Apoptosis ; Autophagy ; Endoplasmic Reticulum ; Endoplasmic Reticulum Chaperone BiP ; Endoplasmic Reticulum Stress ; Hedyotis ; Humans ; Laryngeal Neoplasms/drug therapy* ; Polysaccharides

The authors report a rare case of reticulum cell sarcoma-microgliomatosis which was extended into the leptomeninges, the Virchow-Robin spaces and choroid plexus invading the cerebral parenchyma in the left temporal area. Histogenesis of this tumor is briefly discussed.
Brain* ; Choroid Plexus ; Lymphoma, Non-Hodgkin* ; Reticulum*

Recent reports revealed that the Na+/-Ca2+ exchangers and feet structures of sarcoplasmic reticulum (SR) are located in close vicinity in the specific compartment. Therefore, we investigated the possibility that the Na+/-Ca2+ exchanger may decrease the tension development by transporting the Ca2+ out of the cell right after it released from SR, on the basis of this anatomical proximity. We examined the negative force-frequency relationship of the developed tension in the electrically field stimulated left atria of postnatal developing rat (1, 3 day, 1 week and 4 week old after birth). Cyclopiazonic acid (3 X 10(-5) M) treatment decreased the developed tension further according to postnatal age. Monensin (3 X 10(-6) M) treatment did not increase the maximal tension in 4 week-old rat, preserving negative staircase, while the negative staircase in the younger rat were flattened. Ca2+ depletion in the buffer elicited more suppression of the maximal tension according to the frequency in all groups except the 4 week-old group. The % decrease of the maximal developed tension of 4 week-old group at 1 Hz to that of 0.1 Hz after Na+ and Ca2+ depletion was only a half of those of the younger groups. Taken together, it is concluded that the Na+/-Ca2+ exchange transports more Ca2+ released from SR out of the cell in proportion to the frequency, and this is responsible for the negative staircase effect of the rat heart.
Animals ; Foot ; Heart* ; Monensin ; Rats* ; Sarcoplasmic Reticulum

The formation and development of cytoplasmic inclusion bodies of type II pneumocyte were investigated using 7 cases of human fetal lungs from 9 to 20 weeks of gestation by transmission electron micropscopy. The results obtained were as follows: 1. The multilamellar bodies, the characteristic inclusion body of type II pneumocyte, have developed in developing epithelium of lung at 9 week of gestation. Another inclusion bodies specific to type II pneumocyte also have developed at that time. 2. The inclusion bodies were formed in association with cytoplasmic reticulum, outer membrane of nuclear envelope, and mitochondria. 3. The inclusion bodies were distributed in cluster at the apical cytoplasm, and classified schematically with the contents as multilamellar, cytoplasmic, granular/f locculent, multivesicular, dense, and multilamellar. But the intermediate and composite forms of inclusion bodies appeared at the time toward 20 week of gestation. In summary, it is suggested that the differentiation of type II pneumocyte starts before 9 week of gestation and 4 main types of inclusion bodies considered as the precursor of multilamellar body were found. Although the inclusion bodies were formed at endoplasmic reticulum or etc, it is likely that they form multilamellar body through the complex process such as fusion of inclusion bodies.
Cytoplasm ; Endoplasmic Reticulum ; Epithelium ; Fetus* ; Humans* ; Inclusion Bodies* ; Lung ; Membranes ; Mitochondria ; Nuclear Envelope ; Pneumocytes* ; Pregnancy ; Reticulum

Apoptosis is an important host defense mechanism against mycobacterial infection. Recent reports suggest that links between apoptosis and endoplasmic reticulum (ER) stress are critical for the regulation of mycobacterial survival; however, the exact regulatory mechanisms are not well known. In this study, we isolated 20 Mycobacterium tuberculosis (Mtb) clinical strains from Korean patients and examined ER stress-mediated apoptosis in Mtb-infected macrophages. Most Mtb strains increased the rates of apoptosis and production of ER stress-sensing molecules in mouse macrophages, similar to Mtb H37Rv infection. Moreover, the intracellular survival of Mtb clinical isolates in macrophages was similar to that of H37Rv. Our data suggest that infection with Mtb downregulated MCP-1 and MCPIP. The regulation of MCPIP may decrease ROS production, leading to a reduction in ER stress-mediated apoptosis.
Animals ; Apoptosis* ; Endoplasmic Reticulum Stress* ; Endoplasmic Reticulum* ; Humans ; Korea* ; Macrophages* ; Mice ; Mycobacterium tuberculosis* ; Mycobacterium*

Histochemical and electron microscopic studies were made on the canal epithelium of the body segment of the rabbit epididymis and following results were obtained. 1) Acid phosphatase activity was marked in the canal epithelium. especially of the proximal body segment of the epididymis. Granules reactive to the acid phosphatase were present in both the above and below the nucleus 2) Electron microscopic finding: Canal epithelium of the body segment of the rabbit epididymis consisted of largely principal cells. Very few light and few basal cells. Principal cells were characterized by having slender microvilli (stereocilia). Luminal vesicles and vacuoles, extensive Golgi areas and many dense bodies in the supranuclear region, remarkable endoplasmic reticulum of mainly agranular type throughout the cytoplasm. Infranuclear cytoplasm contained often abundant mitochodria, many dense bodies and significant amount of granular endoplasmic reticulum. Light cells were characterized by having light cytoplasm, numerous vesicles, many vacuoles and dense bodies. Basal cells were present characterized by haying small nucleus, small number of cell organelles and rather clear cytoplasm From these results, it is suggested that the principal cell may have dual function of secretion and absorption and the light cell may engage mainly in absorptive function.
Absorption ; Acid Phosphatase ; Cytoplasm ; Endoplasmic Reticulum ; Endoplasmic Reticulum, Rough ; Epididymis* ; Epithelium* ; Male ; Microvilli ; Organelles ; Phenobarbital ; Vacuoles

Endoplasmic reticulum (ER) is an important organelle for protein folding, post-transcriptional modification and transport, which plays an important role in maintaining cell homeostasis. A variety of internal and external environmental stimuli can cause the accumulation of misfolded or unfolded proteins in the endoplasmic reticulum, and then result in ER stress. ER stress activates the unfolded protein response (UPR) and initiates a cluster of downstream signals to maintain ER homeostasis. However, severe and persistent ER stress activates UPR, which eventually leads to apoptosis and diseases. In recent years, a lot of researches suggest that ER stress plays an important role in the pathogenesis of various cardiovascular diseases (CVD), including ischemic heart disease, diabetic cardiomyopathy, heart failure, atherosclerosis and vascular calcification, high blood pressure and aortic aneurysm. ER stress might be one of the important targets for treatment of multiple CVD. Herein, the regulation mechanism of ER stress by activating UPR pathways in various common CVD and the new research advances in relationship of ER stress and CVD are briefly reviewed.
Apoptosis ; Cardiovascular Diseases ; physiopathology ; Endoplasmic Reticulum ; Endoplasmic Reticulum Stress ; Humans ; Unfolded Protein Response

Epilepsies are a group of chronic neurological disorders characterized by spontaneous recurrent seizures caused by abnormal synchronous firing of neurons and transient brain dysfunction. The underlying mechanisms are complex and not yet fully understood. Endoplasmic reticulum (ER) stress, as a condition of excessive accumulation of unfolded and/or misfolded proteins in the ER lumen, has been considered as a pathophysiological mechanism of epilepsy in recent years. ER stress can enhance the protein processing capacity of the ER to restore protein homeostasis through unfolded protein response, which may inhibit protein translation and promote misfolded protein degradation through the ubiquitin-proteasome system. However, persistent ER stress can also cause neuronal apoptosis and loss, which may aggravate the brain damage and epilepsy. This review has summarized the role of ER stress in the pathogenesis of genetic epilepsy.
Humans ; Endoplasmic Reticulum Stress/genetics* ; Unfolded Protein Response ; Endoplasmic Reticulum/pathology* ; Apoptosis ; Epilepsy/genetics*

It has been shown that mitochondria not only control their own Ca(2+) concentration ([Ca(2+)]), but also exert an influence over Ca(2+) signaling of the entire cell, including the endoplasmic reticulum or the sarcoplasmic reticulum, the plasma membrane, and the nucleus. That is to say, mitochondria couple cellular metabolic state with Ca(2+) transport processes. This review focuses on the ways in which the mitochondrial Ca(2+) handling system provides integrity and modulation for the cell to cope with the complex actions throughout its life cycle, enumerates some indeterminate aspects about it, and finally, prospects directions of future research.
Biological Transport ; Calcium Signaling ; Cell Membrane ; physiology ; Endoplasmic Reticulum ; physiology ; Mitochondria ; physiology ; Sarcoplasmic Reticulum ; physiology

Neurofi brillary tangles (NFTs) of microtubule-associated protein tau are a pathological hallmark of Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress has been known to be involved in the pathogenesis of AD. However, the exact role of ER stress in tau pathology has not yet been clearly elucidated. In present study, the possible relationship between tau pathology and ER stress was examined in terms of sorcin, which is a calcium binding protein and plays an important role in calcium homeostasis. Our previous yeast two hybrid study showed that sorcin is a novel tau interacting protein. Caspase-3-cleaved tau (T4C3) showed significantly increased tau-sorcin interaction compared to wild type tau (T4). Thapsigargin-induced ER stress and co-expression of constitutively active GSK3β (GSK3β-S9A) also exhibited significantly increased tau-sorcin interactions. T4C3-expressing cells showed potentiated thapsigargin-induced apoptosis and disruption of intracellular calcium homeostasis compared to T4-expressing cells. Overexpression of sorcin signifi cantly attenuated thapsigargin-induced apoptosis and disruption of calcium homeostasis. In contrary, siRNA-mediated knock-down of sorcin showed significantly increased thapsigargin-induced apoptosis and disruption of calcium homeostasis. These data strongly suggest that sequestration of sorcin by aberrant forms of tau compromises the function of sorcin, such as calcium homeostasis and cellular resistance by ER stress, which may consequently result in the contribution to the progression of AD.
Alzheimer Disease ; Apoptosis ; Calcium* ; Carrier Proteins ; Endoplasmic Reticulum ; Endoplasmic Reticulum Stress ; Homeostasis* ; Pathology ; Thapsigargin ; Yeasts