[1] PubMed ID: | 34775377 |
Disease Name: | Atherosclerosis |
Sample: | AS patients |
Dysfunction Pattern: | Regulation(MAPK/NF-κB pathway) |
Validated Method: | Western Blot//Transfection//Colony Formation Assay//Flow Cytometry//qRT-PCR//MTT//ELISA//IHC//EdU Staining |
Description: | Consequently, PVT1 was highly expressed in AS patients. Briefly, silencing PVT1 inhibited AS development by downregulating MAPK/NF-κB pathway. |
Causality: | Yes |
Causal Description: | Silencing PVT1 decreased levels of TG, TC, LDL, IL-6, IL-1β, TNF-α, MMP-2, MMP-9, CRP, TIMP-1, MAPK, and NF-κB, increased HDL, reduced atherosclerotic plaques and macrophage content in mice, inhibited viability, clones and EdU positive rates in HA-VSMCs, but promoted apoptosis and cell cycle arrest. Inhibition of MAPK/NF-κB pathway suppressed proliferation and promoted apoptosis of HA-VSMCs while PVT1 overexpression facilitated AS development. |
Clinical-realted Application: | |
[2] PubMed ID: | 35038974 |
Disease Name: | Atherosclerosis |
Sample: | AS patients and HUVECs |
Dysfunction Pattern: | Interaction(miR-30 c-5p) |
Validated Method: | RNA Pull-Down//Western Blot//Transfection//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//ELISA |
Description: | lncRNA PVT1 was overexpressed in the serum of AS patients and in ox-LDL-stimulated HUVECs relative to controls. Moreover, miR-30 c-5p was verified as a direct target of lncRNA PVT1. Furthermore, we observed that miR-30 c-5p expression was lower in AS patients than in controls. In addition, the influence of lncRNA PVT1 knockdown on ox-LDL-treated HUVECs was significantly reversed by downregulation of miR-30 c-5p. |
Causality: | Yes |
Causal Description: | Knockdown of lncRNA PVT1 facilitated proliferation, reduced apoptosis, and secretion of inflammatory factors in ox-LDL-treated HUVECs. |
Clinical-realted Application: | |
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