An in‐vitro mechanical strain three‐dimensional culture model: periodontal ligament cell viability, apoptosis, and endoplasmic reticulum stress response

2020 ◽  
Vol 128 (2) ◽  
pp. 120-127
Author(s):  
Fiona A. Firth ◽  
Trudy J. Milne ◽  
Benedict Seo ◽  
Mauro Farella
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Endoplasmic Reticulum Stress ◽  
Periodontal Ligament ◽  
Mechanical Strain ◽  
Three Dimensional ◽  
Endoplasmic Reticulum Stress Response ◽  
Periodontal Ligament Cell ◽  
Culture Model

scholarly journals Effect of pioglitazone treatment on endoplasmic reticulum stress response in human adipose and in palmitate-induced stress in human liver and adipose cell lines

2008 ◽  
Vol 295 (2) ◽  
pp. E393-E400 ◽  
Author(s):  
Swapan K. Das ◽  
Winston S. Chu ◽  
Ashis K. Mondal ◽  
Neeraj K. Sharma ◽  
Philip A. Kern ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Insulin Sensitivity ◽  
Endoplasmic Reticulum Stress ◽  
Initiation Factor ◽  
Endoplasmic Reticulum Stress Response ◽  
Human Volunteers ◽  
Inflammatory State ◽  
Subcutaneous Adipose

Obesity and elevated cytokine secretion result in a chronic inflammatory state and may cause the insulin resistance observed in type 2 diabetes. Recent studies suggest a key role for endoplasmic reticulum stress in hepatocytes and adipocytes from obese mice, resulting in reduced insulin sensitivity. To address the hypothesis that thiazolidinediones, which improve peripheral insulin sensitivity, act in part by reducing the endoplasmic reticulum stress response, we tested subcutaneous adipose tissue from 20 obese volunteers treated with pioglitazone for 10 wk. We also experimentally induced endoplasmic reticulum stress using palmitate, tunicamycin, and thapsigargin in the human HepG2 liver cell line with or without pioglitazone pretreatment. We quantified endoplasmic reticulum stress response by measuring both gene expression and phosphorylation. Pioglitazone significantly improved insulin sensitivity in human volunteers ( P = 0.002) but did not alter markers of endoplasmic reticulum stress. Differences in pre- and posttreatment endoplasmic reticulum stress levels were not correlated with changes in insulin sensitivity or body mass index. In vitro, palmitate, thapsigargin, and tunicamycin but not oleate induced endoplasmic reticulum stress in HepG2 cells, including increased transcripts CHOP, ERN1, GADD34, and PERK, and increased XBP1 splicing along with phosphorylation of eukaryotic initiation factor eIF2α, JNK1, and c- jun. Although patterns of endoplasmic reticulum stress response differed among palmitate, tunicamycin, and thapsigargin, pioglitazone pretreatment had no significant effect on any measure of endoplasmic reticulum stress, regardless of the inducer. Together, our data suggest that improved insulin sensitivity with pioglitazone is not mediated by a reduction in endoplasmic reticulum stress.

scholarly journals Activation of ATF6 and an ATF6 DNA Binding Site by the Endoplasmic Reticulum Stress Response

2000 ◽  
Vol 275 (35) ◽  
pp. 27013-27020
Author(s):  
Yan Wang ◽  
Jingshi Shen ◽  
Natalia Arenzana ◽  
Witoon Tirasophon ◽  
Randal J. Kaufman ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Dna Binding ◽  
Endoplasmic Reticulum Stress ◽  
Binding Site ◽  
Endoplasmic Reticulum Stress Response ◽  
Dna Binding Site

scholarly journals Involvement of Endoplasmic Reticulum Stress Response in Orofacial Inflammatory Pain

2014 ◽  
Vol 23 (4) ◽  
pp. 372-380 ◽  
Author(s):  
Eun Sun Yang ◽  
Jin Young Bae ◽  
Tae Heon Kim ◽  
Yun Sook Kim ◽  
Kyoungho Suk ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Endoplasmic Reticulum Stress ◽  
Inflammatory Pain ◽  
Endoplasmic Reticulum Stress Response
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