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PubMedDate not supplied

Neurons bearing presenilins: weapons for defense or suicide?

Apoptotic machinery designed for cell's organized self-destruction involve different systems of proteases which cleave vital proteins and disassemble nuclear and cytoplasmic structures, committing the cell to death. The most studied apoptotic proteolytic system is the caspase family, but calpains and the proteasome could play important roles as well. Alzheimer's disease associated presenilins showed to be a substrate for such proteolytic systems, being processed early in several apoptotic models, and recent data suggest that alternative presenilin fragments could regulate cell survival. Mutations in genes encoding presenilins proved to sensitize neurons to apoptosis by different mechanisms e.g. increased caspase-3 activation, oxyradicals production and calcium signaling dysregulation. Here we review the data involving presenilins in apoptosis and discuss a possible role of presenilins in the regulation of apoptotic biochemical machinery.

Journal Article↗
PubMed1988

Tyrosinase protein is expressed also in some neural crest derived cells which are not melanocytes.

Some neural crest cells give rise to pigment cells in early ontogenesis. We tested here whether tyrosinase--a key enzyme in melanogenesis--was present in some pigment neural crest derivatives in adult hamsters. Interestingly enough, inactive tyrosinase protein was detected, using indirect immunofluorescence, in the satellite cells of spinal ganglia and Schwann cells of sciatic and facial nerves in normal adult animals. The results of cell blotting from spinal ganglia were similar to the fluorescence findings. Thus, our results seem to support the hypothesis that Schwann cells, satellite cells of spinal ganglia, and melanocytes may be more intimately related developmentally than other neural-crest-derived cells. Moreover, since we detected tyrosinase protein in cells which normally do not produce melanosomes, it could be deduced that, during the melanocyte's differentiation from its cell precursor, the expression of tyrosinase protein might precede the point when melanosomes begin to differentiate from known cytoplasmic structures.

Animals↗
PubMed1997

Evidence for genetic control of changes in f-actin polymerization caused by pathogenic microorganisms: in vitro assessment using gingival fibroblasts from human twins.

Attachment to and migration upon a substratum, as well as other functions of connective tissue cells, are regulated mainly by cytoplasmic structural proteins, particularly filamentous actin (f-actin). Pathogenic microorganisms exert negative effects on cytoskeletal proteins. In the present study, normal gingival fibroblasts from 10 sets of human twins (6 fraternal, DZ; 4 identical, MZ) were exposed to soluble extracts from Porphyromonas gingivalis or Fusobacterium nucleatum, then f-actin was stained using FITC-labeled phalloidin. Cells were examined under fluorescence, and a computer-assisted image analyzer quantitated f-actin polymerization as fluorescence intensity on a per-cell basis. Intraclass correlation coefficients for f-actin in MZ/MZ vis-a-vis DZ/DZ paired cell cultures were determined to assess the possible heritability of responses to the microorganism preparations. F-actin labeling was significantly different between control cultures and those exposed to the extracts. Both F. nucleatum and P. gingivalis effected f-actin and fibroblast morphology. When the data were adjusted for gender and age effects, and for differences in control f-actin levels, fibroblasts from MZ twin pairs were moderately similar in both absolute and relative responses to bacterial challenges; cells from DZ twins showed little similarity when response was measured on the absolute scale, and moderate similarity using the relative scale.

Actins↗
PubMed2005

Strength at the extracellular matrix-muscle interface.

Mechanical force is generated within skeletal muscle cells by contraction of specialized myofibrillar proteins. This paper explores how the contractile force generated at the sarcomeres within an individual muscle fiber is transferred through the connective tissue to move the bones. The initial key point for transfer of the contractile force is the muscle cell membrane (sarcolemma) where force is transferred laterally to the basement membrane (specialized extracellular matrix rich in laminins) to be integrated within the connective tissue (rich in collagens) before transmission to the tendons. Connections between (1) key molecules outside the myofiber in the basement membrane to (2) molecules within the sarcolemma of the myofiber and (3) the internal cytoplasmic structures of the cytoskeleton and sarcomeres are evaluated. Disturbances to many components of this complex interactive system adversely affect skeletal muscle strength and integrity, and can result in severe muscle diseases. The mechanical aspects of these crucial linkages are discussed, with particular reference to defects in laminin-alpha2 and integrin-alpha7. Novel interventions to potentially increase muscle strength and reduce myofiber damage are mentioned, and these are also highly relevant to muscle diseases and aging muscle.

Animals↗
PubMed2006

Citron kinase, a RhoA effector, enhances HIV-1 virion production by modulating exocytosis.

RhoGTPases play important roles in the regulation of protein transport and membrane recycling. Little is known, however, about how RhoGTPases affect HIV-1 virion production, which is dependent on the endosomal sorting pathway. We report that ectopic expression of citron kinase (citron-K), a RhoA effector, preferentially enhances HIV-1 virion production. Depletion of endogenous citron-K inhibits HIV-1 virion production. Citron-N, which lacks the kinase domain, also enhances HIV-1 virion production. The leucine zipper, Rho-binding and zinc finger domains of citron-N are necessary for the enhancement activity. Citron-K also enhances murine leukemia virion production and the HIV-1 late domain is not required for the citron-K-mediated enhancement. Ectopic expression of citron-K leads to the formation of cytoplasmic structures containing citron-K and HIV-1 Gag proteins. HIV-1 and citron-K cooperatively enhance acidic endosome and lysosome compartments. Finally, citron-K promotes exocytosis of microvesicles or exosomes that co-purify with HIV-1 virions. We conclude that citron-K enhances HIV-1 virion production by stimulating the endosomal compartments and exocytosis.

Animals↗
PubMed1984

Electrical membrane responses to secretagogues in parietal cells of the rat gastric mucosa in culture.

Fragments of the gastric fundus of 6-8-day-old rats were maintained in tissue culture. From the explant, adhered to a plastic substrate, epithelial cells migrated and developed to form a monolayer colony. Histological and histochemical studies as well as indirect immunofluorescence studies using anti-parietal cell antibodies testified to the presence of parietal cells in the monolayer during the first week. These parietal cells were distinguished by their vesicular cytoplasmic structures using phase-contrast or differential interference-contrast microscopy. Acridine Orange, an optical probe of H+ accumulation, was taken up preferentially by these parietal cells, exhibiting orange fluorescence within the cells on the third day of culture, in response to stimulation with gastrin, histamine and carbachol. The resting potential of these cultured parietal cells was about -20 mV. On day 2-4 of culture, the cell membrane became hyperpolarized (up to -30 to -40 mV) in response to gastrin, carbachol or histamine in the presence of isobutylmethyl-xanthine (IMX). During hyperpolarization, the membrane resistances decreased significantly. The amplitude and the polarity of secretagogue-induced responses were found to be dependent on the extracellular concentration of K+ (but not Na+ and Cl-). The carbachol-induced responses were inhibited by atropine but not curare. The responses induced by histamine plus IMX were blocked by cimetidine but not pyrilamine. Neither atropine nor cimetidine affected the gastrin-evoked responses. It is concluded that rat parietal cells have separate receptors for acetylcholine (muscarinic), gastrin and histamine (H2), and that an increase in the membrane permeability to K+ is closely associated with the responses of these receptors under these in vitro conditions.

Animals↗
PubMed1989

Reciprocal effects of hyper- and hypoactivity mutations in the Drosophila pattern gene torso.

In Drosophila, five "terminal" polarity genes must be active in females in order for them to produce embryos with normal anterior and posterior ends. Hypoactivity mutations in one such gene, torso, result in the loss of the most posterior domain of fushi tarazu expression and the terminal cuticular structures. In contrast, a torso hyperactivity mutation causes the loss of central fushi tarazu expression and central cuticular structures. Cytoplasmic leakage, transplantation, and temperature-shift experiments suggest that the latter effect is caused by abnormal persistence of the torso product in the central region of the embryo during early development. Thus, the amount and timing of torso activity is key to distinguishing the central and terminal regions of the embryo. Mutations in the tailless terminal gene act as dominant maternal suppressors of the hyperactive torso allele, indicating that the torso product acts through, or in concert with, the tailless product.

Abdomen↗
PubMed1971

Immunological Study on the Host Cell Penetration Factor of Toxoplasma gondii.

The host cell penetration factor (PEF) of Toxoplasma gondii was studied by biochemical and immunological techniques. Sephadex gel filtration of an ammonium sulfate-precipitated PEF yielded two components with different molecular weight, but both having penetration-enhancing activity. The methods for purification removed at least 99.9% of extraneous protein. For demonstration of a significant enhancement of penetration, 0.001 mug of protein was sufficient. Biochemically, they appeared to be acid proteins with the same electrophoretic mobility. Both components showed maximal enhancement of penetration at pH 7.6 and 37 C. PEF antisera reduced the penetrative capacity of Toxoplasma parasites. The penetration-enhancing effect of the two components of PEF was inhibited by antiserum against any of them. Moreover, immunologically identical immunoprecipitates were obtained when antiserum reacted with the two components. The results thus indicated that the two components of PEF were immunogenically identical and that the difference in molecular weights might result from aggregation. Immunofluorescence indicated that PEF was related to cytoplasmic structures located in the anterior end of Toxoplasma. A possible relation between these structures and the paired organelle or the convoluted tubes was discussed. The number of parasites with immunofluorescence was low shortly after host cell penetration and increased during the intracellular life of the parasites after kinetics, previously observed for synthesis of PEF as well as for lysosomal activity of Toxoplasma.

Journal Article↗
PubMed1965

LOCATION OF CHLOROPHYLL IN RHODOSPIRILLUM RUBRUM.

Holt, Stanley C. (University of California, Davis), and Allen G. Marr. Location of chlorophyll in Rhodospirillum rubrum. J. Bacteriol. 89:1402-1412. 1965.-If cells of Rhodospirillum rubrum are broken by sonic and ballistic disruption, the chlorophyll is not found in discrete cytoplasmic structures, but is located in a more extensive structure of the cell, the intracytoplasmic membrane. Direct electron microscopy of sonically disrupted cells of R. rubrum and stereo-electron microscopy of osmotically shocked cells reveal the presence of a tubular network of internal membranes originating from the periphery of the cell.

Cell Biology↗
PubMed1969

Sindbis virus-induced viral ribonucleic acid polymerase.

A cytoplasmic structure containing the viral ribonucleic acid (RNA) polymerase has been isolated by sucrose density centrifugation from cells infected with Sindbis virus. Uninfected cells did not contain any such structure. Preliminary experiments indicated that the structure may be associated with membranes. This structure incorporated (3)H-guanosine triphosphate in vitro in the absence of added template. The RNA synthesized in vitro by the enzyme consisted of single-stranded 40S RNA, the ribonuclease-resistant replicative form, and possibly the replicative intermediate form of viral RNA. The products formed in vitro by the enzyme are identical in sedimentation rates to those formed in the infected cells in vivo.

Animals↗
PubMed2002

Murine cytomegalovirus m02 gene family protects against natural killer cell-mediated immune surveillance.

The murine cytomegalovirus m02 gene family encodes putative type I membrane glycoproteins named m02 through m16. A subset of these genes were fused to an epitope tag and cloned into an expression vector. In transfected and murine cytomegalovirus-infected cells, m02, m04, m05, m06, m07, m09, m10, and m12 localized to cytoplasmic structures near the nucleus, whereas m08 and m13 localized to a filamentous structure surrounding the nucleus. Substitution mutants lacking the m02 gene (SMsubm02) or the entire m02 gene family (SMsubm02-16) grew like their wild-type parent in cultured cells. However, whereas SMsubm02 was as pathogenic as the wild-type virus, SMsubm02-16 was markedly less virulent. SMsubm02-16 produced less infectious virus in most organs compared to wild-type virus in BALB/c and C57BL/6J mice, but it replicated to wild-type levels in the organs of immunodeficient gamma(c)/Rag2 mice, lacking multiple cell types including natural killer cells, and in C57BL/6J mice depleted of natural killer cells. These results argue that one or more members of the m02 gene family antagonize natural killer cell-mediated immune surveillance.

Acute Disease↗
PubMed2003

Cellular gene expression survey of vaccinia virus infection of human HeLa cells.

Vaccinia virus (VV) is a cytocidal virus that causes major changes in host cell machinery shortly after infecting cells. To define the consequences of virus infection on host gene expression, we used microarrays of approximately 15,000 human cDNAs to examine expression levels of mRNAs isolated at 2, 6, and 16 h postinfection from cultures of infected HeLa cells. The majority of profiling changes during VV infection corresponded to downregulation of genes at 16 h postinfection. Differentially expressed genes were clustered into seven groups to identify common regulatory pathways, with most of them (90%) belonging to clusters 6 and 7, which represent genes whose expression was repressed after infection. Cluster 1, however, contained 37 transcripts (2.81%) showing a robust pattern of induction that was maintained during the course of infection. Genes in cluster 1 included those for Wiskott-Aldrich syndrome protein (WASP) family member WASF1, thymosine, adenosine A2a receptor, glutamate decarboxylase 2, CD-80 antigen, KIAA0888 protein, selenophosphate synthetase, pericentrin, and attractin as well as several expressed sequence tags. We analyzed in more detail the fate of WASP protein in VV-infected cells, because a related family member, N-WASP, is involved in viral motility. WASP protein accumulated in the course of infection; its increase required viral DNA replication and de novo protein synthesis, and it localized in cytoplasmic structures distinct from uninfected cells. This study is the first quantitative analysis of host gene expression following VV infection of cultured human cells, demonstrating global changes in the expression profile, and identifies upregulated genes with potential roles in the virus replication cycle.

Blotting, Western↗
PubMed2002

Cell cycle arrest and apoptosis induced by human Polo-like kinase 3 is mediated through perturbation of microtubule integrity.

Human Polo-like kinase 3 (Plk3, previously termed Prk or Fnk) is involved in regulation of cell cycle progression through the M phase (B. Ouyang, H. Pan, L. Lu, J. Li, P. Stambrook, B. Li, and W. Dai, J. Biol. Chem. 272:28646-28651, 1997). Here we report that in most interphase cells endogenous Plk3 was predominantly localized around the nuclear membrane. Double labeling with Plk3 and gamma-tubulin, the latter a major component of pericentriole materials, revealed that Plk3 was closely associated with centrosomes and that its localization to centrosomes was dependent on the integrity of microtubules. Throughout mitosis, Plk3 appeared to be localized to mitotic apparatus such as spindle poles and mitotic spindles. During telophase, a significant amount of Plk3 was also detected in the midbody. Ectopic expression of Plk3 mutants dramatically changed cell morphology primarily due to their effects on microtubule dynamics. Expression of a constitutively active Plk3 (Plk3-A) resulted in rapid cell shrinkage, which led to formation of cells with an elongated, unsevered, and taxol-sensitive midbody. In contrast, cells expressing a kinase-defective Plk3 (Plk3(K52R)) mutant exhibited extended, deformed cytoplasmic structures, the phenotype of which was somewhat refractory to taxol treatment. Expression of both Plk3-A and Plk3(K52R) induced apparent G(2)/M arrest followed by apoptosis, although the kinase-defective mutant was less effective. Taken together, our studies strongly suggest that Plk3 plays an important role in the regulation of microtubule dynamics and centrosomal function in the cell and that deregulated expression of Plk3 results in cell cycle arrest and apoptosis.

Apoptosis↗
PubMed2002

Nir2, a human homolog of Drosophila melanogaster retinal degeneration B protein, is essential for cytokinesis.

Cytokinesis, the final stage of eukaryotic cell division, ensures the production of two daughter cells. It requires fine coordination between the plasma membrane and cytoskeletal networks, and it is known to be regulated by several intracellular proteins, including the small GTPase Rho and its effectors. In this study we provide evidence that the protein Nir2 is essential for cytokinesis. Microinjection of anti-Nir2 antibodies into interphase cells blocks cytokinesis, as it results in the production of multinucleate cells. Immunolocalization studies revealed that Nir2 is mainly localized in the Golgi apparatus in interphase cells, but it is recruited to the cleavage furrow and the midbody during cytokinesis. Nir2 colocalizes with the small GTPase RhoA in the cleavage furrow and the midbody, and it associates with RhoA in mitotic cells. Its N-terminal region, which contains a phosphatidylinositol transfer domain and a novel Rho-inhibitory domain (Rid), is required for normal cytokinesis, as overexpression of an N-terminal-truncated mutant blocks cytokinesis completion. Time-lapse videomicroscopy revealed that this mutant normally initiates cytokinesis but fails to complete it, due to cleavage furrow regression, while Rid markedly affects cytokinesis due to abnormal contractility. Rid-expressing cells exhibit aberrant ingression and ectopic cleavage sites; the cells fail to segregate into daughter cells and they form a long unseparated bridge-like cytoplasmic structure. These results provide new insight into the cellular functions of Nir2 and introduce it as a novel regulator of cytokinesis.

Animals↗
PubMed1992

Epidermal growth factor receptors in the oesophagus.

The quantity and distribution of epidermal growth factor receptors (EGF-R) in oesophageal mucosa was studied in the oesophagus in order to determine its role in oesophageal disease. Fifty five biopsies were taken from different levels of the oesophagus in 25 consecutive patients undergoing endoscopy. Another group of eight patients with histologically proven Barrett's oesophagitis had a biopsy taken from the area of columnar lined oesophagus. A peripheral, membranous pattern was seen predominantly confined to the basal and immediately suprabasal cells in all of the first group of patients. In the superficial cells a few granular cytoplasmic structures were positive. All patients with Barrett's oesophagitis showed EGF-R staining of the surface epithelium. A computerised planimeter was used to determine the proportion of stained areas of squamous cells which were expressed as a percentage of the total area of squamous cells. The difference in the area of cells stained for EGF-R between normal and inflamed oesophageal mucosa (29.5% and 43.1% respectively) was significant (p less than 0.001).

Adult↗
PubMed1993

Segregation of eosinophil proteins in alveolar macrophage compartments in chronic eosinophilic pneumonia.

BACKGROUND: The objective was to characterise the process and consequences of eosinophil activation and lysis in patients with chronic eosinophilic pneumonia and to compare them with those in patients with eosinophil pulmonary infiltrates from other causes. METHODS: Cells from bronchoalveolar lavage fluid of four patients with chronic eosinophilic pneumonia and four patients with eosinophilic infiltrates associated with Sjögren's syndrome, drug hypersensitivity pneumonia, postradiotherapy fibrosis, and pulmonary disease associated with graft versus host disease were studied ultrastructurally and with immunogold labelled antibodies directed against eosinophil proteins: major basic protein, eosinophil cationic protein, and Charcot-Leyden crystal protein. The concentration of eosinophil cationic protein was also measured in bronchoalveolar fluid. RESULTS: In the four patients with chronic eosinophilic pneumonia, ultrastructural studies demonstrated numerous lysed eosinophils. Further, three released eosinophil proteins were detected in distinct cytoplasmic structures in alveolar macrophages. These features were not found in the four patients with eosinophilic pulmonary infiltrates from other causes. CONCLUSION: Eosinophils in chronic eosinophilic pneumonia show signs of activation with release of eosinophil proteins. The appearance of three of these eosinophil proteins in different macrophage compartments suggests that macrophage uptake, with or without intracellular transport of released eosinophil proteins, involves separate mechanisms. This interaction does not lead to macrophage lysis, however, and one or more of these eosinophil proteins might directly affect macrophage function.

Adult↗
PubMed1977

Ultrastructure of Nocardia-like variants of Mycobacterium smegmatis and chemical composition of the basal cell wall layer.

Mycobacterium smegmatis, its orange-red--pigmented (OR) variants, and back mutant strains were examined by electron microscopy using ultrathin sectioning, negative or positive staining, and freeze-fracture-etching methods. The parental and back mutant strains showed almost identical ultrastructures. Specifically, thick ramified fibers measuring about 15 nm in diameter were always visible in the positively stained cell wall, although they were not readily visualized with negative staining or freeze-fracture-etching. In contrast, the cell walls of OR variants contained fibrous networks measuring about 11 nm in diameter, which could be observed by positive and negative staining as well as freeze-fracture-etching. Although cytoplasmic structures appeared similar among the four strains examined, mesosomes were significantly more abundant in the OR variants. The basal layer of the cell wall obtained as a phenol residue consisted of a dense membranous matrix containing scattered fibrous structures in the parental and back mutant strains, and fibrous networks in the OR variants. Chemical analyses showed that the basal layers of all four strains contained the same neutral sugars, amino sugars, and amino acids, i.e., arabinose, galactose, muramic acid, glucosamine, alanine, glutamic acid, and diaminopimelic acid. The alpha-branched, beta-hydroxylated fatty acids contained in the basal layers differ among the four strains, however, with nocardomycolic acids being present in the OR variants and mycolic acids in the parental and back mutant strains. Our previous conclusion that OR variants of M. smegmatis have characteristics similar to those of nocardia is supported by the present study.

Amino Acids↗
PubMed1985

A 105 000 dalton antigen of transformed mouse cells is a stress protein.

Antisera prepared in mice against syngeneic spontaneously transformed AL/N cells (anti-TAL/N serum) identified a number of protein antigens synthesized by simian virus 40 (SV40) transformed cells, among which was a protein with a molecular mass of 105 000 daltons (p105). Of these transformed cell antigens which were immunogenic in a syngeneic system, only p105 was detected in primary mouse kidney cell cultures. p105 isolated from normal and transformed mouse cells was demonstrated to be identical by two-dimensional gel analysis. Relatively small amounts of p105 were synthesized in quiescent primary cultures, while the protein was actively synthesized in SV40-infected as well as in proliferating mouse kidney cells, and its synthesis in quiescent cells could be induced by subjecting the cultures to glucose starvation or heat-shock treatment. Immunofluorescent staining and cellular fractionation showed that p105 is normally localized to cytoplasmic structures. The results suggest that the expression of p105 is intimately associated with the metabolic state of the cell.

Animals↗