scholarly journals Mesenchymal stromal cells protect hepatocytes from lipotoxicity through alleviation of endoplasmic reticulum stress by restoring SERCA activity

2021 ◽  
Author(s):  
Linzhao Li ◽  
Xin Zeng ◽  
Zhenzhen Liu ◽  
Xuanming Chen ◽  
Lan Li ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells

scholarly journals Extracellular Vesicles Derived from Human Umbilical Cord Mesenchymal Stromal Cells Protect Cardiac Cells Against Hypoxia/Reoxygenation Injury by Inhibiting Endoplasmic Reticulum Stress via Activation of the PI3K/Akt Pathway

2020 ◽  
Vol 29 ◽  
pp. 096368972094567
Author(s):  
Changyi Zhang ◽  
Hongwu Wang ◽  
Godfrey C.F. Chan ◽  
Yu Zhou ◽  
Xiulan Lai ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Umbilical Cord ◽  
Extracellular Vesicles ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Cardiac Cells ◽  
Akt Pathway ◽  
Human Umbilical Cord ◽  
Hypoxia Reoxygenation

Endoplasmic reticulum (ER) stress is implicated in the pathogenesis of many diseases, including myocardial ischemia/reperfusion injury. We hypothesized that human umbilical cord mesenchymal stromal cells derived extracellular vesicles (HuMSC-EVs) could protect cardiac cells against hyperactive ER stress induced by hypoxia/reoxygenation (H/R) injury. The H/R model was generated using the H9c2 cultured cardiac cell line. HuMSC-EVs were extracted using a commercially available exosome isolation reagent. Levels of apoptosis-related signaling molecules and the degree of ER stress were assessed by western blot. The role of the PI3K/Akt pathway was investigated using signaling inhibitors. Lactate dehydrogenase leakage and 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) analysis were used for evaluating the therapeutic effects of HuMSC-EVs in vitro. The results showed that ER stress and the rate of apoptosis were increased in the context of H/R injury. Treatment with HuMSC-EVs inhibited ER stress and increased survival in H9c2 cells exposed to H/R. Mechanistically, the PI3K/Akt pathway was activated by treatment with HuMSC-EVs after H/R. Inhibition of the PI3K/Akt pathway by a specific inhibitor, LY294002, partially reduced the protective effect of HuMSC-EVs. Our findings suggest that HuMSC-EVs could alleviate ER stress–induced apoptosis during H/R via activation of the PI3K/Akt pathway.

Endoplasmic reticulum stress is involved in lipopolysaccharide‐induced inflammatory response and apoptosis in goat endometrial stromal cells

2019 ◽  
Vol 86 (7) ◽  
pp. 908-921 ◽  
Author(s):  
Amira Abdalla Abdelshafy Mohamed ◽  
Diqi Yang ◽  
Shouqin Liu ◽  
Pengfei Lin ◽  
Osama Abdalla Abdelshafy Mohamad ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Inflammatory Response ◽  
Endoplasmic Reticulum Stress ◽  
Stromal Cells ◽  
Endometrial Stromal Cells

scholarly journals Stromal cell-contact dependent PI3K and APRIL induced NF-κB signaling complement each other to prevent mitochondrial- and endoplasmic reticulum stress induced cell death of bone marrow plasma cells

2019 ◽  
Author(s):  
Rebecca Cornelis ◽  
Stefanie Hahne ◽  
Adriano Taddeo ◽  
Georg Petkau ◽  
Darya Malko ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Stromal Cells ◽  
Stromal Cell ◽  
Plasma Cells ◽  
Ex Vivo ◽  
Cell Contact ◽  
Pi3k Signaling ◽  
Bone Marrow Plasma

SummaryPersistence of long-lived, memory plasma cells in the bone marrow depends on survival factors available in the bone marrow, provided in niches organized by stromal cells. Here we describe that ex vivo we can prevent apoptosis of bone marrow plasma cells by supplying direct cell contact with stromal cells and the soluble cytokine APRIL. Integrin-mediated contact of bone marrow plasma cells with stromal cells activates the PI3K signaling pathway, leading to critical inactivation of FoxO1/3 and preventing the activation of mitochondrial stress-associated effector caspases 3 and 7. Likely, inhibition of PI3K signaling in vivo ablates bone marrow plasma cells. APRIL signaling, via the NF-κB pathway, blocks activation of the endoplasmic reticulum stress-associated initiator caspase 12. Thus, stromal cell-contact induced PI3K and APRIL-induced NF-κB signaling provide necessary and complementary signals to maintain bone marrow memory plasma cells.

Abstract #403: The Glutathione Mimic Ebselen Inhibits Oxidative Stress but not Endoplasmic Reticulum Stress in Endothelial Cells.

2015 ◽  
Vol 21 ◽  
pp. 85-86
Author(s):  
William Kurban ◽  
Salma Makhoul Ahwach ◽  
Melanie Thomas ◽  
Luisa Onsteed-Haas ◽  
Michael Haas
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress
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