No abstract available.
Animals ; Hepatocytes* ; Organelles* ; Rats*

Autophagy is an important homeostatic cellular recycling mechanism responsible for degrading injured or dysfunctional subcellular organelles and proteins in all living cells. The process of autophagy can be divided into three relatively independent steps: the initiation of phagophore, the formation of autophagosome and the maturation/degradation stage. Different morphological characteristics and molecular marker changes can be observed at these stages. Morphological approaches are useful to produce novel knowledge that would not be achieved through other experimental methods. Here we summarize the morphological methods in monitoring autophagy, the principles in data interpretation and the cautions that should be considered in the study of autophagy.
Autophagy ; Homeostasis ; Humans ; Organelles ; Phagosomes

Autophagy is a self-degradative process that removes misfolded or aggregated proteins, clears damaged organelles, as well as eliminates intracellular pathogens playing a role in innate immunity. Mycobacterium abscessus (M. abscessus) has been reported as a causative organism in nearly 80% of the rapid growing mycobacteria (RGM) pulmonary disease. The strain exhibits two different colony types: the smooth (S) one which is considered wild-type and the rough (R) one which is the mutated strain. In accordance to the colony morphology, the S and R types display varying autophagic responses in the host cells with the R type inducing elevated autophagy compared to the S type. The major difference in the autophagy could be based on the bioactive molecules exposed on the surface of the S and R types. Though autophagy has a vital role to play in the clearance of intracellular pathogens, very little is known on the autophagy induced by M. abscessus. It has been known that the intracellular pathogens employ different strategies to evade the autophagic pathway and to survive within the host cells. This review summarizes the most up-to-date findings on autophagy induced by M. abscessus morphotypes and how M. abscessus evades the autophagic machinery to divide and thrive inside the host cells. In addition, the prospects of autophagic machinery in devising new anti-infective strategies against mycobacterial infection is also been discussed.
Autophagy* ; Immunity, Innate ; Lung Diseases ; Mycobacterium* ; Organelles

Autophagy is a self-degradative process that removes misfolded or aggregated proteins, clears damaged organelles, as well as eliminates intracellular pathogens playing a role in innate immunity. Mycobacterium abscessus (M. abscessus) has been reported as a causative organism in nearly 80% of the rapid growing mycobacteria (RGM) pulmonary disease. The strain exhibits two different colony types: the smooth (S) one which is considered wild-type and the rough (R) one which is the mutated strain. In accordance to the colony morphology, the S and R types display varying autophagic responses in the host cells with the R type inducing elevated autophagy compared to the S type. The major difference in the autophagy could be based on the bioactive molecules exposed on the surface of the S and R types. Though autophagy has a vital role to play in the clearance of intracellular pathogens, very little is known on the autophagy induced by M. abscessus. It has been known that the intracellular pathogens employ different strategies to evade the autophagic pathway and to survive within the host cells. This review summarizes the most up-to-date findings on autophagy induced by M. abscessus morphotypes and how M. abscessus evades the autophagic machinery to divide and thrive inside the host cells. In addition, the prospects of autophagic machinery in devising new anti-infective strategies against mycobacterial infection is also been discussed.
Autophagy* ; Immunity, Innate ; Lung Diseases ; Mycobacterium* ; Organelles

The eukaryotic cell is compartmentalized by a series of vesicular organelles which constitute the endocytic and exocytic transport pathways. Each vesicular compartment has distinct sets of membrane proteins, structures and functions. Despite continuous vesicular transport, each vesicular compartment maintains its structure and function by use of retention and retrieval signal for its own resident proteins. Proteins in transit along the endocytic and exocytic pathway are transported without admixing with cytoplasmic constituents by successive steps of budding from the donor vesicles, formation of intermediate transport vesicles, transport, targeting to and fusion with acceptor vesicles. Specificity and fidelity of the vesicular transport are conferred by vesicular membrane proteins and small molecular weight GTP-binding proteins of the Rab subfamily. Proteins for export are packaged into specific vesicles for their final destinations. Insertion into and retrieval from the plasma membrane of transport proteins in response to cellular stimulus are a new paradigm of cellular regulatory mechanism. Secretion of neurotransmitters, hormones and enzymes by exocytosis involves a complex set of cytosolic proteins, G-proteins, proteins on the secretory granule membrane and plasma membrane. Much progress has been recently made in identifying proteins and factors involved in the exocytosis. But the molecular interactions among identified proteins and regulatory factors are unknown and remain to be elucidated. Finally our chemiosmotic hypothesis which involves the H+ electrochemical gradient across the secretory granule membrane generated by an ATP-dependent electrogenic H(+)-ATPase as the potential driving force for fusion and release of granule contents will be discussed.
Biological Transport ; *Exocytosis ; Human ; Organelles/*metabolism ; Support, Non-U.S. Gov't

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*

Modern drug delivery system demands high therapeutic efficacy and low toxicity which depends on efficient intracellular transportation of therapeutics to specific organisms, cells, even targeted organelles such as cytosol, nucleus, mitochondria, lysosome and endoplasmic reticulum. Intracellular barriers which prevent drug molecules accessing to their targets mainly include cell membrane, lysosomal degradation and the endomembrane system. Nanocarriers can preserve the bioactivities of protein, enzyme and DNA, and also they are easy to be modified and functionalized. In this paper, we summarized the intracellular fate of nanocarriers, especially how to bypass intracellular barriers and then target cytosol, nucleus, mitochondria, lysosome and endoplasmic reticulum by pharmaceutical modifications.
Animals ; Drug Carriers ; Drug Delivery Systems ; Humans ; Nanoparticles ; Organelles

OBJECTIVES: There have been developed to use targeting ability for antimicrobial, anticancerous, gene therapy and cosmetics through analysis of various membrane proteins isolated from cell organelles. METHODS: It was examined about the lysosomal membrane protein extracted from lysosome isolated from HeLa cell treated by 100 ppm melanin for 24 hours in order to find associated with targeting ability to melanin using by 2-dimensional electrophoresis. RESULTS: The result showed 14 up-regulated (1.5-fold) and 13 down-regulated (2.0-fold) spots in relation to melanin exposure. CONCLUSIONS: It has been found that lysosomal membrane proteins are associated with melanin to decolorize and quantity through cellular activation of lysosome.
Electrophoresis ; Genetic Therapy ; HeLa Cells* ; Humans ; Lysosome-Associated Membrane Glycoproteins* ; Lysosomes ; Melanins* ; Membrane Proteins ; Organelles

In the present study, we attempted to reveal the response of lens on induced traumatic cataract which were removed the anterior capsule with 0.5 mm, 1.0 mm, 2.0 mm, 4.0 mm size in six rabbits. We examined histopathological change of the wounded lenses by means of the slit-lamp and electronmicroscope. We found opacities in wounded area increased regardless of wound diame-ter. Electronmicroscopic findings were similar to normal single-layer cuboidal anterior epithelial cells at 0.5 mm, 1.0 mm, 2.0 mm, 4.0 mm one day after injury. There were, however, elongated epithelial cells with abun-dant fine filaments and slightly edematous lens fiber cells in 0.5 mm, 1.0 mm, 2.0 mm groups at 1 week after injury. These were observed as a small superficial scars at the wound site. We considered these changes as an effort of lens to delay the progression to the total cataract . We noted the widening of intercellular spaces, loss of cell membrane, decrease of intracel-lular organelles and severe change of the lens fiber rows in 4.0 mm group at 3 weeks after injury. We observed these changes as the total cataract in gross. Taken together, we revealed that lens epithelial cells in 0.5 mm, 1.0 mm, 2.0 mm in wound diameter stop the progression toward to the total cataract. However, lens epithelial cells at 4.0 mm in wound diameter could not obstruct the progression toward to the total cataract. We documented different stages of cataract formation and microstructure of the wounded lens, which have different wound sizes.
Cataract* ; Cell Membrane ; Cicatrix ; Epithelial Cells ; Extracellular Space ; Organelles ; Rabbits ; Wounds and Injuries

Mitochondria are small organelles that produce the majority of cellular energy as ATP. Mitochondrial dysfunction has been implicated in the pathogenesis of Parkinson's disease (PD), and rare familial forms of PD provide valuable insight into the pathogenic mechanism underlying mitochondrial impairment, even though the majority of PD cases are sporadic. The regulation of mitochondria is crucial for the maintenance of energy-demanding neuronal functions in the brain. Mitochondrial biogenesis and mitophagic degradation are the major regulatory pathways that preserve optimal mitochondrial content, structure and function. In this mini-review, we provide an overview of the mitochondrial quality control mechanisms, emphasizing regulatory molecules in mitophagy and biogenesis that specifically interact with the protein products of three major recessive familial PD genes, PINK1, Parkin and DJ-1.
Adenosine Triphosphate ; Brain ; Homeostasis* ; Mitochondria ; Mitochondrial Degradation ; Neurons ; Organelles ; Parkinson Disease* ; Quality Control ; Organelle Biogenesis