Proteoglycan synthesis in cultures of murine retinal neurons and photoreceptors

Murillo-Lopez, Fernando; Politi, Luis E.; Adler, Ruben; At, Hewitt

doi:10.1007/bf00741447

Cited by 11 publications

(3 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A number of other studies have also provided evidence for the role of IPM chondroitin sulfate proteoglycans in retinal adhesion [3,5,18]. The reported synthesis of proteoglycans by embryonic neural retinal cells and photoreceptors [20,21] provides support for the synthesis of chondroitin sulfate by retinal cells in our transgenic mouse model. TGF-β is well known to enhance the synthesis of extracellular matrix components like proteoglycans, collagen, and fibronectin [6,8,12].…”

Section: Resultssupporting

confidence: 62%

Neuron-specific TGF-β signaling deficiency results in retinal detachment and cataracts in mice

Honjo

Nagineni

Larsson

et al. 2007

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

We generated a mouse model (cKO) with a conditional deletion of TGF-β signaling in the retinal neurons by crossing TGF-β receptor I (TGF-β RI) floxed mice with nestin-Cre mice. Almost all of the newborn cKO mice had retinal detachment at the retinal pigment epithelium (RPE)/photoreceptor layer junction of the neurosensory retina (NSR). The immunostaining for chondroitin-6-sulfate showed a very weak reaction in cKO mice in contrast to intense staining in the photoreceptor layer in wild-type mice. Macroscopic cataracts, in one or both eyes, were observed in 50% of the mice by six months of age, starting as early as the first month after birth. The cKO mouse model demonstrates that the TGF-β signaling deficiency in retinal cells leads to decreased levels of chondroitin sulfate proteoglycan in the retinal interphotoreceptor matrix. This in turn causes retinal detachment due to the loss of adhesion of the NSR to RPE.

show abstract

Section: Resultssupporting

confidence: 62%

Neuron-specific TGF-β signaling deficiency results in retinal detachment and cataracts in mice

Honjo

Nagineni

Larsson

et al. 2007

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

show abstract

“…We examined embryonic mouse eyes in order to establish the temporal relationship between the appearance of the F22 antigen and retinal development. Since chondroitin sulfate proteoglycans (CS-PG) are present in the IPM as well as in several other extracellular compartments in the eye (Porello and LaVail, 1986;Murillo-Lopez et al, 1991;Snow et al, 19911, we wanted to compare their distribution with that of the F22 antigen in order to have a broader basis for the specific characterization of the F22 distribution. The ages E11.5-13.5 were chosen due to the specific differentiation of ganglion cells and the transient expression of CS-PGs at this time (Snow et al, 1991;Brittis et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Redistribution of insoluble interphotoreceptor matrix components during photoreceptor differentiation in the mouse retina

Mieziewska

Szél

Veen

et al. 1994

J of Comparative Neurology

View full text Add to dashboard Cite

The development of the nervous system is largely influenced by the extracellular matrix (ECM). In the neural retina, the photoreceptors are surrounded by a unique ECM, the interphotoreceptor matrix (IPM). The IPM plays a central and possibly crucial role in the development, maintenance and specific function of the photoreceptors. Therefore, the characterization of IPM components is necessary to understand the mechanisms regulating photoreceptor differentiation. The IPM in the mouse retina was examined during photoreceptor morphogenesis with the monoclonal antibody (MAb) F22, which recognizes a 250 kDa component of the interphotoreceptor matrix. The binding pattern of MAb F22 revealed a striking redistribution in the expression of the 250 kDa F22 antigen in late stage of postnatal photoreceptor differentiation in the mouse retina. The F22 staining was detectable in the IPM around the inner segments on the third postnatal day (P3). The MAb F22 initially labeled the region around inner segments, but as the outer segments elongated, the F22 distribution became concentrated to the matrix around the rod and cone outer segments until P16-17. At P17, the F22 label around rods began to disappear, while the label around cones became more defined. The shift in label distribution was largely completed by P20. Residual rod-associated label disappeared within a few days. In the adult animal, the F22 antibody labeled the cone-associated matrix only, and this labeling pattern remained stationary. The change in the distribution of MAb F22 demonstrated by immunolabeling was not accompanied by changes in the size of the molecule; F22 antigen isolated from the IPM of P13-15, and from adult IPM migrated with the same molecular weight on SDS gels. The distribution of MAb F22 was compared to that of chondroitin sulfate proteoglycans which are abundant in the IPM. The labeling patterns of MAbs CS-56, C6-S and C4-S were distinct from that of MAb F22. A general decrease of the label intensity was seen with two chondroitin sulfate MAbs (CS-56 and C4-S) between 16 days and 4 months, but a total loss of rod-associated label was not observed. All three chondroitin sulfate MAbs labeled the retina at embryonic day (E) 11.5-13.5, a time of outgrowth of ganglion cell axons, but the F22 antigen was not detected in the retina at this stage of development. The results demonstrate that the F22 and the chondroitin sulfate antibodies are recognizing different molecules that have distinct roles in retinal morphogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)

show abstract

“…accumulations of HSPG are in the basal lamina along the vitreal border, the so-called "inner limiting membrane" of the retina . Embryonic and neonatal retina cells synthesize substantial amounts of CSPG and HSPG (Needham et al ., 1988;Threlkeld et al, 1989;Burg and Cole, 1990;Murillo-Lopez et al, 1991). In normal adult retinas, synthesis of CSPG predominates (Morris et al, 1977 ;Landers and Hollyfield, 1992).…”

mentioning

confidence: 99%

Increased Retinal Synthesis of Heparan Sulfate Proteoglycan and HNK‐1 Glycoproteins Following Photoreceptor Degeneration

Landers

Rayborn

Myers

et al. 1994

Journal of Neurochemistry

View full text Add to dashboard Cite

In an earlier analysis of the retinal biosynthesis of proteoglycan, we noted that, following photoreceptor degeneration in the rd (retinal degeneration) mouse, the remaining inner retina exhibited a marked elevation in synthesis of heparan sulfate proteoglycan (HSPG), well above the level observed in the normal (nondegenerate) retina, as well as a pronounced increase in sulfation of protein substrates. Biochemical and autoradiographic results of 35S‐amino acid utilization reported here confirm that the 35SO42− differences seen previously are accompanied by increased protein synthesis in the rd retina. An intact photoreceptor cell layer is neither a barrier to nor a sink for the amino acid precursor. Further, we have examined sulfate utilization in four other rodent strains with photoreceptor degenerations. In each of the models examined, an increase in retinal synthesis of 35SO42−‐labeled HSPG and glycoproteins occurs following photoreceptor degeneration. We have metabolically labeled with Na235SO4 isolated retinal cultures from the following: (a) mice with light‐induced photoreceptor degeneration; (b) rd mice; (c) transgenic mice with photoreceptor degeneration; (d) RCS rats; and (e) rats with light‐induced photoreceptor degeneration. Comparisons were made with concurrent cultures of control nondegenerate retinal tissues. Protein and proteoglycan‐enriched fractions were prepared from the incubation media and guanidine HCI/detergent extracts of the retinas by ion‐exchange chromatography. The 35SO42−‐proteoglycans were identified by chondroitinase ABC and nitrous acid treatments. Retinas lacking photoreceptors produced at least five times the amount of 35SO42−‐HSPG found in control incubations. The RCS and light‐damaged rats also showed increased synthesis of 35SO42−‐chondroitin sulfate proteoglycan relative to the control, though the increase was of lesser magnitude than the HSPG effect. 35SO42−‐protein in degenerate and light‐damaged retinas always contained at least twice the radioactivity found in comparable control preparations. The bulk of the increased radiolabeling was found in N‐linked oligosaccharides, including several recognized by the HNK‐1 antibody. These data suggest that a sustained increase in HSPG and HNK‐1 glycoprotein synthesis is a consistent response of inner retinal cells following loss of photoreceptors and is independent of the cause of photoreceptor degeneration.

show abstract

Proteoglycan synthesis in cultures of murine retinal neurons and photoreceptors

Cited by 11 publications

References 37 publications

Neuron-specific TGF-β signaling deficiency results in retinal detachment and cataracts in mice

Neuron-specific TGF-β signaling deficiency results in retinal detachment and cataracts in mice

Redistribution of insoluble interphotoreceptor matrix components during photoreceptor differentiation in the mouse retina

Increased Retinal Synthesis of Heparan Sulfate Proteoglycan and HNK‐1 Glycoproteins Following Photoreceptor Degeneration

Contact Info

Product

Resources

About