Autophagy is a physiological process which delivers the mutant cytoplasmic proteins and dysfunctional subcellular organs into lysosomes for degradation to generate fuel in the deficiency conditions. It is mainly classified into macroautophagy, microautophagy and chaperon-mediated autophagy (CMA), as well as the selective autophagy such as mitophagy and aggrephagy. This review mainly introduces the key molecular markers of macroautophagy, CMA and mitophagy.
Autophagy ; Humans ; Lysosomes ; Mitochondrial Degradation ; Molecular Chaperones

OBJECTIVE: To evaluate the change of cell surface CXC chemokine receptor 4 (CXCR4) expression of stem cells from apical papilla (SCAP) after the inhibition of endocytotic pathway, thus to provide experimental basis for the mechanism of SCAP migration. METHODS: The immunofluorescence analysis was conducted to examine the co-expression of CXCR4 and endocytotic compartments, including early endosomes, recycling endosomes and lysosomes in SCAP. Several Rab proteins were applied as markers of organelles in the endocytotic pathway, including Rab5 for early endosomes, Rab11A for recycling endosomes, and Lamp1 for lysosomes. The co-localization of CXCR4 with these endodontic compartments was further observed by proximity ligation assay (PLA). SCAP was treated with two kinds of endocytotic inhibitors, Blebbistatin and Dynasore, at a concentration of 80 μmol/L, respectively. The conditioning time was 1 hour. Flow cytometry was carried out to evaluate the proportion of SCAP that expressed CXCR4 on cell surface. The data were analysed by analysis of variance (ANOVA). RESULTS: The red staining of CXCR4 on immunofluorescence confocal microscopy predominantly overlapped with the green staining of Rab5 and Rab11A, and partly overlapped with Lamp1. It indicated that most CXCR4 molecules were located in early endosomes and recycling endosomes, and some were located in lysosomes. The PLA results revealed that the co-localizaiton of CXCR4 with endocytotic compartments could be observed in early endosomes, recycling endosomes and lysosomes. According to the results of flow cytometry, the proportion of SCAP that expressed CXCR4 on cell surface was as low as 0.13%±0.10%. After the inhibition of endocytosis by pretreating the cells with the following two inhibitors, Blebbistatin and Dynasore, the percentage of SCAP that positively expressed CXCR4 on cell surface was significantly increased to 13.34%±1.31% in Blebbistatin group and 4.03%±0.92% in Dynasore group (F=16.721, P<0.001). Moreover, the number of SCAP that expressed CXCR4 on cell surface in Blebbistatin group was significantly higher than that in Dynasore group (P<0.001). CONCLUSION The inhibition of endocytotic pathway could increase the number of SCAP that expressed CXCR4 on cell surface, and provide potency for the migration of SCAP.
Endocytosis ; Endosomes ; Lysosomes ; Receptors, CXCR4 ; Stem Cells

Autophagy is an intracellular degradation system that delivers cytoplasmic contents to the lysosome for degradation. It is a "self-eating" process and plays a "house-cleaner" role in cells. The complex process consists of several sequential steps-induction, autophagosome formation, fusion of lysosome and autophagosome, degradation, efflux transportation of degradation products, and autophagic lysosome reformation. In this review, the cellular and molecular regulations of late stage of autophagy, including cellular events after fusion step, are summarized.
Animals ; Autophagy ; physiology ; Humans ; Lysosomes ; metabolism ; physiology

Homeostasis ; Lysosomes/metabolism* ; Lipid Metabolism ; Glycosphingolipids/metabolism*

Myeloid body formation is an ultrastructural feature of gentamicin induced nephrotoxicity in human being and experimental animals. The origin of the myeloid body is not satisfactorily understood and morphological verification of the developing process of this structure is not fully accomplished. We injected 100 mg/kg/12 hour of gentamicin in 20 Spraque-Dawley rats and examined the ultrastructural feature of the proximal convoluted tubular cells of the kidney every 30 minutes in the first 4 hours, and in 5 hours, 6 hours, 12 hours, 24 hours and 48 hours after injection of gentamicin, with a TEM and a SEM. Myeloid bodies were noted as concentric layers of membranous structures of degenerated endoplasmic reticulum and mitochondria in the lysosome. The number and size of the myeloid body containing lysosomes were increased with time. We can deduce from this observation that injured cell organelles by diffusible gentamicin within the cells are autophagocytosed by lysosomes which were also injured by the drug from pinocytotic vesicles, and incompletely digested organellar remnants are retained in the lysosomes as myeloid bodies. So we think that the myeloid body formation is a result of an exaggerated and a pathologic autophagocytic process due to cell injury induced by gentamicin.
Animals ; Endoplasmic Reticulum ; Gentamicins* ; Humans ; Kidney ; Lysosomes ; Mitochondria ; Organelles ; Rats*

OBJECTIVE: This study is aimed to see ultrastructural changes of pineal gland in rats exposed to microwaves. METHODS: We conducted an experiment by exposing rats at the electromagnetic wave frequency of 2.45GHz, using with an EMR(electromagnetic radiation) emitting apparatus to study the effect of electromagnetic wave on the pineal gland. Paying especial attention to measure damages to pineal gland cells in the brain, we set the levels of EMR according to the duration of electromagnetic wave exposure at 1.2 joules(20min exposure), 2.4 joules(40min exposure), 3.6 joules(60 min exposure), and 4.8 joules(80min exposure) per 1cm2. RESULTS: Compared with normal cells, main histologic changes were observed with an electron microscope included swelling of the pineal gland cells, a decrease in the electron density of interstitial tissue, an increase in the distances between pineal gland cells, an increase in number of lipid-droplets, and swelling of mitochondria. Especially in those pineal cells exposed to EMR for 80 min, severe swelling of mitochondria and a slight increase in lysosome were observed. CONCLUSION: The authors could identify the harmful effect of microwave by observing abnormal ultrastructural changes of pineal cell in rat according to the increasement of electromagnetic radiation.
Animals ; Brain ; Electromagnetic Radiation ; Lysosomes ; Microwaves* ; Mitochondria ; Pineal Gland* ; Rats*

Autophagy is a highly evolutionarily conserved physiological mechanism of organism, including several stages such as autophagosomes formation, the fusion of lysosomes and autophagosomes, and autophagosomes degradation. In physiological conditions, autophagy is responsible for clearing the spoiled organelles and long-lived proteins to maintain the homeostasis of cells and organism. Meanwhile, autophagy is also involved in the formation and development of diseases, but the mechanism has not been confirmed yet. The relationship between autophagy and hypoxic ischemic brain injuries represented by stroke is a research hotpot in recent years, but there is no clear conclusion about autophagy's role and mechanism in hypoxic ischemic brain injuries. We reviewed the activation, function and mechanism of autophagy in hypoxic ischemic brain injuries, in order to provide some perspectives on these researches.
Animals ; Autophagy ; Homeostasis ; Humans ; Hypoxia-Ischemia, Brain ; physiopathology ; Lysosomes

Humans ; Lysosomal Storage Diseases ; prevention & control ; therapy ; Lysosomes ; metabolism

Autophagy is an intracellular degradation process that maintains cellular homeostasis. It is essential for protecting organisms from environmental stress. Autophagy can help the host to eliminate invading pathogens, including bacteria, viruses, fungi, and parasites. However, pathogens have evolved multiple strategies to interfere with autophagic signaling pathways or inhibit the fusion of autophagosomes with lysosomes to form autolysosomes. Moreover, host cell matrix degradation by different types of autophagy can be used for the proliferation and reproduction of pathogens. Thus, determining the roles and mechanisms of autophagy during pathogen infections will promote understanding of the mechanisms of pathogen‍‒‍host interactions and provide new strategies for the treatment of infectious diseases.
Autophagy ; Bacteria ; Host-Pathogen Interactions ; Lysosomes ; Signal Transduction

OBJECTIVE: To analyze the characteristics of lysosomal enzymes in mucolipidosis (ML) type II α/β and type III α/β for the choice of enzyme evaluating indicators. METHODS: Multiple lysosomal enzymes including α-iduronidase (IDUA), α -N-acetylglucosaminidase (NAGLU), β-galactosidase-1 (GLB1), β-glucuronidase (GUSB), α-galactosidase A (GLA), glucocerebrosidase (GBA) and arylsulphatase A (ASA) in plasma and leukocyte of two Chinese pedigrees with ML type II α/β and type III α/β and healthy controls were determined. Previous publications on ML type II α/β and type III α/β during the last five years were retrieved from PubMed, CNKI and WanFang databases by using "mucolipidosis" as key word. RESULTS: The activities of several lysosomal enzymes were increased in the plasma of both patients: ASA, IDUA (20-fold) > GUSB (10-fold) > GLB1, GLA (5-fold) > NAGLU (2-fold), whilst there was no significant change in GBA. The activities of several lysosomal enzymes in the leukocyte of the two patients were normal. 15 lysosomal enzymes have been used in 22 previous studies, the most frequently used were hexosaminidase A and B (Hex A+B) (12 papers), α-mannosidase (α-man) (11 papers) and GUSB (10 papers). The degree of Hex A+B and α-man elevation was most obvious (24.4-fold and 24.7-fold on average respectively), followed by ASA (22.4-fold on average), GUSB is 18.8-fold on average. CONCLUSION Based on the lysosomal enzyme analysis of the two cases and literature review, ASA, GUSB, Hex A+B and α-man are recommended as the evaluating indicators for lysosomal enzyme analysis of ML type II α/β and type III α/β.
China ; Hexosaminidase A ; Humans ; Iduronidase ; Lysosomes ; Mucolipidoses/genetics* ; Pedigree