ArticleMolecular and cellular biochemistry2022
Endoplasmic reticulum stress induces mitochondrial dysfunction but not mitochondrial unfolded protein response in SH-SY5Y cells.
Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- ER stress inhibitor 4PBA attenuates hindlimb unloading-induced cardiac mitochondrial and metabolic dysfunction.Pflugers Archiv : European journal of physiology · 2025Article
- 3,3'-Diindolylmethane inhibits the proliferation of esophageal squamous cell carcinoma cells via downregulation of STIM1.Oncology letters · 2024Article
- Acute endoplasmic reticulum stress-induced mitochondria respiratory chain damage: The role of activated calpains.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Pathological implications of cellular stress in cardiovascular diseases.The international journal of biochemistry & cell biology · 2023Review
- Metal-Binding Proteins Cross-Linking with Endoplasmic Reticulum Stress in Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In the present study we have shown that treatment of SH-SY5Y cells with either thapsigargin or tunicamycin is associated with a significant decrease in ROUTINE and ATP-coupled mitochondrial respiration as well as a decrease in spare and maximal respiratory capacity. We have also shown that treating cells with either thapsigargin or tunicamycin is associated with significant changes in mitochondrial membrane potential (ΔΨm) generation, which is mainly associated with the reversal of the succinyl-CoA ligase reaction and a decreased activity of complex II. Despite the induction of endoplasmic reticulum (ER) specific unfolded protein response (UPR), as documented by increased expression of HRD1, ER stress did not induce mitochondrial UPR since the expression of both mitochondrial protease LONP1 and mitochondrial chaperone HSP60 was not significantly altered. Inhibition of IRE1α ribonuclease with STF-083010 did not protect the SH-SY5Y cells from ER stress-induced mitochondrial dysfunction. STF-083010 itself had significant impact on both mitochondrial respiration and generation of ΔΨm, which has mainly been associated with the uncoupling of respiratory chain from ATP synthesis.
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Registered trials
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