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A A Moscona

Publications and source records attributed to A A Moscona.

At least 37 records · Page 2Linked to original sources
PubMed1984

Comparative characterization of monoclonal antibodies to carbonic anhydrase.

Monoclonal antibodies (Mabs) were generated to avian carbonic anhydrase-C and characterized; their reactivity with human, murine, bovine, chicken and fish erythrocyte carbonic anhydrase-C, and with human carbonic anhydrase-B was investigated by ELISA and electroblot techniques. Reactivity of the Mabs with native and SDS-denatured carbonic anhydrase was compared. Mabs that recognize antigenic determinants shared by all the carbonic anhydrases examined were identified. The results demonstrate the potential usefulness of these particular probes for investigating various aspects of function, evolution, development and regulation of this important, but not well understood group of enzymes.

Animals↗
PubMed1984

Cell disorganization and malformation in neural retina caused by antibodies to R-cognin: ultrastructural study.

Retina tissue from 6-day chick embryos was organ-cultured for 3 days in the presence of antibodies to R-cognin, a surface antigen of retina cells. The antibodies which are known to bind to this antigen caused a striking malformation: interruption of the outer limiting membrane and extensive cell disorganization resulting in exteriorization of many cells and forming of chaotic masses on the surface of the tissue. Controls did not show these effects. These results further confirm that R-cognin is involved in the mechanism of histotypic contacts and recognition of retina cells, and that it plays an essential role in cell organization and histogenesis in the retina.

Animals↗
PubMed1984

Cellular compartmentalization of carbonic anhydrase-C and glutamine synthetase in developing and mature mouse neural retina.

Using immunohistochemical methods, we have determined the cellular localization of the enzymes, glutamine synthetase (GS) and carbonic anhydrase-C (CA-C), in mouse neural retina during development and in the mature tissue. GS is always confined exclusively to the Müller glial cells; it is first detectable in these cells post-natally on about day 12, i.e. shortly before the eyes open. Also CA-C in the mature retina is localized in the Müller cells but, in addition, it is found in certain amacrine neurons as well. CA-C is first detectable in the retina already several days before birth; at that time it is found in most of the cells, with the exception of the emerging ganglion cells. However, with advancing differentiation, CA-C becomes progressively restricted to Müller cells and to a sub-category of amacrine neurons, and persists only in these cells in the mature retina. The present results extend our previous studies on these enzymes in the avian retina; they demonstrate that also in mammalian retina, different temporal and cellular patterns of GS and CA-C expression and localization earmark distinct phases of structural and functional differentiation of the retina. The striking developmental changes in the cellular localization of CA-C, and the finding of this enzyme in certain amacrine neurons as well as in Müller cells, raise questions about the role of CA-C in the retina, and about mechanisms regulating its expression in specific cell types.

Animals↗
PubMed1984

Variable CA II compartmentalization in vertebrate retina.

We have generated a series of polyclonal and monoclonal antibodies to mammalian, avian, and osteichthian CA II for the purpose of studying its distribution in vertebrate nervous systems. In mature chicken retina, CA II is immunohistochemically detectable only in Müller glial cells. However, during embryonic development, CA II expression is suddenly "switched-on" early as a general constituent of all retinoblasts, later becoming restricted to Müller cells and transiently to a distinct type of amacrine neuron. A similar developmental pattern occurs in mouse. However, at maturity high CA II levels remain in certain amacrine neurons in addition to Müller cells. Comparative analyses of mature retinas of lower vertebrates show that reptiles parallel chicken with high CA II only in Müller cells, certain amphibians show CA II staining in Müller cells, amacrine neurons as in mouse, and in horizontal neurons, teleost and elasmobranch fish possess high CA II in Müller cells and the horizontal neurons, and lamprey eel shows CA II staining primarily in horizontal cells. An evolutionary sequence that will be discussed is thus suggested.

Aging↗
PubMed1984

Effect of embryonic age on aggregability, histogenesis and biochemical differentiation in the embryonic chick and quail neural retina.

In this paper, the different ages of the chicken and quail embryonic retina cell aggregates are used to examine the aggregation, histogenesis, and the induction of glutamine synthetase (GS) elicited by hydrocortisone. The results show that the GS inducibility in the retina cells increases at a slow rate, then rises sharply on the 9th day, and after 9 days, the GS inducibility of aggregates decreases with the increase of embryonic age. The observed value of induced GS activity in the chick retina cells coaggregate with quail embryonic retina cells is less than the expected value. Bispecific cell coaggregates were observed when the 9-day chicken embryonic retina cells and the 71/2-day quail embryonic retina cells were combined and coaggregated, the chicken and quail cells formed three retinal rosettes. When the 9-day chicken embryonic retina cells were commingled with the 13-day quail embryonic retina cells, in the coaggregates, only one retinal rosette was formed.

Animals↗
PubMed1983

Hormonal induction of glutamine synthetase in cultures of embryonic retina cells: requirement for neuron-glia contact interactions.

Cortisol induces glutamine synthetase (GS) in gliocytes of chick embryo neural retina. Using adherent cultures of retina cells we have demonstrated that responsiveness of the gliocytes to GS induction by the hormone requires contact with neurons. GS is not inducible in high-density cultures depleted of neurons and consisting only of gliocytes. In neuron-containing cultures, induced GS was detected immunohistochemically only in those gliocytes that were closely juxtaposed with clusters of neurons. Unlike the induction of GS, the expression of carbonic anhydrase-C (which does not require cortisol) persisted in these glia cells also in the absence of neurons. The nature and role of glia-neuron interactions in the hormonal induction of GS are briefly discussed.

Animals↗
PubMed1983

Localization of retina cognin in embryonic neural retina tissue by immuno-scanning electron microscopy.

The retina cognin (a retina-specific cell-surface glycosylated protein that mediates self-recognition and morphogenetic contact associations of embryonic retina cells) was visualized by immunolabeling and scanning electron microscopy on the surface of cells within retina tissue of 9- and 16-day chick embryos. The photoreceptor processes which are free of contact with cells in the neural retina, were found to be devoid of surface cognin from early on in their development. These results extend previous studies on cognin localization and regeneration on separated retina cells in vitro and conclusively correlate its presence and surface topology with its postulated role.

Animals↗
PubMed1983

Transformation of retinal glia cells into lens phenotype: expression of MP26, a lens plasma membrane antigen.

We describe experiments in which dissociated cells from differentiated, post-mitotic neural retina of late chicken embryos (13 and 16 days) rapidly and consistently transform (transdifferentiate) in vitro into lens-like phenotype and form spherical lentoids. Using immunohistochemical and other tests, we have established that the lentoids arise from the progeny of definitive retinal glia cells (Müller cells). An early event in their transformation is the appearance in the cell surface of MP26, a plasma membrane protein characteristic of lens but not found in the retina. The results support the hypothesis that the phenotype of definitive glia cells in the retina is stabilized by contact-mediated interactions with neurons; disruption of cell contacts and cell separation alter surface properties of the glia cells, decontrol their phenotype, and predispose them to phenotype transformation.

Animals↗
PubMed1982

Changes in patterns and synthesis of proteins in embryonic neural retina studied by 2-dimensional gel electrophoresis.

Changes in protein patterns during early differentiation of embryonic neural retina (chick) were studied by 2-dimensional gel electrophoresis. The procedures employed here made it possible to visualize the overall population of proteins present in the tissue at a given time and, on the same gel to distinguish labeled from unlabeled proteins. 2-Dimensional gels were stained by a highly sensitive silver stain to visualize, map and quantitate proteins (and polypeptides) resolved by electrophoresis; the same gels were then autoradiographed in order to differentiate between actively synthesized and pre-existing proteins at each development stage. The effectiveness of this combinative analysis was first verified by identifying and localizing glutamine synthetase, an inducible enzyme marker of retina differentiation. Next, protein patterns in retina tissue at 2 embryonic ages were compared. Of the large number of spots visualized by the above methods approximately 10% showed distinct qualitative-quantitative developmental changes; these were grouped into 7 classes representative of major modes of alteration of protein patterns during cell differentiation.

Animals↗
PubMed1982

Cell contact-dependent regulation of hormonal induction of glutamine synthetase in embryonic neural retina.

Glutamine synthetase (GS) is a differentiation marker in the neural retina of the chick embryo. GS is localized specifically in Müller glia cells, and it can be precociously induced by adrenal corticosteroids (such as cortisol). The induction depends on cortisol-elicited gene expression and results in de novo synthesis of GS and in a multifold increase in its level. GS is inducible only when Müller cells are closely associated with retina neurons. When retina tissue from 10-day embryos is dissociated into single cells and these are maintained either in suspension or in monolayer culture, GS cannot be induced. However, if identically prepared cells are reaggregated and allowed to reconstruct retinotypic associations, they are inducible for GS. Measurements of cytoplasmic cortisol-receptors showed that cell dissociation results in a rapid and marked reduction in the level (or activity) of these receptors. Their low level persists if the cells are maintained in a dispersed state. However, if the cells are reaggregated and reestablish tissue-like contacts, the level of cortisol receptors increases, as does GS inducibility. The results indicate that, in the embryonic neural retina, histotypic cell contacts are involved in regulating the level of cytoplasmic cortisol receptors and of the responsiveness of Müller glia cells to the induction of GS. Whether the two aspects are causally related is a matter for future study.

Animals↗
PubMed1981

Development of differential affinities and positional information in embryonic retina cells: inhibition by BrdU.

Embryonic neural retina cells fail to develop surface properties for type-specific cell recognition if they are transiently exposed to BrdU during an early, critical age. Such cells do not proceed with histogenetic positioning, organization and differentiation and, instead, form a malformed cell mass. This effect of BrdU is correlated with BrdU incorporation into DNA, and it can be prevented by simultaneous treatment of the cells with cytosine arabinoside. The proposed working hypothesis is that, in this system, BrdU interferes with expression of genes controlling cognitive specification of the cell surface.

Animals↗
PubMed1981

Induction of glutamine synthetase in embryonic neural retina: its suppression by the gliatoxic agent alpha-aminoadipic acid.

Competence for cortisol-mediated induction of glutamine synthetase (GS) is a differentiation marker of embryonic neural retina. Earlier work has indicated that the induction and accumulation of GS is localized in the Müller glia cells. This localization was presently confirmed by the finding that the gliatoxin D,L-alpha-amino-adipic acid (AAA) reduces responsiveness to GS induction by 60--90% due to preferential damage to Müller cells. The tests were performed on organ cultures of retina tissue from chick embryos, and on retina cell aggregates in which there is tissue reconstruction. The presence of GS-inducible Müller cells was monitored by immuno-staining of tissue sections with anti-GS antiserum. Reduction of GS inducibility due to pretreatment with AAA resulted in virtual absence of cells that immunostained for GS. The preferential toxicity of AAA for Müller cells was also demonstrated by cell viability tests; it was further corroborated by the finding that treatment with AAA greatly reduced the level of carbonic anhydrase activity, another enzyme localized predominantly in Müller cells, but did not affect gamma-aminobutyric acid transaminase and choline acetyl transferase, neuronal enzymes. Susceptibility of Müller cells to AAA was found to increase with embryonic development of the retina. We suggest that acquisition of susceptibility for AAA represents another differentiation marker of embryonic Müller cells.

2-Aminoadipic Acid↗