccharide (LPS)-induced inflammation injury in HK-2 cells. We established LPS-induced septic acute kidney injury (AKI) model in HK-2 cells. LPS-induced HK-2 cells were transfected with pc-PVT1, pc-NC, si-PVT1 or si-NC. Cell viability and apoptosis rate were detected by MTT assay and Annexin V-FITC/PI Apoptosis Detection kit, respectively. The relationships of PVT1 and inflammatory factors were evaluated by RNA Immunoprecipitation (RIP) assay. The levels of inflammatory factors, apoptosis-related proteins and the expressions of proteins related to c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB) signaling pathway were detected by ELISA or Western blotting. Compared with cells with pc-NC, cell viability was remarkably decreased and cell apoptosis rate was increased in LPS-induced cells with pc-PVT1 (p<0.05). The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β were significantly increased in LPS-induced cells with pc-PVT1 compared with cells with pc-NC (p<0.05). All these changes were reversed in LPS-induced cells with si-PVT1 and si-NC (p<0.05). RTP assay revealed that PVT1 could bind to TNF-α. Furthermore, down-regulated PVT1 remarkably reduced the expressions of p-JNK and p-c-Jun, p-IκBα and p-p65 (p<0.05); while increased expressions of these proteins and inflammatory factors induced by up-regulated PVT1 were reversed by JNK or NF-κB inhibitors. PVT1 may promote inflammatory response by binding to TNF-α and inhibiting JNK/NF-κB signaling pathway in LPS-induced septic AKI cells.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app