ArticleMolecular biology of the cell2013
JNK1/2 regulates ER-mitochondrial Ca2+ cross-talk during IL-1β-mediated cell death in RINm5F and human primary β-cells.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Review
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- Organelle-specific crosstalk between calcium and redox signaling in pancreatic β-cells in physiology and type 2 diabetes.Frontiers in network physiology · 2026Review
- UCP2 inhibition eliminates pancreatic β cell autoinflammation in T2DM with islet-mitochondrial sequential targeting nanomedicines.Nature communications · 2025Article
- Integrative Metabolome and Proteome Analysis of Cerebrospinal Fluid in Parkinson's Disease.International journal of molecular sciences · 2024Review
- Melatonin enhanced the cardioprotective effects of HTK solution on Langendorff-perfused mouse hearts subjected to ischemia/reperfusion.Iranian journal of basic medical sciences · 2024Article
- Control of human pancreatic beta cell kinome by glucagon-like peptide-1 receptor biased agonism.Diabetes, obesity & metabolism · 2023Article
- Systemic inflammation after stroke: implications for post-stroke comorbidities.EMBO molecular medicine · 2022Review
- GRP75 mediates endoplasmic reticulum-mitochondria coupling during palmitate-induced pancreatic β-cell apoptosis.The Journal of biological chemistry · 2021Article
- Mechanism of Endoplasmic Reticulum Stress in Cerebral Ischemia.Frontiers in cellular neuroscience · 2021Review
- Impact of Conventional and Atypical MAPKs on the Development of Metabolic Diseases.Biomolecules · 2020Review
- A Putative Prohibitin-Calcium Nexus inJournal of diabetes research · 2020Review
- EGCG Upregulates UCPDrug design, development and therapy · 2020Article
- Pterostilbene Attenuates Early Brain Injury Following Subarachnoid Hemorrhage via Inhibition of the NLRP3 Inflammasome and Nox2-Related Oxidative Stress.Molecular neurobiology · 2017Article
- Cadmium-induced apoptosis of Siberian tiger fibroblasts via disrupted intracellular homeostasis.Biological research · 2016Article
- Decoding the oxidative stress hypothesis in diabetic embryopathy through proapoptotic kinase signaling.American journal of obstetrics and gynecology · 2015Review
- Inhibition of transient receptor potential melastatin 7 (TRPM7) channel induces RA FLSs apoptosis through endoplasmic reticulum (ER) stress.Clinical rheumatology · 2014Article
- Mitochondrial metabolism directs stemness and differentiation in P19 embryonal carcinoma stem cells.Cell death and differentiation · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated interleukin-1β (IL-1β) induces apoptosis in pancreatic β-cells through endoplasmic reticulum (ER) stress induction and subsequent c-jun-N-terminal kinase 1/2 (JNK1/2) activation. In earlier work we showed that JNK1/2 activation is initiated before ER stress and apoptotic induction in response to IL-1β. However, the detailed regulatory mechanisms are not completely understood. Because the ER is the organelle responsible for Ca(2+) handling and storage, here we examine the effects of IL-1β on cellular Ca(2+) movement and mitochondrial dysfunction and evaluate the role of JNK1/2. Our results show that in RINm5F cells and human primary β-cells, IL-1β alters mitochondrial membrane potential, mitochondrial permeability transition pore opening, ATP content, and reactive oxygen species production and these alterations are preceded by ER Ca(2+) release via IP3R channels and mitochondrial Ca(2+) uptake. All these events are prevented by JNK1/2 small interfering RNA (siRNA), indicating the mediating role of JNK1/2 in IL-1β-induced cellular alteration. This is accompanied by IL-1β-induced apoptosis, which is prevented by JNK1/2 siRNA and the IP3R inhibitor xestospongin C. This suggests a regulatory role of JNK1/2 in modulating the ER-mitochondrial-Ca(2+) axis by IL-1β in apoptotic cell death.
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