Ion transport and membrane interactions in vascular health and disease /

Detalles Bibliográficos
Clasificación:Libro Electrónico
Otros Autores: Sturek, Michael (Editor )
Formato: Electrónico eBook
Idioma:Inglés
Publicado: Cambridge, MA : Academic Press, 2022.
Colección:Current topics in membranes ; v. 90.
Temas:
Ion channels.
Membranes (Biology)
Canaux ioniques.
Membranes (Biologie)
Ion channels
Acceso en línea:Texto completo
Texto completo
Tabla de Contenidos:
  • Intro
  • Ion Transport and Membrane Interactions in Vascular Health and Disease
  • Copyright
  • Contents
  • Contributors
  • Preface
  • Acknowledgments
  • Chapter One: Introduction to ion transport and membrane interactions in vascular health and disease
  • 1. Vascular specificity in health and disease
  • 2. Metabolic disease milieu and experimental approaches and models
  • 3. Snapshot of ion transport and membrane interactions
  • 4. Conclusions and future directions
  • Acknowledgments
  • References
  • Chapter Two: An unexpected effect of risperidone reveals a nonlinear relationship between cytosolic Ca uptake
  • 1. Introduction
  • 2. Materials and methods
  • 2.1. Materials and compounds
  • 2.2. Cell culture and preparation
  • 2.3. Transfection
  • 2.4. Buffers and solutions
  • 2.5. Loading with fura-2/am
  • 2.6. Genetically-encoded fluorescent sensors
  • 2.7. Microscopes and acquisition
  • 2.8. Data analysis
  • 2.9. Statistics
  • 3. Results
  • 3.1. Risperidone inhibited cytosolic Ca transients
  • 3.2. The effect of risperidone on endothelial Ca was exclusively due to its inhibitory effect on histamine-triggered sign ...
  • 3.3. Risperidone inhibited histamine-induced mitochondrial Ca signals
  • 3.4. Risperidone appears more potent in preventing histamine-induced mitochondrial Ca elevations
  • 3.5. Using various concentrations of risperidone, a linear cytosolic Ca elevation upon histamine was achieved
  • 3.6. The correlation between cytosolic and mitochondrial Ca elevations is biphasic but linear after a certain threshold
  • 4. Discussion
  • Conflict of interest
  • Acknowledgments
  • Author contributions
  • References
  • Chapter Three: Regulation of exosome release by lysosomal acid ceramidase in coronary arterial endothelial cells: Role of ...
  • 1. Introduction
  • 2. Materials and methods.
  • 2.1. Isolation and culture of CAECs from mouse coronary artery
  • 2.2. GCaMP3 Ca imaging
  • 2.3. Isolation of lysosomes from CAECs
  • 2.4. Whole-lysosome patch clamp recording
  • 2.5. Structured illumination microscopy
  • 2.6. Nanoparticle tracking analysis
  • 2.7. Dynamic analysis of lysosome movement in CAECs
  • 2.8. Statistical analysis
  • 3. Results
  • 3.1. Elevation of exosome release and reduction of lysosome-MVB interaction in CAECs lacking Asah1 gene
  • 3.2. Inhibition of exosome release from CAECs lacking Asah1 gene by sphingosine
  • 3.3. Regulation of lysosome trafficking and lysosome-MVB interaction by ML-SA1 and sphingosine in CAECs
  • 3.4. Characterization of TRPML channels in CAECs
  • 3.5. Blockade of TRPML1 channel by Asah1 gene deletion in CAECs
  • 3.6. Rescue of TRPML1 channel activity by sphingosine in CAECs lacking Asah1 gene
  • 3.7. Contribution of dynein activity to lysosomal regulation of exosome release in CAECs
  • 4. Discussion
  • References
  • Chapter Four: Vascular CaV1.2 channels in diabetes
  • 1. Introduction
  • 2. General L-type Ca channel CaV1.2 structure
  • 3. Regulation of vascular CaV1.2 channels
  • 3.1. Splice variants
  • 3.2. Phosphorylation
  • 4. Effects of hyperglycemia on CaV1.2
  • 5. Mechanisms of hyperglycemia-induced regulation of vascular CaV1.2 channels
  • 5.1. PKA
  • 5.2. AC5
  • 5.3. P2Y11
  • 5.4. A-kinase anchoring proteins (AKAPs)
  • 6. Conclusions and future directions
  • Acknowledgments
  • References
  • Chapter Five: Multiphasic changes in smooth muscle Ca transporters during the progression of coronary atherosclerosis
  • 1. Overview of vascular smooth muscle intracellular Ca regulation in health
  • 2. Smooth muscle phenotypic modulation and [Ca]i handling alterations
  • 3. Metabolic syndrome ``milieu��
  • 4. Atherogenesis.
  • 5. Function/dysfunction of Ca transporters during coronary atherosclerosis progression in swine
  • 6. SERCA stimulation induces coronary smooth muscle proliferation in early atherosclerosis
  • 6.1. Methods
  • 6.1.1. Organ culture of epicardial conduit coronary arteries
  • 6.1.2. Proliferation assay
  • 6.1.3. Immunohistochemistry
  • 6.1.4. Statistical analysis
  • 6.2. Results
  • 7. Similarity of swine and human coronary atherosclerosis and smooth muscle Ca signaling
  • 8. Multiphasic model of coronary smooth muscle Ca transporter regulation in atherosclerosis
  • 9. Conclusions and future directions
  • Acknowledgments
  • References
  • Chapter Six: Specificity of Ca channel modulation in atherosclerosis and aerobic exercise training
  • 1. General information on main types of K channels
  • 1.1. Voltage-gated K channels (Kv)
  • 1.2. ATP-sensitive K channels (KATP)
  • 1.3. Inward rectifier K channels (Kir)
  • 1.4. Calcium-activated K channels (BKCa)
  • 2. Physiological roles of KCa channels
  • 3. Effects of chronic exercise on reduction of cardiovascular disease and underlying K channel adaptations
  • 4. Conclusions and future directions
  • Acknowledgments
  • References
  • Chapter Seven: K+ channels in the coronary microvasculature of the ischemic heart
  • 1. Introduction
  • 2. Porcine model of ischemic heart disease
  • 3. Role of K channels in basal active tone of arterioles from ischemic myocardium
  • 4. Kv channels in arteriolar smooth muscle cells of ischemic myocardium
  • 5. BKCa channels in arteriolar smooth muscle cells of ischemic myocardium
  • 6. Role of additional K channel subfamilies in control of basal tone and vasodilation
  • 7. Conclusion
  • References.

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