hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In Vitro
Heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) is a protein involved in the regulation of RNA processing, cell metabolism, migration, proliferation, and apoptosis. However, the effect of hnRNPA2/B1 on injured endothelial cells (ECs) remains unclear. We investigated the effect of hnRNPA2/...
Saved in:
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2020-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2020/6458791 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832565980575825920 |
|---|---|
| author | Yi Chen Dan Tang Linjie Zhu Tianjie Yuan Yingfu Jiao Hexin Yan Weifeng Yu |
| author_facet | Yi Chen Dan Tang Linjie Zhu Tianjie Yuan Yingfu Jiao Hexin Yan Weifeng Yu |
| author_sort | Yi Chen |
| collection | DOAJ |
| description | Heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) is a protein involved in the regulation of RNA processing, cell metabolism, migration, proliferation, and apoptosis. However, the effect of hnRNPA2/B1 on injured endothelial cells (ECs) remains unclear. We investigated the effect of hnRNPA2/B1 on lipopolysaccharide- (LPS-) induced vascular endothelial injury in human umbilical vein endothelial cells (HUVECs) and the underlying mechanisms. LPS was used to induce EC injury, and the roles of hnRNPA2/B1 in EC barrier dysfunction and inflammatory responses were measured by testing endothelial permeability and the expression of inflammatory factors after the suppression and overexpression of hnRNPA2/B1. To explore the underlying mechanism by which hnRNPA2/B1 regulates endothelial injury, we studied the VE-cadherin/β-catenin pathway and NF-κB activation in HUVECs. The results showed that hnRNPA2/B1 was elevated in LPS-stimulated HUVECs. Moreover, knockdown of hnRNPA2/B1 aggravated endothelial injury by increasing EC permeability and promoting the secretion of the inflammatory cytokines TNF-α, IL-1β, and IL-6. Overexpression of hnRNPA2/B1 can reduce the permeability and inflammatory response of HUVEC stimulated by LPS in vitro, while increasing the expression of VE-Cadherin and β-catenin. Furthermore, the suppression of hnRNPA2/B1 increased the LPS-induced NF-κB activation and reduced the VE-cadherin/β-catenin pathway. Taken together, these results suggest that hnRNPA2/B1 can regulate LPS-induced EC damage through regulating the NF-κB and VE-cadherin/β-catenin pathways. |
| format | Article |
| id | doaj-art-2bff4b8fbde84bb6a5622f039fcf965d |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-2bff4b8fbde84bb6a5622f039fcf965d2025-02-03T01:05:23ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/64587916458791hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In VitroYi Chen0Dan Tang1Linjie Zhu2Tianjie Yuan3Yingfu Jiao4Hexin Yan5Weifeng Yu6Department of Anesthesiology and Critical Care Medicine, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai /200217, ChinaDepartment of Anesthesiology and Critical Care Medicine, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai /200217, ChinaDepartment of Anesthesiology and Critical Care Medicine, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai /200217, ChinaDepartment of Anesthesiology and Critical Care Medicine, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai /200217, ChinaDepartment of Anesthesiology and Critical Care Medicine, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai /200217, ChinaDepartment of Anesthesiology and Critical Care Medicine, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai /200217, ChinaDepartment of Anesthesiology and Critical Care Medicine, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai /200217, ChinaHeterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) is a protein involved in the regulation of RNA processing, cell metabolism, migration, proliferation, and apoptosis. However, the effect of hnRNPA2/B1 on injured endothelial cells (ECs) remains unclear. We investigated the effect of hnRNPA2/B1 on lipopolysaccharide- (LPS-) induced vascular endothelial injury in human umbilical vein endothelial cells (HUVECs) and the underlying mechanisms. LPS was used to induce EC injury, and the roles of hnRNPA2/B1 in EC barrier dysfunction and inflammatory responses were measured by testing endothelial permeability and the expression of inflammatory factors after the suppression and overexpression of hnRNPA2/B1. To explore the underlying mechanism by which hnRNPA2/B1 regulates endothelial injury, we studied the VE-cadherin/β-catenin pathway and NF-κB activation in HUVECs. The results showed that hnRNPA2/B1 was elevated in LPS-stimulated HUVECs. Moreover, knockdown of hnRNPA2/B1 aggravated endothelial injury by increasing EC permeability and promoting the secretion of the inflammatory cytokines TNF-α, IL-1β, and IL-6. Overexpression of hnRNPA2/B1 can reduce the permeability and inflammatory response of HUVEC stimulated by LPS in vitro, while increasing the expression of VE-Cadherin and β-catenin. Furthermore, the suppression of hnRNPA2/B1 increased the LPS-induced NF-κB activation and reduced the VE-cadherin/β-catenin pathway. Taken together, these results suggest that hnRNPA2/B1 can regulate LPS-induced EC damage through regulating the NF-κB and VE-cadherin/β-catenin pathways.http://dx.doi.org/10.1155/2020/6458791 |
| spellingShingle | Yi Chen Dan Tang Linjie Zhu Tianjie Yuan Yingfu Jiao Hexin Yan Weifeng Yu hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In Vitro Mediators of Inflammation |
| title | hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In Vitro |
| title_full | hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In Vitro |
| title_fullStr | hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In Vitro |
| title_full_unstemmed | hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In Vitro |
| title_short | hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In Vitro |
| title_sort | hnrnpa2 b1 ameliorates lps induced endothelial injury through nf κb pathway and ve cadherin β catenin signaling modulation in vitro |
| url | http://dx.doi.org/10.1155/2020/6458791 |
| work_keys_str_mv | AT yichen hnrnpa2b1ameliorateslpsinducedendothelialinjurythroughnfkbpathwayandvecadherinbcateninsignalingmodulationinvitro AT dantang hnrnpa2b1ameliorateslpsinducedendothelialinjurythroughnfkbpathwayandvecadherinbcateninsignalingmodulationinvitro AT linjiezhu hnrnpa2b1ameliorateslpsinducedendothelialinjurythroughnfkbpathwayandvecadherinbcateninsignalingmodulationinvitro AT tianjieyuan hnrnpa2b1ameliorateslpsinducedendothelialinjurythroughnfkbpathwayandvecadherinbcateninsignalingmodulationinvitro AT yingfujiao hnrnpa2b1ameliorateslpsinducedendothelialinjurythroughnfkbpathwayandvecadherinbcateninsignalingmodulationinvitro AT hexinyan hnrnpa2b1ameliorateslpsinducedendothelialinjurythroughnfkbpathwayandvecadherinbcateninsignalingmodulationinvitro AT weifengyu hnrnpa2b1ameliorateslpsinducedendothelialinjurythroughnfkbpathwayandvecadherinbcateninsignalingmodulationinvitro |