scholarly journals Mitochondrial calcium signalling and cell death: Approaches for assessing the role of mitochondrial Ca2+ uptake in apoptosis

Cell Calcium ◽  
2006 ◽  
Vol 40 (5-6) ◽  
pp. 553-560 ◽  
Author(s):  
György Hajnóczky ◽  
György Csordás ◽  
Sudipto Das ◽  
Cecilia Garcia-Perez ◽  
Masao Saotome ◽  
...  
Keyword(s):  
Cell Death ◽  
Calcium Signalling ◽  
Mitochondrial Calcium

scholarly journals Controlling metabolism and cell death: At the heart of mitochondrial calcium signalling

2009 ◽  
Vol 46 (6) ◽  
pp. 781-788 ◽  
Author(s):  
Marta Murgia ◽  
Carlotta Giorgi ◽  
Paolo Pinton ◽  
Rosario Rizzuto
Keyword(s):  
Cell Death ◽  
Calcium Signalling ◽  
Mitochondrial Calcium

Intricate role of mitochondrial calcium signalling in mitochondrial quality control for regulation of cancer cell fate

Mitochondrion ◽  
2021 ◽  
Vol 57 ◽  
pp. 230-240
Author(s):  
Srimanta Patra ◽  
Kewal Kumar Mahapatra ◽  
Prakash Priyadarshi Praharaj ◽  
Debasna Pritimanjari Panigrahi ◽  
Chandra Sekhar Bhol ◽  
...  
Keyword(s):  
Quality Control ◽  
Cell Fate ◽  
Cancer Cell ◽  
Calcium Signalling ◽  
Mitochondrial Calcium ◽  
Mitochondrial Quality Control

scholarly journals Mitochondrial calcium signalling in cell death

FEBS Journal ◽  
2005 ◽  
Vol 272 (16) ◽  
pp. 4013-4022 ◽  
Author(s):  
Sara Leo ◽  
Katiuscia Bianchi ◽  
Marisa Brini ◽  
Rosario Rizzuto
Keyword(s):  
Cell Death ◽  
Calcium Signalling ◽  
Mitochondrial Calcium

scholarly journals Identification of a Novel MICU1 Nonsense Variant Causes Myopathy with Extrapyramidal Signs in an Iranian Consanguineous Family

2020 ◽  
Author(s):  
Fatemeh Bitarafan ◽  
Mehrnoosh Khodaeian ◽  
Elham Amjadi Sardehaei ◽  
Fatemeh Zahra Darvishi ◽  
Navid Almadani ◽  
...  
Keyword(s):  
Cell Death ◽  
Elevated Serum ◽  
Mitochondrial Calcium ◽  
Molecular Testing ◽  
Iranian Patient ◽  
Whole Exome ◽  
Serum Creatine Phosphokinase ◽  
Extrapyramidal Signs ◽  
Hepatic Transaminase

Abstract Background: Ca2+ as a universal second messenger regulates basic biological functions including cell cycle, cell proliferation, cell differentiation and cell death. Lack of the protein mitochondrial calcium uptake1 (MICU1) which has been regarded as a gatekeeper of Ca ions, leads to the abnormal mitochondrial Ca2+ handling, excessive production of reactive oxygen species (ROS), and increased cell death. Mutations in MICU1 gene (NM_006077.3) causes a very rare neuromuscular disease, Myopathy with extrapyramidal signs (MPXPS), due to primary alterations in mitochondrial calcium signaling which demonstrates the key role of mitochondrial Ca2+ uptake. To date 6 variants have been reported in MICU1 gene in approximately 21 pedigrees.Case presentation: here we report a 44-year-old Iranian patient presented with learning disability, muscle weakness, easy fatigability, reduced tendon reflexes, ataxia, elevated hepatic transaminase, elevated serum creatine phosphokinase and gait disturbance. We Identified a novel nonsense variant c.385C>T; p.(R129*) in MICU1 gene by whole exome sequencing and segregation analysis.Conclusions: Our finding along with previous studies provides more evidence on the clinical presentation of the disease caused by pathogenic mutations in MICU1. Finding more variants and expanding the spectrum of the disease increases the diagnostic rate of molecular testing in screening of this kind of diseases and in turn improves the quality of counseling for at risk couples and helps them to minimize the risks of having affected children.

scholarly journals Identification of a novel MICU1 nonsense variant causes myopathy with extrapyramidal signs in an Iranian consanguineous family

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Fatemeh Bitarafan ◽  
Mehrnoosh Khodaeian ◽  
Elham Amjadi Sardehaei ◽  
Fatemeh Zahra Darvishi ◽  
Navid Almadani ◽  
...  
Keyword(s):  
Cell Death ◽  
Elevated Serum ◽  
Mitochondrial Calcium ◽  
Molecular Testing ◽  
Iranian Patient ◽  
Whole Exome ◽  
Hepatic Transaminases ◽  
Extrapyramidal Signs ◽  
Ca Ions

Abstract Background Ca2+ as a universal second messenger regulates basic biological functions including cell cycle, cell proliferation, cell differentiation, and cell death. Lack of the protein mitochondrial calcium uptake1 (MICU1), which has been regarded as a gatekeeper of Ca ions, leads to the abnormal mitochondrial Ca2+ handling, excessive production of reactive oxygen species (ROS), and increased cell death. Mutations in MICU1 gene causes a very rare neuromuscular disease, myopathy with extrapyramidal signs (MPXPS), due to primary alterations in mitochondrial calcium signaling which demonstrates the key role of mitochondrial Ca2+ uptake. To date, 13 variants have been reported in MICU1 gene in 44 patients presented with the vast spectrum of symptoms. Case presentation Here, we report a 44-year-old Iranian patient presented with learning disability, muscle weakness, easy fatigability, reduced tendon reflexes, ataxia, gait disturbance, elevated hepatic transaminases, elevated serum creatine kinase (CK), and elevated lactate dehydrogenase (LDH). We identified a novel nonsense variant c.385C>T; p.(R129*) in MICU1 gene by whole exome sequencing (WES) and segregation analysis. Conclusions Our finding along with previous studies provides more evidence on the clinical presentation of the disease caused by pathogenic mutations in MICU1. Finding more variants and expanding the spectrum of the disease increases the diagnostic rate of molecular testing in screening of this kind of diseases and in turn improves the quality of counseling for at risk couples and helps them to minimize the risks of having affected children.

scholarly journals Bcl-2 Family of Proteins in the Control of Mitochondrial Calcium Signalling: An Old Chap with New Roles

2021 ◽  
Vol 22 (7) ◽  
pp. 3730
Author(s):  
Jordan L. Morris ◽  
Germain Gillet ◽  
Julien Prudent ◽  
Nikolay Popgeorgiev
Keyword(s):  
Cell Death ◽  
Cell Migration ◽  
Cell Survival ◽  
Calcium Signalling ◽  
Mitochondrial Pathway ◽  
Signalling Pathways ◽  
Mitochondrial Outer Membrane ◽  
Mitochondrial Calcium ◽  
New Class ◽  
Mitochondrial Outer Membrane Permeabilization

Bcl-2 family proteins are considered as one of the major regulators of apoptosis. Indeed, this family is known to control the mitochondrial outer membrane permeabilization (MOMP): a central step in the mitochondrial pathway of apoptosis. However, in recent years Bcl-2 family members began to emerge as a new class of intracellular calcium (Ca2+) regulators. At mitochondria-ER contacts (MERCs) these proteins are able to interact with major Ca2+ transporters, thus controlling mitochondrial Ca2+ homeostasis and downstream Ca2+ signalling pathways. Beyond the regulation of cell survival, this Bcl-2-dependent control over the mitochondrial Ca2+ dynamics has far-reaching consequences on the physiology of the cell. Here, we review how the Bcl-2 family of proteins mechanistically regulate mitochondrial Ca2+ homeostasis and how this regulation orchestrates cell death/survival decisions as well as the non-apoptotic process of cell migration.

Ceramides induce programmed cell death in Arabidopsis cells in a calcium-dependent manner

2005 ◽  
Vol 386 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Helen E. Townley ◽  
Kerrie McDonald ◽  
Gareth I. Jenkins ◽  
Marc R. Knight ◽  
Christopher J. Leaver
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Calcium Signalling ◽  
Plant Cells ◽  
Calcium Transient ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Calcium Dependent ◽  
Arabidopsis Cells

Abstract While the role of C2-ceramide in the induction of programmed cell death (PCD) in animal systems has been well documented, little is known of its role in plant cells. Here we show that C2-ceramide induces PCD in Arabidopsis suspension cultures, which is preceded by the generation of a calcium transient and an increase in reactive oxygen species (ROS). Inhibition of the calcium transient prevented cell death, whereas inhibition of ROS had no effect on cell survival. These observations suggest that calcium signalling plays a role in ceramide-induced PCD but is independent of the generation of ROS.

scholarly journals The role of cGMP-signalling and calcium-signalling in photoreceptor cell death: perspectives for therapy development

2021 ◽  
Author(s):  
Soumyaparna Das ◽  
Yiyi Chen ◽  
Jie Yan ◽  
Gustav Christensen ◽  
Soumaya Belhadj ◽  
...  
Keyword(s):  
Cell Death ◽  
Photoreceptor Cell ◽  
Second Messengers ◽  
Calcium Signalling ◽  
Clinical Applications ◽  
Photoreceptor Degeneration ◽  
Therapeutic Approaches ◽  
Cgmp Signalling ◽  
Key Aspects

AbstractThe second messengers, cGMP and Ca2+, have both been implicated in retinal degeneration; however, it is still unclear which of the two is most relevant for photoreceptor cell death. This problem is exacerbated by the close connections and crosstalk between cGMP-signalling and calcium (Ca2+)-signalling in photoreceptors. In this review, we summarize key aspects of cGMP-signalling and Ca2+-signalling relevant for hereditary photoreceptor degeneration. The topics covered include cGMP-signalling targets, the role of Ca2+ permeable channels, relation to energy metabolism, calpain-type proteases, and how the related metabolic processes may trigger and execute photoreceptor cell death. A focus is then put on cGMP-dependent mechanisms and how exceedingly high photoreceptor cGMP levels set in motion cascades of Ca2+-dependent and independent processes that eventually bring about photoreceptor cell death. Finally, an outlook is given into mutation-independent therapeutic approaches that exploit specific features of cGMP-signalling. Such approaches might be combined with suitable drug delivery systems for translation into clinical applications.

Sign in / Sign up

Export Citation Format

Share Document