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Books on the topic 'Leader cells in cell migration'

Author: Grafiati
Published: 6 September 2023

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1

In vivo migration of immune cells. Boca Raton, Fla: CRC Press, 1987.

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2

1949-, Husband Alan J., ed. Migration and homing of lymphoid cells. Boca Raton, Fla: CRC Press, 1988.

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3

Stem cell migration: Methods and protocols. New York: Humana Press, 2011.

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4

Frank, Entschladen, and Zänker Kurt S, eds. Cell migration: Signalling and mechanisms. Basel: Karger, 2010.

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5

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.
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6

Olszewski, Waldemar. In Vivo Migration of Immune Cells. Taylor & Francis Group, 2021.

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7

Filippi, Marie-Dominique, and Hartmut Geiger. Stem Cell Migration: Methods and Protocols. Humana Press, 2016.

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8

Okeyo, Kennedy Omondi Omondi, Hiromi Miyoshi, and Taiji Adachi. Innovative Approaches to Cell Biomechanics: From Cell Migration to On-Chip Manipulation. Springer, 2016.

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9

Miyoshi, Hiromi, Taiji Adachi, and Kennedy Omondi Okeyo. Innovative Approaches to Cell Biomechanics: From Cell Migration to On-Chip Manipulation. Hiromi Miyoshi Kennedy Omondi Okeyo Taiji Adachi, 2015.

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10

Miyoshi, Hiromi, Taiji Adachi, and Kennedy Omondi Okeyo. Innovative Approaches to Cell Biomechanics: From Cell Migration to On-Chip Manipulation. Springer, 2015.

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11

Miyoshi, Hiromi, Taiji Adachi, and Kennedy Omondi Okeyo. Innovative Approaches to Cell Biomechanics: From Cell Migration to on-Chip Manipulation. Springer Japan, 2015.

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12

Luckner, Martin. Secondary Metabolism and Cell Differentiation. Springer, 2011.

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13

Stickel, Eberhard, and Martin Luckner. Secondary Metabolism and Cell Differentiation. Springer, 2011.

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14

Lopez-Arvizu, Carmen, Carmel Bogle, and Harolyn M. E. Belcher. Neurobiology of Fetal Alcohol Spectrum Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0179.

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Prenatal exposure to ethanol can result in a wide range of clinical presentations that are grouped under the term “Fetal Alcohol Spectrum Disorders” (FASD). The direct cellular teratogenic effects of ethanol on fetal neurodevelopment include damage to cell survival, proliferation, and migration mechanisms. Dysregulation of neurotransmission and alteration of genetic transcription have also been implicated in the neurotoxic effects of prenatal ethanol exposure. These deleterious events lead to brain volume reduction, corpus callosum dysgenesis, cerebellar, and other neuroanatomical anomalies that have been observed in individuals with FASD. Beyond direct ethanol-induced insults, the impact that ethanol has on maternal nutrition, metabolism, hormonal regulation, and placental physiology also adversely effects fetal development. The complex interactions between numerous neurobiological and psychosocial mechanisms that hinder optimal fetal neurodevelopment are reflected by the heterogeneous clinical presentation of FASD, including impaired growth, dysmorphic facial features, and cognitive and behavioral disorders.
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15

Ali, Ased. Pathogenesis of urinary tract infection. Edited by Rob Pickard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0001.

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The realization of the harms resulting from indiscriminate use of antibiotics for minor infection has added impetus to the need to understand better the interaction between urogenital tract epithelium and invading bacteria during the initial stages of urinary tract infection (UTI). It is thought that uropathogenic Escherichia coli clones develop in the gut and migrate across the perineum to the urethra and up into the bladder. The response of the epithelium to bacterial adherence and the evolution of the invading bacteria will then govern the clinical consequences. These can vary between rapid invasion and further migration to produce systemic sepsis to tolerance of the bacteria in a planktonic state in asymptomatic bacteriuria. The key to these differences is the activation of epithelial pathogen-associated molecular pattern receptors by expressed proteins on the bacterial cell wall. Increased understanding of these interactions will lead to non-antibiotic-based strategies for clinical management of urinary infection.
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16

Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.

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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
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17

Lopez-Sanchez, Carmen, Virginio Garcia-Lopez, Gary C. Schoenwolf, and Virginio Garcia-Martinez. From epiblast to mesoderm: elaboration of a fate map for cardiovascular progenitors. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0003.

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The origin and migration of cardiovascular progenitors have been identified using multiple cell fate mapping techniques monitoring marked epiblast cells through time at carefully defined stages of early gastrulation. These studies have revealed that ordered groups of cells from the epiblast move into the anterior region of the primitive streak, and then migrate anterior laterally to define the first heart field in the mesodermal layer. Subsequently, the right and left components of the first heart field fuse into a single straight heart at the embryonic midline. Additional cells derived from the second heart field are added to the cardiac tube and contribute to further heart development. Heterotopic and heterochronic transplantation studies have revealed that cardiac precursor cells are plastic and do not form a specific subpopulation of the cardiac mesoderm. Specification of the heart fields occurs after ingression of precardiac cells through the primitive streak.
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18

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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19

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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20

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Abstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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21

Cahill, Thomas J., and Paul R. Riley. Epicardial and coronary vascular development. Edited by Miguel Torres. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0009.

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The coronary circulation is essential for human life. In embryonic development, abnormal formation of the coronary vasculature can cause death in utero or after birth. In adulthood, atherosclerosis of the coronary arteries is the commonest cause of death worldwide. The last decade has witnessed significant strides forward in our understanding of coronary development. Multiple sources of coronary endothelial cells have been identified using genetic tools for fate mapping. The epicardium, the outermost layer of the developing heart, has emerged as both a source of cell progenitors and key signalling mediators. Knowledge of the specific genes underlying formation, function, and heterogeneity of the epicardium is expanding. Significant challenges remain, however, in understanding the spatiotemporal signalling patterns required for organized migration, differentiation, and patterning of the vasculature. In addition, dissecting how coronary development is perturbed in patients with congenital coronary anomalies is a major ongoing focus of research.
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22

Woolf, Eric C., and Adrienne C. Scheck. Ketogenic Diet as Adjunctive Therapy for Malignant Brain Cancer. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0013.

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Malignant brain tumors are devastating, and increased survival requires new therapeutic modalities. Metabolic dysregulation results in an increased need for glucose in tumor cells, suggesting that reduced tumor growth could be achieved with decreased glucose availability either through pharmacological means or use of a high-fat, low-carbohydrate ketogenic diet (KD). KD provides increased blood ketones to support energy needs of normal tissues and has been shown to reduce tumor growth, angiogenesis, inflammation, peritumoral edema, migration, and invasion. Furthermore, this diet can enhance the activity of radiation and chemotherapy in a mouse model of glioma, thus increasing survival. In vitro studies indicate that increasing ketones in the absence of glucose reduction can also inhibit cell growth and potentiate the effects of radiation. Thus, emerging data provide strong support for the use of KD in the treatment of malignant gliomas and thus far has led to a limited number of clinical trials.
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23

Banjara, Manoj, and Damir Janigro. Effects of the Ketogenic Diet on the Blood-Brain Barrier. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0030.

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Ketone bodies (KBs) are always present in the blood, and their levels increase after high-fat diet intake, prolonged exercise, or extended fasting. Thus, one can predict effects on the brain capillary endothelium from high levels of ketones in the blood. Prolonged exposure of blood-brain barrier (BBB) endothelial cells to KBs induces expression of monocarboxylate transporters and enhances brain uptake of KBs. In addition, cell migration and expression of gap junction proteins are up-regulated by KBs. Thus, beneficial effects of the ketogenic diet may depend on increased brain uptake of KBs to match metabolic demand and repair of a disrupted BBB. As the effects of KBs on the BBB and their transport mechanisms across the BBB are better understood, it will be possible to develop alternative strategies to optimize the therapeutic benefits of KBs for brain disorders where the BBB is compromised.
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