The interplay between mitochondria and store‐operated Ca<sup>2+</sup> entry: Emerging insights into cardiac diseases

Nan, Jinliang; Li, Jiamin; Lin, Yanwen; Rahman, Muhammad Saif Ur; Li, Zhengzheng; Zhu, Lingjun

doi:10.1111/jcmm.16941

Cited by 22 publications

(12 citation statements)

References 193 publications

(295 reference statements)

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“…ATP-induced [Ca 2+ ] i signals were altered in HUVECs from the FGR-HDP group, including slower t p and lower sustained phase. The initial phase of the ATP-[Ca 2+ ] i signal is primarily mediated by P2Y2 receptors ( 20 ), whose activation generates inositol triphosphate (IP 3 ) and Ca 2+ release from Ca 2+ stores, whereas the sustained phase of the [Ca 2+ ] i signals is determined by SOCE ( 59 ). The present result suggest that the kinetics of the IP 3 -induced Ca 2+ release and SOCE-mediated Ca 2+ influx are diminished in FGR-HDP cells.…”

Section: Discussionmentioning

confidence: 99%

Ca²⁺ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder

Cortés,

Alonso,

Vinet

et al. 2024

Biomed Rep

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Fetal growth restriction associated with hypertensive disorders of pregnancy (FGR-HDP) is a prevalent pathology with a higher risk of perinatal morbimortality. In this condition, placental insufficiency and endothelial dysfunction serve key roles. The present prospective cohort study monitored 11 patients with an FGR-HDP and 15 with full-term normotensive pregnancies and studied post-natal intracellular calcium concentration ([Ca 2+ ] i ) signals in human umbilical vein endothelial cells (HUVECs). Small fetuses with placental insufficiency were identified using fetal biometry with Doppler velocimetry. Mean gestational age and birth weight were 31.8±4.1 weeks and 1,260±646 g for FGR-HDP and 39.2±0.8 weeks and 3,320±336 g for normal births, respectively. Abnormal umbilical artery Doppler waveforms were found in 64% of neonates with FGR-HDP. A significant percentage (86%) of FGR newborns were admitted to the neonatal intensive care unit at Gustavo Fricke hospital, Viña del Mar, Chile, with one case of death after birth. [Ca 2+ ] i signals were measured by microfluorimetry in Fluo-3-loaded HUVECs from primary cultures. Altered [Ca 2+ ] i signals were observed in HUVECs from FGR-HDP, where the sustained phase of ATP-induced [Ca 2+ ] i responses was significantly reduced compared with the normotensive group. Also, the [Ca 2+ ] i signals induced with 10 mM Ca 2+ after depletion of internal Ca 2+ stores were significantly higher. The present study provides a better comprehension of the role of altered cytosolic Ca 2+ dynamics in endothelial dysfunction and an in vitro model to assess novel therapeutic approaches for decreasing or preventing complications in FGR-HDP.

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Section: Discussionmentioning

confidence: 99%

Ca²⁺ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder

Cortés,

Alonso,

Vinet

et al. 2024

Biomed Rep

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“…Our pathway enrichment results also support this hypothesis. Both mitochondrial production of ROS and calcium are known to regulate the signaling between mitochondria and ER [ 56 , 57 ]. Although the exact mechanism is still unknown, we can hypothesize that disruptions in mitochondrial translation pathways play a crucial role in ROS production and calcium communication between ER and mitochondria.…”

Section: Discussionmentioning

confidence: 99%

A Genome-Wide Functional Screen Identifies Enhancer and Protective Genes for Amyloid Beta-Peptide Toxicity

Picón-Pagès

Bosch-Morató

Subirana

et al. 2023

IJMS

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Alzheimer’s disease (AD) is known to be caused by amyloid β-peptide (Aβ) misfolded into β-sheets, but this knowledge has not yet led to treatments to prevent AD. To identify novel molecular players in Aβ toxicity, we carried out a genome-wide screen in Saccharomyces cerevisiae, using a library of 5154 gene knock-out strains expressing Aβ1–42. We identified 81 mammalian orthologue genes that enhance Aβ1–42 toxicity, while 157 were protective. Next, we performed interactome and text-mining studies to increase the number of genes and to identify the main cellular functions affected by Aβ oligomers (oAβ). We found that the most affected cellular functions were calcium regulation, protein translation and mitochondrial activity. We focused on SURF4, a protein that regulates the store-operated calcium channel (SOCE). An in vitro analysis using human neuroblastoma cells showed that SURF4 silencing induced higher intracellular calcium levels, while its overexpression decreased calcium entry. Furthermore, SURF4 silencing produced a significant reduction in cell death when cells were challenged with oAβ1–42, whereas SURF4 overexpression induced Aβ1–42 cytotoxicity. In summary, we identified new enhancer and protective activities for Aβ toxicity and showed that SURF4 contributes to oAβ1–42 neurotoxicity by decreasing SOCE activity.

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“…Moreover, mitochondrial dysfunction can also be a cause of the elevated activity of the SOC channels. Mitochondrial calcium handling, mitochondrial motility, and ATP production play crucial roles in the formation of high Ca 2+ microdomains near SOC channels and consequently in calcium-dependent inactivation of ORAI channels [ 69 , 70 , 71 ]. Future studies should be focused on the coupling of aberrant calcium signaling and mitochondrial dysfunction in neurons, including possible compensatory mechanisms in various neuronal types which may result in selective neuronal vulnerability in different neurodegenerative pathologies.…”

Section: Discussionmentioning

confidence: 99%

An Efficient 2D Protocol for Differentiation of iPSCs into Mature Postmitotic Dopaminergic Neurons: Application for Modeling Parkinson’s Disease

Lebedeva

Шарова

Grekhnev

et al. 2023

IJMS

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About 15% of patients with parkinsonism have a hereditary form of Parkinson’s disease (PD). Studies on the early stages of PD pathogenesis are challenging due to the lack of relevant models. The most promising ones are models based on dopaminergic neurons (DAns) differentiated from induced pluripotent stem cells (iPSCs) of patients with hereditary forms of PD. This work describes a highly efficient 2D protocol for obtaining DAns from iPSCs. The protocol is rather simple, comparable in efficiency with previously published protocols, and does not require viral vectors. The resulting neurons have a similar transcriptome profile to previously published data for neurons, and have a high level of maturity marker expression. The proportion of sensitive (SOX6+) DAns in the population calculated from the level of gene expression is higher than resistant (CALB+) DAns. Electrophysiological studies of the DAns confirmed their voltage sensitivity and showed that a mutation in the PARK8 gene is associated with enhanced store-operated calcium entry. The study of high-purity DAns differentiated from the iPSCs of patients with hereditary PD using this differentiation protocol will allow for investigators to combine various research methods, from patch clamp to omics technologies, and maximize information about cell function in normal and pathological conditions.

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The interplay between mitochondria and store‐operated Ca²⁺ entry: Emerging insights into cardiac diseases

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 22 publications

References 193 publications

Ca²⁺ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder

Ca²⁺ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder

A Genome-Wide Functional Screen Identifies Enhancer and Protective Genes for Amyloid Beta-Peptide Toxicity

An Efficient 2D Protocol for Differentiation of iPSCs into Mature Postmitotic Dopaminergic Neurons: Application for Modeling Parkinson’s Disease

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The interplay between mitochondria and store‐operated Ca2+ entry: Emerging insights into cardiac diseases

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 22 publications

References 193 publications

Ca2+ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder

Ca2+ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder

A Genome-Wide Functional Screen Identifies Enhancer and Protective Genes for Amyloid Beta-Peptide Toxicity

An Efficient 2D Protocol for Differentiation of iPSCs into Mature Postmitotic Dopaminergic Neurons: Application for Modeling Parkinson’s Disease

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The interplay between mitochondria and store‐operated Ca²⁺ entry: Emerging insights into cardiac diseases

Ca²⁺ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder

Ca²⁺ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder