scholarly journals HIPK2 sustains inflammatory cytokine production by promoting endoplasmic reticulum stress in macrophages

2020 ◽  
Vol 20 (6) ◽  
pp. 1-1
Author(s):  
Long Xu ◽  
He Fang ◽  
Dayuan Xu ◽  
Guangyi Wang
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production

Dendritic cells sub-sets are associated with inflammatory cytokine production in progressive vitiligo disease

2021 ◽  
Author(s):  
Niharika Srivastava ◽  
Anuradha Bishnoi ◽  
Davinder Parsad ◽  
Muthu Sendhil Kumaran ◽  
Keshavamurthy Vinay ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production

Long non-coding RNA SNHG14 aggravates LPS-induced acute kidney injury through regulating miR-495-3p/HIPK1

2021 ◽  
Author(s):  
Ni Yang ◽  
Hai Wang ◽  
Li Zhang ◽  
Junhua Lv ◽  
Zequn Niu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Acute Kidney Injury ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Kidney Injury ◽  
Interaction Network ◽  
High Morbidity ◽  
Abrupt Decrease ◽  
Inflammatory Cytokine Production ◽  
Non Coding Rna

Abstract Acute kidney injury (AKI) is a complex syndrome with an abrupt decrease of kidney function, which is associated with high morbidity and mortality. Sepsis is the common cause of AKI. Mounting evidence has demonstrated that long non-coding RNAs (lncRNAs) play critical roles in the development and progression of sepsis-induced AKI. In this study, we aimed to illustrate the function and mechanism of lncRNA SNHG14 in lipopolysaccharide (LPS)-induced AKI. We found that SNHG14 was highly expressed in the plasma of sepsis patients with AKI. SNHG14 inhibited cell proliferation and autophagy and promoted cell apoptosis and inflammatory cytokine production in LPS-stimulated HK-2 cells. Functionally, SNHG14 acted as a competing endogenous RNA (ceRNA) to negatively regulate miR-495-3p expression in HK-2 cells. Furthermore, we identified that HIPK1 is a direct target of miR-495-3p in HK-2 cells. We also revealed that the SNHG14/miR-495-3p/HIPK1 interaction network regulated HK-2 cell proliferation, apoptosis, autophagy, and inflammatory cytokine production upon LPS stimulation. In addition, we demonstrated that the SNHG14/miR-495-3p/HIPK1 interaction network regulated the production of inflammatory cytokines (TNF-α, IL-6, and IL-1β) via modulating NF-κB/p65 signaling in LPS-challenged HK-2 cells. In conclusion, our findings suggested a novel therapeutic axis of SNHG14/miR-495-3p/HIPK1 to treat sepsis-induced AKI.

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