Cytoplasmic Components in Hepatic Cell Lysosomes

Autophagy in the liver

“…Ashford and Porter reported "autophagy-like" structures in glucagon-perfused rat liver in 1962. 8 Soon it was confirmed that glucagon can stimulate autophagy in the liver. 9,25 The glucagon receptor is Gprotein-coupled.…”

“…7 Much of the pioneering work in the autophagy field is conducted in the liver or using isolated hepatocytes, such as determination of the morphology and membrane compositions of autophagosomes and characterization of the kinetics of protein degradation, regulation by hormones and amino acids, and involvement of the mammalian target of rapamycin (mTOR) pathway in induction. 2,[8][9][10][11][12] It is now clear that macroautophagy is important for many physiological and pathological processes. 4,6,13 It is required for normal development and participates in the clearance of apoptotic cells during embryogenesis.…”

Lysosomal Changes in Rat Hepatic Parenchymal Cells After Glucagon Administrationi

“…The autophagic vacuoles or autophagolysosomes are limited by a single or occasionally double membranes, containing clearly recognizable cytoplasmic organelles such as mitochondria or the endoplasmic reticulum. The origin of the limiting membrane of autophagolysosomes has been the matter of controversy and thcrc have been several hypotheses reported concerning its origin; (1) The membrane arises by de novo formation (Ashford and Porter, 1962;Napolitano, 1967), (2) The membrane originates from the plasma membrane (Quatacker, 1971), (3) The membrane is derived from the rough-or smooth-endoplasmic reticulum (Arstila and Trump, 1969;Coe et al, 1971; by the wrapping mechanism Ogawa et al, 1972). If a flattened sac surrounds and subsequently encloses an area of cytoplasm during the autophagolysosome formation, there must be a stage of autophagic vacuoles covered by two (inner and outer) membranes without regard to the origin of membranes.…”

“…Ashford and Porter (1962) showed that it was possible to induce an autophagocytosis in livers by perfusion of glucagon. found biochemically that an intraperitoneal injection of glucagon causes a marked increase in size, mechanical fragility and osmotic sensitivity of rat liver lysosomes 30 min after the administration of glucagon, and presumed that these changes weer related to autophagic vacuole formation.…”

Burkholderia cenocepacia J2315-mediated destruction of Staphylococcus aureus NRS77 biofilms.

“…CF lungs are in a hyper-inflammatory state due to chronic bacterial infections as well as the accumulation of misfolded and degraded proteins inside the cell. The cellular process of autophagy normally assists in removal of unwanted proteins and cytosolic debris through fusion of phagosomes with degradative lysosomes [9]. Defects in autophagy have been observed in CF-derived cell lines and have been shown to lead to increased inflammation in the lung airways [10][11][12].…”