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Biomedical subjects

L Degenstein

Publications and source records attributed to L Degenstein.

26 records · Page 2Linked to original sources
PubMed1986

Retinoic acid inhibits conversion of dissociated Müller glia into lens-like cells.

In monolayer cultures of dissociated retina cells, Müller gliocytes undergo conversion into a lens-like cell type (lentoidal cells): they become unable to adhere to neurons and accumulate lens antigens. Retinoic acid (RA) retards these changes. We present evidence that RA prevents the rapid loss of gliocyte adhesivity to neurons; and that, by promoting restoration of glia cell contacts with neurons, RA protects the gliocytes from phenotype alteration.

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PubMed1985

Antiserum to lens antigens immunostains Müller glia cells in the neural retina.

Antiserum to a lens fraction enriched for alpha-crystallin selectively immunostains Müller glia cells in the neural retina of several vertebrate species. Also, in embryonic retina (chicken), this antiserum reacts with Müller cells and, at early stages of development, with their apparent precursors. Thus, antibodies to a lens product(s) detect a Müller glia cell marker that begins to be expressed very early in their ontogeny and can be useful in studies on differentiation, function, and pathologies of this cell type.

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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↗
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

Normal development and precocious induction of glutamine synthetase in the neural retina of the quail embryo.

The developmental pattern of glutamine synthetase (GS) in the neural retina of the quail embryo is described and correlated with retina growth and differentiation. We show that GS in the quail retina can be precociously induced by cortisol, and that the enzyme is localized in Müller glia cells. The results are compared with the development and induction of GS in chick retina.

Animals↗