Our previous work has shown that interleukin-6 (IL-6) implements its neuroprotective effect by inhibiting the intracellular Ca(2+) overload in neurons. Here, we examined whether regulation of L-type calcium channels (LCCs) activities is involved in the neuroprotective action of IL-6. In cultured cerebellar granule neurons (CGNs), patch-clamp recording showed that the whole-cell Ca(2+) current and LCC current were significantly reduced by IL-6 pretreatment (120 ng/ml, for 24 h). Calcium imaging data indicated that IL-6 significantly suppressed high K(+)-induced intracellular Ca(2+) overload and LCC Ca(2+) influx. Moreover, expression of the LCC subunit, Ca(v)1.2, was remarkably downregulated by IL-6 in cultured CGNs. These findings suggest that IL-6 exerts a neurotrophic effect by preventing Ca(2+) overload, at least partly through inhibition of LCC activity in cultured CGNs.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717850 | PMC |
| http://dx.doi.org/10.1007/s12576-012-0215-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Background: Alzheimer's disease (AD) is a complex neurodegenerative disorder marked by progressive memory loss and cognitive decline. The precise molecular mechanisms underlying AD pathogenesis remain uncertain, underscoring the need for further investigation to identify novel therapeutic targets. We recently demonstrated that mitochondrial calcium (Ca) overload significantly contributes to the development of AD, capable of independently driving AD-like pathology.
View Article and Find Full Text PDFMicrotubule acetylation and PERK activation facilitate eribulin-induced mitochondrial calcium accumulation and cell death.
Cell Mol Life Sci
December 2024
Department of Life Science, Chung-Ang University, Seoul, 06974, Republic of Korea.
Over the past few decades, microtubules have been targeted by various anticancer drugs, including paclitaxel and eribulin. Despite their promising effects, the development of drug resistance remains a challenge. We aimed to define a novel cell death mechanism that targets microtubules using eribulin and to assess its potential in overcoming eribulin resistance.
View Article and Find Full Text PDFCardiomyocyte-specific Piezo1 deficiency mitigates ischemia-reperfusion injury by preserving mitochondrial homeostasis.
Redox Biol
December 2024
Innovation Research Center, Shandong University of Traditional Chinese Medicine, Jinan, 250307, China; Lingnan Medical Research Center, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, 510260, China; School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, LS2 9JT, UK. Electronic address:
Ca overload and mitochondrial dysfunction play crucial roles in myocardial ischemia-reperfusion (I/R) injury. Piezo1, a mechanosensitive cation channel, is essential for intracellular Ca homeostasis. The objective of this research was to explore the effects of Piezo1 on mitochondrial function during myocardial I/R injury.
View Article and Find Full Text PDFEffect of 2-Aminoethoxydiphenyl Borate on the State of Skeletal Muscles in Dystrophin-Deficient Mice.
Front Biosci (Landmark Ed)
December 2024
Department of Biochemistry, Cell Biology and Microbiology, Mari State University, 424001 Yoshkar-Ola, Russia.
Objective: Ca overload of muscle fibers is one of the factors that secondarily aggravate the development of Duchenne muscular dystrophy (DMD). The purpose of this study is to evaluate the effects of the Ca channel modulator 2-aminoethoxydiphenyl borate (APB) on skeletal muscle pathology in dystrophin-deficient mice.
Methods: Mice were randomly divided into six groups: wild type (WT), WT+3 mg/kg APB, WT+10 mg/kg APB, , +3 mg/kg APB, +10 mg/kg APB.
Simultaneous Imaging of pH and Peroxynitrite in the Endoplasmic Reticulum and Mitochondria: Revealing Organelle Interactions in Alzheimer's Disease Pathogenesis.
Anal Chem
December 2024
Key Laboratory of Photochemical Conversion and Optoelectronic Materials, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing 100190, China.
pH and peroxynitrite (ONOO) are two critical biomarkers to unveil the corresponding status of endoplasmic reticulum (ER) stress and mitochondrial dysfunction, which are closely related to Alzheimer's disease (AD). Simultaneously monitoring pH and ONOO fluctuations in the ER and mitochondria during AD progression is pivotal for clarifying the interplay between the disorders of the two organelles and revealing AD pathogenesis. Herein, we designed and synthesized a dual-channel fluorescent probe (DCFP) to visualize pH and ONOO in the ER and mitochondria.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!