scholarly journals Differential Levels of Endoplasmic Reticulum Stress in Peripheral Blood Mononuclear Cells from Patients with Sudden Sensorineural Hearing Loss

2020 ◽  
Vol 26 ◽  
Author(s):  
Zhibiao Liu ◽  
Bing Fei ◽  
Xiaoping Du ◽  
Yanhong Dai ◽  
Wandong She
Keyword(s):  
Endoplasmic Reticulum ◽  
Hearing Loss ◽  
Endoplasmic Reticulum Stress ◽  
Sensorineural Hearing Loss ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Sudden Sensorineural Hearing Loss ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Does Metformin Modulate Endoplasmic Reticulum Stress and Autophagy in Type 2 Diabetic Peripheral Blood Mononuclear Cells?

2018 ◽  
Vol 28 (17) ◽  
pp. 1562-1569 ◽  
Author(s):  
Noelia Diaz-Morales ◽  
Francesca Iannantuoni ◽  
Irene Escribano-Lopez ◽  
Celia Bañuls ◽  
Susana Rovira-Llopis ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Type 2 Diabetic

scholarly journals Postprandial inflammation is not associated with endoplasmic reticulum stress in peripheral blood mononuclear cells from healthy lean men

2014 ◽  
Vol 112 (4) ◽  
pp. 573-582 ◽  
Author(s):  
Jana Kračmerová ◽  
Eva Czudková ◽  
Michal Koc ◽  
Lucia Mališová ◽  
Michaela Šiklová ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Inflammatory Cytokines ◽  
Peripheral Blood Mononuclear Cells ◽  
Mononuclear Cells ◽  
Cell Populations ◽  
Peripheral Blood Mononuclear ◽  
Expression Levels ◽  
Blood Mononuclear Cells

The consumption of lipids and simple sugars induces an inflammatory response whose exact molecular trigger remains elusive. The aims of the present study were to investigate (1) whether inflammation induced by a single high-energy, high-fat meal (HFM) is associated with endoplasmic reticulum stress (ERS) in peripheral blood mononuclear cells (PBMC) and (2) whether these inflammatory and ERS responses could be prevented by the chemical chaperone ursodeoxycholic acid (UDCA). A total of ten healthy lean men were recruited to a randomised, blind, cross-over trial. Subjects were given two doses of placebo (lactose) or UDCA before the consumption of a HFM (6151 kJ; 47·4 % lipids). Blood was collected at baseline and 4 h after the HFM challenge. Cell populations and their activation were analysed using flow cytometry, and plasma levels of inflammatory cytokines were assessed by ELISA and Luminex technology. Gene expression levels of inflammatory and ERS markers were analysed in CD14+ and CD14− PBMC using quantitative RT-PCR. The HFM induced an increase in the mRNA expression levels of pro-inflammatory cytokines (IL-1β, 2·1-fold; IL-8, 2·4-fold; TNF-α, 1·4-fold; monocyte chemoattractant protein 1, 2·1-fold) and a decrease in the expression levels of miR181 (0·8-fold) in CD14+ monocytes. The HFM challenge did not up-regulate the expression of ERS markers (XBP1, HSPA5, EDEM1, DNAJC3 and ATF4) in either CD14+ or CD14− cell populations, except for ATF3 (2·3-fold). The administration of UDCA before the consumption of the HFM did not alter the HFM-induced change in the expression levels of ERS or inflammatory markers. In conclusion, HFM-induced inflammation detectable on the level of gene expression in PBMC was not associated with the concomitant increase in the expression levels of ERS markers and could not be prevented by UDCA.

Sign in / Sign up

Export Citation Format

Share Document