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CRAC (Calcium Release Activated Calcium) channel is one of the most important channels regulating calcium influx and has been involved in many autoimmune diseases. The contribution of CRAC channel in the pathogenesis of Type 1 Diabetes (T1D) has not been described much. Thus, we aimed to study the expression of CRAC channel and inflammatory cytokines like IL-1β (Interleukin -1β) and TNF-α (Tumor Necrosis Factor-α) in the spleen-derived cytotoxic T cells, Bone marrow monocytes (BMM) and macrophages differentiated from BMM in the alloxan induced T1D mice. BALB/c mice treated with alloxan and vehicle control for 12 and 24 h. Spleen derived T cells; Bone marrow derived monocytes were isolated from the control and diabetic BALB/c mice as well as macrophages differentiated from the control and diabetic BMM. We observed increased expression of CRAC channel components like STIM1 (Stromal Interaction Molecule), ORAI1 and ORAI2 and inflammatory cytokines like IL-1β and TNF-α in the spleen derived cytotoxic T cells and Macrophages differentiated from BMM as well as the downregulated expression of the same and CRAC channel in BMM of 12 and 24 h alloxan induced BALB/c mice. This study suggests that differential expression of CRAC channel correlated with the expression of inflammatory cytokines, thus CRAC channel might be responsible for the increased production of inflammatory cytokines in the alloxan induced T1D mice.
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http://dx.doi.org/10.1080/08923973.2020.1716788 | DOI Listing |
Biomed Pharmacother
September 2025
Department and Graduate Institute of Pharmacology, College of Pharmacy, National Defense Medical University, Taipei, Taiwan; Department of Pharmacy Practice, Tri-Service General Hospital, National Defense Medical University, Taipei, Taiwan; School of Pharmacy, College of Pharmacy, National Defense M
Parkinson's disease (PD) is characterized by chronic neuroinflammation and progressive dopaminergic neurodegeneration, driven primarily by the activation of microglia and associated apoptotic pathways. The intermediate-conductance calcium-activated potassium channel KCNN4 has recently emerged as a potential therapeutic target, yet its role in chronic neurodegenerative conditions remains underexplored. In this study, we investigated whether pharmacological inhibition of KCNN4 using TRAM-34 can modulate both inflammatory and apoptotic responses in an LPS-induced mouse model of PD.
View Article and Find Full Text PDFBiomolecules
August 2025
School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds LS29JT, UK.
Cardiovascular and metabolic disorders significantly reduce healthspan and lifespan, with oxidative stress being a major contributing factor. Oxidative stress, marked by elevated reactive oxygen species (ROS), disrupts cellular and systemic functions. One proposed mechanism involves TRPM2 (Transient Receptor Potential Melastatin2)-dependent Ca dysregulation.
View Article and Find Full Text PDFPLoS One
August 2025
Department of Neurology, The PLA Rocket Force Characteristic Medical Center, Beijing, China.
Objective: To investigate the functional and molecular mechanisms by which Piezo1regulates HT-22 hippocampal neuronal autophagy, and to explore whether Piezo1 regulates hippocampal neuronal autophagy via the Ca2+/Calpain, CaMKKβ, or Calcineurin pathways.
Methods: The impacts of Piezo1 inhibition, activation and gene knockdown on the autophagy of HT22 neurons was investigated by Western blotting, PCR and immunofluorescence. The changes of intracellular calcium (Ca2+) concentration were also observed.
J Immunol
August 2025
Department of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Chimeric antigen receptor (CAR) T-cell therapy has proven to be a promising treatment for multiple types of cancer. Yet, the mechanisms regulating CAR T-cell function as well as the side effects remain an area of active research. The formation of the immunological synapse is essential for the activation of signaling pathways including the Ca2+-dependent one.
View Article and Find Full Text PDFJ Ginseng Res
September 2025
Department of Physiology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand.
Background: Ginsenoside Re (Re) has been shown to activate small-conductance calcium-activated potassium (SK) current in human coronary artery endothelial cells (HCAECs). We aimed to investigate whether Re increased SK current via glucocorticoid receptor (GR), its non-genomic pathway phosphoinositide 3-kinase-protein kinase B (PI3K-Akt/PKB), and endothelial nitric oxide synthase (eNOS), and whether SK mediated Re-induced increase in nitric oxide (NO), prostacyclin (PGI), epoxyeicosatrienoic acid (EET), and/or hydrogen peroxide (HO).
Methods: Whole-cell patch clamp technique was employed to study Re-activated HCAEC currents, using specific inhibitors of the proposed mediating pathway.