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Sommaire: keratin 818 regulation of hepatic cell death and metabolism
List of tables
List of figures
List of abbreviations
Chapter 1 : Introduction
1.1 LIVER
1.1.1 Functional organization of liver tissue
1.1.2 Hépatocytes
1.1.3 Liver as a metabolic hub
1.2 HEPATIC GLUCOSE HOMEOSTASIS
1.2.1 Glucose production
1.2.1.1 Glycogenolysis
1.2.1.2 Gluconeogenesis
1.2.2 Liver Glucose uptake
1.2.3 Glycogen synthesis
1.2.3.1 Glycogen synthase
1.2.3.2 Glucose regulation of GS
1.2.4 Glucose transporters
1.2.5 Insulin regulation of liver glucose homeostasis
1.2.6 Metabolic liver diseases (MLDs)
1.2.6.1 Diabetes Mellitus
1.2.6.2 Cancer
1.2.6.3 Nonalcoholic fatty liver disease (NAFLD)
1.3 OXIDATIVE STRESS AND CELL DEATH IN THE LIVER
1.3.1 Reactive oxygen species (ROS)
1.3.2 Cellular antioxidant system
1.3.2.1 The glutathione system
1.3.3 ROS in hepatic cell death
1.3.3.1 Types of cell death
1.3.4 Redox-sensitive signaling in the liver
1.3.4.1 Mitogen-activated protein (MAP) kinase family
1.3.4.2 Protein kinase C (PKC) family
1.3.5 Metabolic regulation of cell death
1.4 INTERMEDIATE FILAMENTS (IFs)
1.4.1 IF types
1.4.2 IF structure
1.4.3 Keratin IFs
1.4.4 Liver keratins
1.4.5 Posttranslational modifications of keratins
1.4.5.1 Phosphorylation
1.4.5.2 Other modifications
1.4.6 Mechanical functions of keratins
1.4.7 Non-mechanical functions of keratins 8/18
1.4.7.1 K8/K18 involvement in hepatic cell death
1.4.8 Role of keratins in liver diseases
– 1.4.8.1 Keratin mutations associated with liver diseases
1.4.8.2 Keratin involvement in metabolic liver diseases
1.5 CONTEXT OF THE RESEARCH PROJECT
Chapter 2 : Keratin-PKC interaction in ROS-induced hepatic cell death through mitochondrial signaling
PREFACE
MANUSCRIPT
ADDENDUM
Chapter 3 : Keratin 8/18 regulation of insulin-regulated glucose metabolism in hepatic cells through modulation of glucose transport and downstream signaling
PREFACE
MANUSCRIPT
Chapter 4 : Conclusion and Perspectives
4.1 Keratin-plectin scaffold at the mitochondria may modulate cell death signaling
4.2 Involvement of glucose in the ROS-induced hepatic cell death
4.3 PKC5 involvement in the K8/K18 modulation of insulin signaling in hepatic cells
4.4 K8/K18 modulation of energy metabolism in hepatic cell death and growth
4.5 K8/K18 regulation of hepatic cell glucose influx
4.6 A pathologic outlook on the K8/K18 regulation of energy metabolism
4.7 K8/K18 as a metabolic and death regulator in the hepatic cells: A new model
BIBLIOGRAPHY
Appendix 1
Appendix II
Appendix III
Extrait du mémoire keratin 818 regulation of hepatic cell death and metabolism
Chapter 1 : Introduction
1.1 LIVER
The liver, located in the upper right comer of the abdomen, is the largest internal organ of the body (/). The organ is closely associated with the small intestine, processing the nutrient-enriched venous blood from the portal vein. Because of its strategic location in the circulatory system, the liver functions both as an effector and a sensor organ. It maintains the organism’s energy supply in all metabolic states. Moreover, it is also a center of defense, preparing xenobiotics for elimination and destruction of foreign macromolecules; a control station of the hormonal system, inactivating hormones and releasing (pro)hormones; and a blood reservoir.
In addition, the liver senses and reports the stat of hydrophilic nutrient supply via vagal and splanchnic afférents to the central nervous system, thus contributing to the control of food intake (2).
keratin 818 regulation
1.1.1 Functional organization of liver tissue
The acinus is the smallest functional unit of the liver (3). It is based on the blood supply, thus representing a microcirculatory unit (Fig.1). The acinus consists of an irregular shaped, roughly- ellipsoidal mass of hépatocytes extends from a terminal portal venule and a terminal hepatic arteriole, which deliver their blood into the sinusoids, to the central vein, which delivers the blood to the hepatic vein. The upstream region around the terminal portal vein and arteriole is called the periportal zone; the area around the central vein is known as the perivenous zone. Apart from the parenchymal hépatocytes, there are four major types of non-parenchymal cells in the liver (2). (a) Sinusoidal endothelial cells lacking a basement membrane form the wall of the sinusoids. The small space between endothelial cells and hépatocytes is known as the space of Disse, (b) Kupffer cells are resident liver macrophages attached to the sinusoidal wall on the luminal surface, especially at branching points, (c) Stellate cells, also called Ito cells, lipocytes, or fat-storing cells, encircle the sinusoidal wall with long processes from the space of Disse, (d) Large granular lymphocytes, called pit cells, are loosely attached to the luminal surface of the sinusoids, to Kupffer cells and endothelial cells. Notably, in addition to producing cytokines, activated Kupffer cells are the major source of pathologic reactive oxygen species (ROS) in the liver (4).
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