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Article: Tissue Specificity: Store-Operated Ca

Bootman, Martin D / Rietdorf, Katja

Advances in experimental medicine and biology

2017 Volume 993, Page(s) 363–387

Abstract: ... Calcium ( ... ...

Abstract	Calcium (Ca
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-319-57732-6_19
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Investigating interactions between epicardial adipose tissue and cardiac myocytes: what can we learn from different approaches?

Rietdorf, Katja / MacQueen, Hilary

British journal of pharmacology

2017 Volume 174, Issue 20, Page(s) 3542–3560

Abstract: Heart disease is a major cause of morbidity and mortality throughout the world. Some cardiovascular conditions can be modulated by lifestyle factors such as increased exercise or a healthier diet, but many require surgical or pharmacological ... ...

Abstract	Heart disease is a major cause of morbidity and mortality throughout the world. Some cardiovascular conditions can be modulated by lifestyle factors such as increased exercise or a healthier diet, but many require surgical or pharmacological interventions for their management. More targeted and less invasive therapies would be beneficial. Recently, it has become apparent that epicardial adipose tissue plays an important role in normal and pathological cardiac function, and it is now the focus of considerable research. Epicardial adipose tissue can be studied by imaging of various kinds, and these approaches have yielded much useful information. However, at a molecular level, it is more difficult to study as it is relatively scarce in animal models and, for practical and ethical reasons, not always available in sufficient quantities from patients. What is needed is a robust model system in which the interactions between epicardial adipocytes and cardiac myocytes can be studied, and physiologically relevant manipulations performed. There are drawbacks to conventional culture methods, not least the difficulty of culturing both cardiac myocytes and adipocytes, each of which has special requirements. We discuss the benefits of a three-dimensional co-culture model in which in vivo interactions can be replicated. Linked articles: This article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue - Potential Pharmacological Targets? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc.
MeSH term(s)	Adipokines/physiology ; Adipose Tissue/physiology ; Animals ; Humans ; Myocytes, Cardiac/physiology ; Pericardium/physiology
Chemical Substances	Adipokines
Language	English
Publishing date	2017-01-22
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.13678
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Article ; Online: Atrial myocytes demonstrate the diversity of cardiac calcium signalling.

Bootman, Martin D / Rietdorf, Katja

Channels (Austin, Tex.)

2015 Volume 9, Issue 5, Page(s) 219–220

MeSH term(s)	Animals ; Calcium Signaling ; Myocytes, Cardiac/metabolism
Language	English
Publishing date	2015-11-03
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2262854-X
ISSN	1933-6969 ; 1933-6950
ISSN (online)	1933-6969
ISSN	1933-6950
DOI	10.1080/15384101.2015.1086203
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Article ; Online: Autophagy and cancer drug resistance in dialogue: Pre-clinical and clinical evidence.

Qin, Yi / Ashrafizadeh, Milad / Mongiardini, Vera / Grimaldi, Benedetto / Crea, Francesco / Rietdorf, Katja / Győrffy, Balázs / Klionsky, Daniel J / Ren, Jun / Zhang, Wei / Zhang, Xianbin

Cancer letters

2023 Volume 570, Page(s) 216307

Abstract: The emergence of drug resistance is a major challenge for oncologists. Resistance can be categorized as acquired or intrinsic; the alteration of several biological mechanisms contributes to both intrinsic and acquired resistance. Macroautophagy/autophagy ...

Abstract	The emergence of drug resistance is a major challenge for oncologists. Resistance can be categorized as acquired or intrinsic; the alteration of several biological mechanisms contributes to both intrinsic and acquired resistance. Macroautophagy/autophagy is the primary process in eukaryotes for the degradation of macromolecules and organelles. This process is critical in maintaining cellular homeostasis. Given its function as either a pro-survival or a pro-death phenomenon, autophagy has a complex physio-pathological role. In some circumstances, autophagy can confer chemoresistance and promote cell survival, whereas in others it can promote chemosensitivity and contribute to cell death. The role of autophagy in the modulation of cancer drug resistance reflects its impact on apoptosis and metastasis. The regulation of autophagy in cancer is mediated by various factors including AMP-activated protein kinase (AMPK), MAPK, phosphoinositide 3-kinase (PI3K)-AKT, BECN1 and ATG proteins. Non-coding RNAs are among the main regulators of autophagy, e.g., via the modulation of chemoresistance pathways. Due to the significant contribution of autophagy in cancer drug resistance, small molecule modulators and natural compounds targeting autophagy have been introduced to alter the response of cancer cells to chemotherapy. Furthermore, nanotherapeutic approaches based on autophagy regulation have been introduced in pre-clinical cancer therapy. In this review we consider the potential for using autophagy regulators for the clinical treatment of malignancies.
MeSH term(s)	Humans ; Drug Resistance, Neoplasm ; Phosphatidylinositol 3-Kinases/metabolism ; Apoptosis ; Phosphatidylinositol 3-Kinase ; Autophagy ; Neoplasms/drug therapy
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137)
Language	English
Publishing date	2023-07-12
Publishing country	Ireland
Document type	Review ; Journal Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2023.216307
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Article ; Online: Deleterious effects of calcium indicators within cells; an inconvenient truth.

Bootman, Martin D / Allman, Sarah / Rietdorf, Katja / Bultynck, Geert

Cell calcium

2018 Volume 73, Page(s) 82–87

Abstract: The study of cellular ... ...

Abstract	The study of cellular Ca
MeSH term(s)	Animals ; Calcium/analysis ; Calcium/metabolism ; Calcium Signaling/drug effects ; Calcium Signaling/physiology ; Cell Membrane/chemistry ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Egtazic Acid/analogs & derivatives ; Egtazic Acid/analysis ; Egtazic Acid/metabolism ; Egtazic Acid/pharmacology ; Humans ; Indicators and Reagents/analysis ; Indicators and Reagents/metabolism ; Indicators and Reagents/pharmacology
Chemical Substances	Indicators and Reagents ; Egtazic Acid (526U7A2651) ; 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (K22DDW77C0) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2018-04-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	757687-0
ISSN	1532-1991 ; 0143-4160
ISSN (online)	1532-1991
ISSN	0143-4160
DOI	10.1016/j.ceca.2018.04.005
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Article ; Online: Cardiac pathology in neuronal ceroid lipofuscinoses (NCL): More than a mere co-morbidity.

Rietdorf, Katja / Coode, Emily E / Schulz, Angela / Wibbeler, Eva / Bootman, Martin D / Ostergaard, John R

Biochimica et biophysica acta. Molecular basis of disease

2019 Volume 1866, Issue 9, Page(s) 165643

Abstract: The neuronal ceroid lipofuscinoses (NCLs) are mostly seen as diseases affecting the central nervous system, but there is accumulating evidence that they have co-morbidities outside the brain. One of these co-morbidities is a decline in cardiac function. ... ...

Abstract	The neuronal ceroid lipofuscinoses (NCLs) are mostly seen as diseases affecting the central nervous system, but there is accumulating evidence that they have co-morbidities outside the brain. One of these co-morbidities is a decline in cardiac function. This is becoming increasingly recognised in teenagers and adolescents with juvenile CLN3, but it may also occur in individuals with other NCLs. The purpose of this review is to summarise the current knowledge of the structural and functional changes found in the hearts of animal models and people diagnosed with NCL. In addition, we present evidence of structural changes that were observed in a systematic comparison of the cardiomyocytes from CLN3
MeSH term(s)	Animals ; Disease Models, Animal ; Heart Diseases/diagnosis ; Heart Diseases/metabolism ; Humans ; Membrane Glycoproteins/metabolism ; Molecular Chaperones/metabolism ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Neuronal Ceroid-Lipofuscinoses/diagnosis ; Neuronal Ceroid-Lipofuscinoses/metabolism
Chemical Substances	CLN3 protein, mouse ; Membrane Glycoproteins ; Molecular Chaperones
Language	English
Publishing date	2019-12-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2019.165643
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Article ; Online: Examining Cardiomyocyte Dysfunction Using Acute Chemical Induction of an Ageing Phenotype.

Masoud, Said / McDonald, Fraser / Bister, Dirk / Kotecki, Claire / Bootman, Martin D / Rietdorf, Katja

International journal of molecular sciences

2019 Volume 21, Issue 1

Abstract: Much effort is focussed on understanding the structural and functional changes in the heart that underlie age-dependent deterioration of cardiac performance. Longitudinal studies, using aged animals, have pinpointed changes occurring to the contractile ... ...

Abstract	Much effort is focussed on understanding the structural and functional changes in the heart that underlie age-dependent deterioration of cardiac performance. Longitudinal studies, using aged animals, have pinpointed changes occurring to the contractile myocytes within the heart. However, whilst longitudinal studies are important, other experimental approaches are being advanced that can recapitulate the phenotypic changes seen during ageing. This study investigated the induction of an ageing cardiomyocyte phenotypic change by incubation of cells with hydroxyurea for several days ex vivo. Hydroxyurea incubation has been demonstrated to phenocopy age- and senescence-induced changes in neurons, but its utility for ageing studies with cardiac cells has not been examined. Incubation of neonatal rat ventricular myocytes with hydroxyurea for up to 7 days replicated specific aspects of cardiac ageing including reduced systolic calcium responses, increased alternans and a lesser ability of the cells to follow electrical pacing. Additional functional and structural changes were observed within the myocytes that pointed to ageing-like remodelling, including lipofuscin granule accumulation, reduced mitochondrial membrane potential, increased production of reactive oxygen species, and altered ultrastructure, such as mitochondria with disrupted cristae and disorganised myofibres. These data highlight the utility of alternative approaches for exploring cellular ageing whilst avoiding the costs and co-morbid factors that can affect longitudinal studies.
MeSH term(s)	Animals ; Calcium/metabolism ; Cellular Senescence/physiology ; Heart Diseases/metabolism ; Heart Diseases/physiopathology ; Heart Ventricles/metabolism ; Heart Ventricles/physiopathology ; Longitudinal Studies ; Membrane Potential, Mitochondrial/physiology ; Mitochondria/metabolism ; Mitochondria/physiology ; Myocardial Contraction/physiology ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/physiology ; Phenotype ; Rats ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-12-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21010197
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Article ; Online: Examining Cardiomyocyte Dysfunction Using Acute Chemical Induction of an Ageing Phenotype

Said Masoud / Fraser McDonald / Dirk Bister / Claire Kotecki / Martin D. Bootman / Katja Rietdorf

International Journal of Molecular Sciences, Vol 21, Iss 1, p

2019 Volume 197

Abstract	Much effort is focussed on understanding the structural and functional changes in the heart that underlie age-dependent deterioration of cardiac performance. Longitudinal studies, using aged animals, have pinpointed changes occurring to the contractile myocytes within the heart. However, whilst longitudinal studies are important, other experimental approaches are being advanced that can recapitulate the phenotypic changes seen during ageing. This study investigated the induction of an ageing cardiomyocyte phenotypic change by incubation of cells with hydroxyurea for several days ex vivo. Hydroxyurea incubation has been demonstrated to phenocopy age- and senescence-induced changes in neurons, but its utility for ageing studies with cardiac cells has not been examined. Incubation of neonatal rat ventricular myocytes with hydroxyurea for up to 7 days replicated specific aspects of cardiac ageing including reduced systolic calcium responses, increased alternans and a lesser ability of the cells to follow electrical pacing. Additional functional and structural changes were observed within the myocytes that pointed to ageing-like remodelling, including lipofuscin granule accumulation, reduced mitochondrial membrane potential, increased production of reactive oxygen species, and altered ultrastructure, such as mitochondria with disrupted cristae and disorganised myofibres. These data highlight the utility of alternative approaches for exploring cellular ageing whilst avoiding the costs and co-morbid factors that can affect longitudinal studies.
Keywords	cardiac ; ageing ; calcium ; remodelling ; alternans ; arrhythmia ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2019-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Spontaneous, pro-arrhythmic calcium signals disrupt electrical pacing in mouse pulmonary vein sleeve cells.

Rietdorf, Katja / Bootman, Martin D / Sanderson, Michael J

PloS one

2014 Volume 9, Issue 2, Page(s) e88649

Abstract: The pulmonary vein, which returns oxygenated blood to the left atrium, is ensheathed by a population of unique, myocyte-like cells called pulmonary vein sleeve cells (PVCs). These cells autonomously generate action potentials that propagate into the left ...

Abstract	The pulmonary vein, which returns oxygenated blood to the left atrium, is ensheathed by a population of unique, myocyte-like cells called pulmonary vein sleeve cells (PVCs). These cells autonomously generate action potentials that propagate into the left atrial chamber and cause arrhythmias resulting in atrial fibrillation; the most common, often sustained, form of cardiac arrhythmia. In mice, PVCs extend along the pulmonary vein into the lungs, and are accessible in a lung slice preparation. We exploited this model to study how aberrant Ca(2+) signaling alters the ability of PVC networks to follow electrical pacing. Cellular responses were investigated using real-time 2-photon imaging of lung slices loaded with a Ca(2+)-sensitive fluorescent indicator (Ca(2+) measurements) and phase contrast microscopy (contraction measurements). PVCs displayed global Ca(2+) signals and coordinated contraction in response to electrical field stimulation (EFS). The effects of EFS relied on both Ca(2+) influx and Ca(2+) release, and could be inhibited by nifedipine, ryanodine or caffeine. Moreover, PVCs had a high propensity to show spontaneous Ca(2+) signals that arose via stochastic activation of ryanodine receptors (RyRs). The ability of electrical pacing to entrain Ca(2+) signals and contractile responses was dramatically influenced by inherent spontaneous Ca(2+) activity. In PVCs with relatively low spontaneous Ca(2+) activity (<1 Hz), entrainment with electrical pacing was good. However, in PVCs with higher frequencies of spontaneous Ca(2+) activity (>1.5 Hz), electrical pacing was less effective; PVCs became unpaced, only partially-paced or displayed alternans. Because spontaneous Ca(2+) activity varied between cells, neighboring PVCs often had different responses to electrical pacing. Our data indicate that the ability of PVCs to respond to electrical stimulation depends on their intrinsic Ca(2+) cycling properties. Heterogeneous spontaneous Ca(2+) activity arising from stochastic RyR opening can disengage them from sinus rhythm and lead to autonomous, pro-arrhythmic activity.
MeSH term(s)	Action Potentials/physiology ; Animals ; Atrial Fibrillation/physiopathology ; Caffeine ; Calcium Signaling/drug effects ; Calcium Signaling/physiology ; Electric Stimulation ; Fluorescence ; Lung/cytology ; Lung/metabolism ; Mice ; Microscopy, Phase-Contrast ; Myocytes, Smooth Muscle/metabolism ; Nifedipine ; Pulmonary Veins/cytology ; Pulmonary Veins/metabolism ; Ryanodine ; Ryanodine Receptor Calcium Release Channel/metabolism ; Statistics, Nonparametric
Chemical Substances	Ryanodine Receptor Calcium Release Channel ; Ryanodine (15662-33-6) ; Caffeine (3G6A5W338E) ; Nifedipine (I9ZF7L6G2L)
Language	English
Publishing date	2014-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0088649
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Article ; Online: The regulation of autophagy by calcium signals: Do we have a consensus?

Bootman, Martin D / Chehab, Tala / Bultynck, Geert / Parys, Jan B / Rietdorf, Katja

Cell calcium

2017 Volume 70, Page(s) 32–46

Abstract: Macroautophagy (hereafter called 'autophagy') is a cellular process for degrading and recycling cellular constituents, and for maintenance of cell function. Autophagy initiates via vesicular engulfment of cellular materials and culminates in their ... ...

Abstract	Macroautophagy (hereafter called 'autophagy') is a cellular process for degrading and recycling cellular constituents, and for maintenance of cell function. Autophagy initiates via vesicular engulfment of cellular materials and culminates in their degradation via lysosomal hydrolases, with the whole process often being termed 'autophagic flux'. Autophagy is a multi-step pathway requiring the interplay of numerous scaffolding and signalling molecules. In particular, orthologs of the family of ∼30 autophagy-regulating (Atg) proteins that were first characterised in yeast play essential roles in the initiation and processing of autophagic vesicles in mammalian cells. The serine/threonine kinase mTOR (mechanistic target of rapamycin) is a master regulator of the canonical autophagic response of cells to nutrient starvation. In addition, AMP-activated protein kinase (AMPK), which is a key sensor of cellular energy status, can trigger autophagy by inhibiting mTOR, or by phosphorylating other downstream targets. Calcium (Ca
MeSH term(s)	Animals ; Autophagy ; Calcium Channels/metabolism ; Calcium Signaling ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Lysosomes/metabolism ; Mitochondria/metabolism
Chemical Substances	Calcium Channels ; Inositol 1,4,5-Trisphosphate Receptors
Language	English
Publishing date	2017-08-19
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	757687-0
ISSN	1532-1991 ; 0143-4160
ISSN (online)	1532-1991
ISSN	0143-4160
DOI	10.1016/j.ceca.2017.08.005
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