scholarly journals Endoplasmic reticulum refilling and mitochondrial calcium extrusion promoted in neurons by NCX1 and NCX3 in ischemic preconditioning are determinant for neuroprotection

2014 ◽  
Vol 21 (7) ◽  
pp. 1142-1149 ◽  
Author(s):  
M J Sisalli ◽  
A Secondo ◽  
A Esposito ◽  
V Valsecchi ◽  
C Savoia ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Ischemic Preconditioning ◽  
Mitochondrial Calcium ◽  
Calcium Extrusion

Endoplasmic Reticulum & Mitochondrial Calcium homeostasis: The Interplay with Viruses

Mitochondrion ◽  
2021 ◽  
Author(s):  
SwagatikaPanda ◽  
Suchismita Behera ◽  
Mohd. Faraz Alam ◽  
Gulam Hussain Syed
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Homeostasis ◽  
Mitochondrial Calcium

scholarly journals Overexpression of SERCA2a Alleviates Cardiac Microvascular Ischemic Injury by Suppressing Mfn2-Mediated ER/Mitochondrial Calcium Tethering

2021 ◽  
Vol 9 ◽  
Author(s):  
Feng Tian ◽  
Ying Zhang
Keyword(s):  
Endoplasmic Reticulum ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Ischemic Injury ◽  
Calcium Overload ◽  
Mitochondrial Calcium ◽  
Myocardial Infarct Size ◽  
Hypoxic Injury

Our previous research has shown that type-2a Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a) undergoes posttranscriptional oxidative modifications in cardiac microvascular endothelial cells (CMECs) in the context of excessive cardiac oxidative injury. However, whether SERCA2a inactivity induces cytosolic Ca2+ imbalance in mitochondrial homeostasis is far from clear. Mitofusin2 (Mfn2) is well known as an important protein involved in endoplasmic reticulum (ER)/mitochondrial Ca2+ tethering and the regulation of mitochondrial quality. Therefore, the aim of our study was to elucidate the specific mechanism of SERCA2a-mediated Ca2+ overload in the mitochondria via Mfn2 tethering and the survival rate of the heart under conditions of cardiac microvascular ischemic injury. In vitro, CMECs extracted from mice were subjected to 6 h of hypoxic injury to mimic ischemic heart injury. C57-WT and Mfn2KO mice were subjected to a 1 h ischemia procedure via ligation of the left anterior descending branch to establish an in vivo cardiac ischemic injury model. TTC staining, immunohistochemistry and echocardiography were used to assess the myocardial infarct size, microvascular damage, and heart function. In vitro, ischemic injury induced irreversible oxidative modification of SERCA2a, including sulfonylation at cysteine 674 and nitration at tyrosine 294/295, and inactivation of SERCA2a, which initiated calcium overload. In addition, ischemic injury-triggered [Ca2+]c overload and subsequent [Ca2+]m overload led to mPTP opening and ΔΨm dissipation compared with the control. Furthermore, ablation of Mfn2 alleviated SERCA2a-induced mitochondrial calcium overload and subsequent mito-apoptosis in the context of CMEC hypoxic injury. In vivo, compared with that in wild-type mice, the myocardial infarct size in Mfn2KO mice was significantly decreased. In addition, the findings revealed that Mfn2KO mice had better heart contractile function, decreased myocardial infarction indicators, and improved mitochondrial morphology. Taken together, the results of our study suggested that SERCA2a-dependent [Ca2+]c overload led to mitochondrial dysfunction and activation of Mfn2-mediated [Ca2+]m overload. Overexpression of SERCA2a or ablation of Mfn2 expression mitigated mitochondrial morphological and functional damage by modifying the SERCA2a/Ca2+-Mfn2 pathway. Overall, these pathways are promising therapeutic targets for acute cardiac microvascular ischemic injury.

scholarly journals Astroglial calcium transfer from endoplasmic reticulum to mitochondria determines synaptic integration

2020 ◽  
Author(s):  
Roman Serrat ◽  
Ana Covelo ◽  
Vladimir Kouskoff ◽  
Sebastien Delcasso ◽  
Andrea Ruiz ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Signaling ◽  
Intracellular Calcium ◽  
Hippocampal Slices ◽  
Cytosolic Calcium ◽  
Brain Network ◽  
Synaptic Integration ◽  
Mitochondrial Calcium ◽  
Intracellular Calcium Signaling ◽  
Electrophysiological Recordings

SummaryIntracellular calcium signaling underlies the astroglial control of synaptic transmission and plasticity. Mitochondria-endoplasmic reticulum contacts (MERCs) are key determinants of calcium dynamics, but their functional impact on astroglial regulation of brain information processing is currently unexplored. We found that the activation of astrocyte mitochondrial-associated CB1 receptors (mtCB1) determines MERCs-dependent intracellular calcium signaling and synaptic integration. The stimulation of mtCB1 receptors promotes calcium transfer from the endoplasmic reticulum to mitochondria through specific mechanisms regulating the activity of the mitochondrial calcium uniporter (MCU) channel. Physiologically, mtCB1-dependent mitochondrial calcium uptake determines the precise dynamics of cytosolic calcium events in astrocytes upon endocannabinoid mobilization. Accordingly, electrophysiological recordings in hippocampal slices showed that genetic exclusion of mtCB1 receptors or specific astroglial MCU inhibition blocks lateral synaptic potentiation, a key example of astrocyte-dependent integration of distant synapses activity. Altogether, these data reveal an unforeseen link between astroglial MERCs and the regulation of brain network functions.

Bcl-2 Modulates Endoplasmic Reticulum and Mitochondrial Calcium Stores in PC12 Cells

2011 ◽  
Vol 37 (2) ◽  
pp. 238-243 ◽  
Author(s):  
Hanako Hirata ◽  
Guiomar S. Lopes ◽  
Aron Jurkiewicz ◽  
Lucia Garcez-do-Carmo ◽  
Soraya S. Smaili
Keyword(s):  
Endoplasmic Reticulum ◽  
Pc12 Cells ◽  
Mitochondrial Calcium ◽  
Calcium Stores

Involvement of the mitochondrial calcium uniporter in cardioprotection by ischemic preconditioning

Life Sciences ◽  
2006 ◽  
Vol 78 (7) ◽  
pp. 738-745 ◽  
Author(s):  
Shi-zhong Zhang ◽  
Qin Gao ◽  
Chun-mei Cao ◽  
Iain C. Bruce ◽  
Qiang Xia
Keyword(s):  
Ischemic Preconditioning ◽  
Mitochondrial Calcium ◽  
Mitochondrial Calcium Uniporter ◽  
Calcium Uniporter
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