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PubMed1988

Monoclonal antibody EBM/11: high cellular specificity for human macrophages.

A monoclonal antibody, EBM/11, was raised against isolated human lung macrophages. Immunohistochemically this antibody reacted with freshly isolated lung macrophages and blood monocytes, mononuclear cells (presumptive macrophages) in sections of lung, skin, stomach, small and large bowel, pancreas, spleen, tonsil, placenta, liver, gall bladder, heart, thyroid, pituitary, brain, and peritubular and mesangial cell in kidney. Microglial cells and osteoclasts also labelled with EBM/11. The antibody reacted with cytoplasmic structures rather than with cell membranes. The epitope recognised by EBM/11 was present on four polypeptides (of 120, 70, 64 and 22 kilodaltons). It did not react with any other cell type in the tissues screened except the epithelium of renal proximal tubules. This antibody may be useful in identifying and elucidating the function of macrophages in pathological processes.

Antibodies, Monoclonal↗
PubMed1976

Cancer, retrodifferentiation, and the myth of Faust.

The close relationship at the molecular level between cellular differentiation and neoplasia has been evidenced by the discovery in adult individuals of fetospecific antigens and fetal type isozymes associated with many spontaneous and experimentally induced malignant tumors. One question in relation with this finding is whether cancerous tumors develop from the differentiation of a tissue reserve of stem cells or by a process of retrodifferentiation, i.e., the nucleocytoplasmic stepwise reversion of cells toward stationary states with simplified structure and less information content. The question is not merely academic; elucidation of the nature of the target cells from which neoplastic growth emerges has obviously physiopathological and therapeutic implications. This contribution is an analysis of the nature and the mechanism of cellular retrodifferentiation and a discussion of its possible role in regeneration and metaplasia, as well as in neoplastic development. Throughout living systems, retrodifferentiation appears as a common adaptive process for the maintenance of cell integrity against deleterious agents of varied etiology (physical, chemical,and viral). While preserving the entire information encoded on its genome, cells undergoing retrodifferentiation lose morphological and functional complexity by virtue of a process of self-deletion of cytoplasmic structures and the transition to a more juvenile pattern of gene expression. This results in a progressive uniformization of originally distinct cell phenotypes and to a decrease of responsiveness to regulatory signals operational in adult cells. Retrodifferentiation is normally counterbalanced by a process of reontogeny that tends to restore the terminal phenotypes from where the reversion started. This explains why retrodifferentiation remains invariably associated to cell regeneration and tissue repair. There is an ever growing evidence that neoplastic transformation in vivo and in vitro is frequently preceded and/or accompanied by biochemical, morphological, and behavioral transitions characteristic of a cell undergoing retrodifferentiation. Contrary to what occurs in regenerating tissues, the "unbalanced" character of tumor-associated retrodifferentiation seems to be a property linked to cancer. The question arises why a unique mechanism of cell rejuvenation is in physiological conditions (regeneration), followed by a process of reontogeny, while in neoplasia the process remains incomplete or does not occur and leads to the emergence of a population of persistently dividing cells. It is to be hoped that a careful study of retrodifferentiation in physiological and tumoral models will help to distinguish that which in neoplastic development can be relevant to an adaptive cell behavior from that which might eventually be the result of specific or constitutive alterations.

Adaptation, Physiological↗
PubMed1995

Recombinant expression of the brush border myosin I heavy chain.

Although the specific functions of myosin I motors are not known, their localization to membrane structures suggests a function in membrane motility. Different myosin I isoforms in the same cell or in different cells can possess different localizations. To determine if the localization and biochemical activity of the best-characterized mammalian myosin I, chicken intestinal epithelium brush border myosin I, was dependent on determinants of the membrane or actin cytoskeleton specific to epithelial cells, we transfected the cDNA for the heavy chain of this myosin into COS cells. Transient transfection of COS cells with the chicken brush border myosin heavy chain resulted in the production of recombinant myosin I. Recombinant brush border myosin I localized to protrusions of the plasma membrane, particularly at spreading edges, and also to unknown cytoplasmic structures. Some cells expressing particularly high levels of brush border myosin I possessed a highly irregular surface. Recombinant brush border myosin I purified from COS cells bound to actin filaments in an ATP-dependent manner and decorated actin filaments to form a characteristic appearance. The recombinant myosin also catalyzed calcium-sensitive, actin-activated MgATPase activity similar to that of the native enzyme. Thus, any cellular factor required for the general membrane localization or biochemical activity of brush border myosin I is present in COS cells as well as intestinal epithelium.

Actins↗
PubMed1987

Tunneling cell processes in myocytes of stretched mouse atria.

Serial section electron micrographs of mouse atria stretched in vitro show that myocytes have cell processes which tunnel into adjacent myocytes for 8 microns or more. The tunneling cell processes (TCP) (diam 4-6.2 microns) lack myofibrils and organelles associated with atrial peptide secretion. The glycogen-rich TCP cytoplasmic matrix contains conspicuous tubules and vesicles originating from endoplasmic reticulum and resembling free sarcoplasmic reticulum (SR). TCP are surrounded by a plasmalemma derived from their myocyte of origin, the plasmalemma of the tunneled myocyte, and an intervening narrow compartment continuous with the interstitial space. Profiles having the characteristics cytoplasmic structure of TCP are also found both in the interstitial space between myocytes and near the longitudinal terminations where myocyte ends about on the interstitial space. We suggest that TCP tubules and vesicles may proliferate and/or transport in response to stretch, might be free SR, and may respond to stretch-activated changes in ionic composition or potential of the surrounding myocyte and narrow intercellular compartment.

Animals↗
PubMed1978

Transient acantholytic dermatosis with involvement of oral mucosa.

Histologic, immunologic and electron microscopic studies were performed in a patient with transient acantholytic dermatosis which involved oral mucosa. Hitologic and electron microscopic findings were almost identical in both cutaneous and mucous membrane lesions, and these were similar to pemphigus vulgaris; suprabasilar separation with acantholytic cells. Desmosome-desmosome complexes were separated without disruption of cell membranes and cytoplasmic structures were well-preserved without dyskeratosis. Lamina lucida, however, was often separated in mucous membrane lesions, in contrast to the normal lamina lucida in cutaneous lesions of such cases or in pemphigus vulgaris. Direct and indirect immunofluorescence studies for pemphigus were repeatedly negative. This study shows that transient acantholytic dermatosis may involve mucous membrane and may resemble pemphigus vulgaris histologically and ultrastructurally except for the widened lamina lucida of the mucous membrane.

Acantholysis↗
PubMed1993

Effects of difloxacin on the metabolism of glycosaminoglycans and collagen in organ cultures of articular cartilage.

Fluoroquinolones, including difloxacin, are potent antibacterial compounds which, as a side effect, cause lesions in articular-epiphyseal cartilage complexes (AECC) of growing animals. To evaluate the effects of difloxacin on the structure of AECC and the metabolism of sulfated glycosaminoglycans (GAG) and collagen, explants of AECC were obtained from 18 healthy, 3-month-old Beagle dogs and cultured in medium which either had no difloxacin or had the drug at one of three concentrations (40, 80, or 160 micrograms/ml). Rates of synthesis of GAG and collagen were reduced by concentrations of difloxacin that were at or above 80 micrograms/ml. The rate of synthesis of total protein, however, was reduced only at the highest dose level. Catabolism of GAG and collagen was unaffected by the treatment. The principal ultrastructural changes in affected chondrocytes were distension of rough endoplasmic reticulum with electron-dense material that was probably protein, and vacuolation of cytoplasm. Structural changes were not observed in the extracellular matrix. It, therefore, appeared plausible that difloxacin affected chondrocytes by interfering with secretion of the matrix components, GAG and collagen.

Animals↗
PubMed1997

Death substrates come alive.

Interleukin 1 beta-converting enzyme (ICE)-like proteases (caspases) play an important role in programmed cell death (apoptosis), and elucidating the consequences of their proteolytic activity is central to our understanding of the molecular mechanisms of cell death. Diverse structural and regulatory proteins and enzymes, including protein kinase C delta, the retinoblastoma protein (a protein involved in cell survival), the DNA repair enzyme DNA-dependent protein kinase and the nuclear lamins, undergo specific and limited endoproteolytic cleavage by various caspases during apoptosis. Since individual caspases can cleave multiple substrates, the consequences of cleavage of only a single substrate are still poorly understood. Nevertheless, proteolytic activation of protein kinase C delta may be an important early step in the cell death pathway, and cleavage of the retinoblastoma protein could suppress its cell survival function, whereas proteolytic inactivation of DNA repair enzymes might compromise the ability of the cell to reverse DNA fragmentation. On the other hand, cleavages of nuclear and cytoplasmic structural proteins (e.g. the lamins and Gas2) appear to be required for or contribute to the dramatic rearrangements in cellular architecture that are necessary for the completion of the cell death process. An emerging theme is that parallel and sequential proteolytic activation and inactivation of key protein substrates occurs during the multiple steps of apoptosis.

Animals↗
PubMed1980

Immunocytochemical localization of intracellular antigens with SEM.

A method for the localization of intracellular antigens with a scanning electron microscope using peroxidase-labelling antibodies is described. A search for a hydrogen donor which may be deposited at the sites of antigen by enzymatic action and emit secondary electrons or generate backscatter electrons was made. It was found that when 4-chloro-1-naphthol was used, the peroxidase deposited reaction product which resulted in a strong secondary electron emission at the site of antigen. With this method, the presence of luteinizing hormone in secretion granules and other cytoplasmic structures of gonadotropic cells was demonstrated. The level of detection of intracellular antigens with this method is not as high as that detectable with light microscopical examination of the same specimens, that is, more reaction product at the site of antigen is required to be detectable with scanning electron microscopy than with light microscopy. In spite of the lack of high sensitivity, the intracellular antigens may be localized with the method described.

Animals↗
PubMedDate not supplied

Confronting cisternae and ciliated cells in malignant pleural mesothelioma: an ultrastructural study.

The incidence of malignant mesothelioma of the pleura has recently increased in Japan, and ultrastructural and immunohistochemical studies can help in the histopathologic diagnosis. Confronting cisternae consist of dense laminae between the cisternae of rough endoplasmic reticula. Cylindric confronting cisternae have recently been found in patients with acquired immunodeficiency syndrome. The pathologic significance of this unusual structure is still obscure, but it has been proposed that trapped ribosomes on the confronting unit membranes of rough endoplasmic reticula produce the dense laminae. In this study, prominent confronting cisternae were found in more than half the tumor cells, and accumulation of an electrondense fine granular substance surrounded by Golgi vesicles (so-called vesicular rosettes) were noted and found to be continuous with the dense laminae. The nature and origin of the vesicular rosettes are important with regard to the formation and significance of confronting cisternae. Oligocilia have been found in various metaplastic and neoplastic cells and are thought to be nonspecific. There has been only one report of ciliated cells and confronting cisternae in a malignant peritoneal mesothelioma, however, indicating that these unusual cytoplasmic structures might be related to some epithelial-type mesotheliomas.

Adult↗
PubMed1992

Sample preparation of animal tissues and cell cultures for secondary ion mass spectrometry (SIMS) microscopy.

Sample preparation is a critical step in the elemental analysis of animal tissues and cell cultures with ion microscopy. Since live cells cannot be analyzed with ion microscopy, a careful sample fixation is necessary which preserves the native structural and chemical integrity of a specimen. The evaluation of morphological and chemical integrity of a fixed specimen is necessary before any physiological explanation of ion fluxes is interpreted based on ion microscopy. For diffusible ion localization studies, strict cryogenic procedures are recommended. Examples are shown for diffusible ion microanalysis in frozen-freeze-dried tissues and cell cultures. Ion microscopy studies of tightly bound elements/molecules may be conducted in chemically fixed and/or plastic embedded specimens. Since it is not generally known which elements/molecules are tightly bound to the tissue matrix, a confirmation of elemental distribution with cryogenic procedures is desirable. A recent approach of combining laser scanning confocal fluorescence microscopy and ion microscopy on the same frozen freeze-dried cell is also discussed for recognizing smaller cytoplasmic structures in ion microscopy images.

Animals↗
PubMed1975

Ultrastructural changes in livers of tumour bearing rats.

An ultrastructural study of the livers of rats bearing transplanted mammary carcinomata from 4 to 12 weeks after transplantation revealed changes mainly in cytoplasmic structure of hepatocytes. The significant findings were pleomorphism of mitochondria, presence of large number of myelin figures, marked increase in microbodies, dilatation of rough endoplasmic reticulum, proliferation of smooth endoplasmic reticulum, intracytoplasmic cholesterol clefts and absence of increase in lysosomes. These alterations have been compared with that of others who have used different animal model systems to study the effect of tumour in livers of host. Centrioles in Küpffer cells are described for the first time in this study.

Animals↗
PubMed1984

The protein A-gold technique. Use in the immunoelectron microscopic study of the teleost growth hormone.

By the application of the protein A-gold technique for immunocytochemistry of the tilapia pituitary growth hormone (GH), our electron micrographs revealed that the antigenicity of tilapia GH and the cytoplasmic structure were well preserved in the tissues fixed with periodate-lysine-paraformaldehyde followed by osmium tetroxide postfixation. Using the specific antiserum against tilapia GH, the immunoreactive gold particles of 20-40 nm in size were located on secretory granules (200-300 nm in diameter) exclusively of one cell type in the proximal pars distalis identified as GH cells on the basis of their ultrastructural characteristics. This technique is considered to be fairly efficient for the detection of intracellular antigenic sites on ultrathin sections.

Animals↗
PubMed1987

The normal structure of regional feline gastric mucosae: scanning electron microscopic study.

Regions of cat's stomach can be identified by looking at the surface epithelial cells by scanning electron microscopy (SEM). The luminal surface of cells of the cardiac region were elongated, of the fundus rounded, of the corpus polygonal shaped, and of the pyloric region diamond shaped. The quantity and distribution of microvilli covering the epithelial cells varies, being abundant and evenly distributed in the cardiac region and gradually decreasing in number toward the gastro-duodenal junction, where they were confined to cell perimeters. The colliculi varied in shape and distribution from few in the fundus and corpus to numerous in the pyloric region. Large numbers of gastric pits were present in the corpus. They diminish toward both the cardia and gastro-duodenal junction. The cardiac and pyloric glands were coiled. The gastric glands (glandula gastrica propria) were straight tubules in the fundus and coiled in the corpus. All luminal surfaces of glandular epithelial cells were covered with microvilli, but the regional distribution of microvilli on the cell was variable. Parietal, mucous neck, and chief (zymogen) cells were identified by their cytoplasmic structure. Parietal cells had long apical microvilli, mucous neck cells contained large numbers of globular mucous granules, and chief cells were vacuolated. A few G cells (Endocrinocytus gastrointestinalis) were seen in the cardiac region, large numbers in the pyloric region, and not found in fundus or corpus.

Animals↗
PubMed1997

The C. elegans MEX-1 protein is present in germline blastomeres and is a P granule component.

In the nematode Caenorhabditis elegans, germ cells arise from early embryonic cells called germline blastomeres. Cytoplasmic structures called P granules are present in the fertilized egg and are segregated into each of the germline blastomeres during the first few cleavages of the embryo. Mutations in the maternally expressed gene mex-1 disrupt the segregation of P granules, prevent the formation of germ cells, and cause inappropriate patterns of somatic cell differentiation. We have cloned the mex-1 gene and determined the distribution pattern of the mex-1 gene products. The MEX-1 protein contains two copies of an unusual 'finger' domain also found in the PIE-1 protein of C. elegans. PIE-1 has been shown to be expressed in germline blastomeres, and is a component of P granules. We show here that MEX-1 also is present in germline blastomeres and is a P granule component, although MEX-1 is a cytoplasmic protein while PIE-1 is present in both the nucleus and cytoplasm. We further show that MEX-1 is required to restrict PIE-1 expression and activity to the germline blastomeres during the early embryonic cleavages.

Amino Acid Sequence↗
PubMed1983

Myeloid bodies in drug-induced acute tubular necrosis.

A growing list of drugs, metals, and chemicals has been implicated as the cause of functional and structural damage specifically to the proximal tubular epithelium. Renal biopsies were obtained from three patients who had developed nephrotoxic agent-related acute renal failure. Two of the patients had received gentamicin and viomycin; the third patient had heavy exposure to chromium. All three biopsies showed acute tubular necrosis (ATN) on light microscopy. Electron microscopy revealed that the proximal tubular cells and, to a lesser degree, the distal tubular cells, contained abundant, variably sized myeloid bodies. In our previous experimental study of viomycin-induced ATN in rats, similar ultrastructural findings of a gradual increase in the number of myeloid bodies in the proximal tubular cells were also observed. The constant presence of myeloid bodies in the tubular epithelial cells following drug-induced tubular necrosis suggests that they may represent lysosomal isolation of drug-bound cytoplasmic structures, as a cellular mechanism to degrade toxic substances and, therefore, may serve as an ultrastructural marker of cellular drug uptake and drug disposition.

Acute Kidney Injury↗
PubMed1984

Aggregate-carrying membranes during ADH stimulation and washout in toad bladder.

Aggregates of intramembrane particles are found in cytoplasmic structures that we now term "aggrephores." Antidiuretic hormone (ADH) causes aggrephores to fuse with the luminal membrane. Aggregates subsequently become dispersed in the membrane and behave as sites for water flow. In the present studies we examined further the behavior of aggrephores. 1) Bladders stimulated for 10, 30, or 60 min in the absence of an osmotic gradient had two to three times more fusions as those stimulated in the presence of a gradient, indicating that aggrephore fusion frequency is influenced by water flow. 2) ADH stimulation did not change the projected luminal surface area of granular cells. Thus fused aggrephores remain fixed while aggregates move from the aggrephore to flat areas of luminal membrane. 3) Horseradish peroxidase, present in the mucosal baths of bladders stimulated with and then washed of ADH, was found in the lumen of cytoplasmic aggrephores; aggrephores therefore detach from the luminal membrane during washout. The same bladders had about twice as many multivesicular body-type lysosomes as unstimulated bladders, suggesting that, after detachment, aggrephores may join or become lysosomes. 4) Colchicine did not affect the rate of disappearance of fusion sites during washout, whereas cytochalasin B slowed it, suggesting that aggrephore detachment depends of microfilaments, but not microtubules.

Animals↗
PubMed1988

[Differential cytology of malignant melanoma].

On the basis of 285 fine needle biopsies and smear preparations of malignant melanoma (both primaries and metastases), we present a catalogue of highly characteristic cytologic features: dissociation of melanoma cells, excessive dimension of the tumor cells, characteristic staining of the cytoplasm, structure of the nucleus, features of the nucleoli, aberrations of mitoses and amitoses. With the help of the cytologic catalogue, we are able to differentiate melanoma in a contrasting way from other diseases such as pigmented seborrheic keratosis, basal cell carcinoma, squamous cell carcinoma, and various lymphomas. Thus the differential cytology of malignant melanoma can be referred to for general criteria of malignancy on the one hand, as well as for the diagnosis of the specific tumor type and the epicrisis of uncertain histologic aspects on the other.

Cell Nucleus↗
PubMed1996

Cytoplasmic sequestration of wild-type p53 protein impairs the G1 checkpoint after DNA damage.

Wild-type p53 protein is abnormally sequestered in the cytoplasm of a subset of primary human tumors including neuroblastomas (NB) (U. M. Moll, M. LaQuaglia, J. Benard, and G. Riou, Proc. Natl. Acad. Sci. USA 92:4407-4411, 1995; U. M. Moll, G. Riou, and A. J. Levine, Proc. Natl. Acad. Sci.USA 89:7262-7266, 1992). This may represent a nonmutational mechanism for abrogating p53 tumor suppressor function. To test this hypothesis, we established the first available in vitro model that accurately reflects the wild-type p53 sequestration found in NB tumors. We characterized a series of human NB cell lines that overexpress wild-type p53 and show that p53 is preferentially localized to discrete cytoplasmic structures, with no detectable nuclear p53. These cell lines, when challenged with a variety of DNA strand-breaking agents, all exhibit impaired p53-mediated G1 arrest. Induction analysis of p53 and p53-responsive genes show that this impairment is due to suppression of nuclear p53 accumulation. Thus, this naturally occurring translocation defect compromises the suppressor function of p53 and likely plays a role in the tumorigenesis of these tumors previously thought to be unaffected by p53 alterations.

Cytoplasm↗