Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “retinal development”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,027 records · Page 57Linked to original sources
PubMed1982

[Clinical and experimental results in the treatment of massive periretinal proliferation (MPP), a retinal detachment with a most unfavorable prognosis].

Today eyes with massive periretinal proliferation which are often seen after uncured retinal detachments or after perforating injuries can be cured at least in 25 to 35% of the cases, even with modern surgical techniques. This is due to proliferation of cells, which enter through different pathways--retinal tears, perforating wounds of sclera and chorioidea, damaged retina or retinal vessels--into the vitreous and form membranes, which prevent the retina to attach. In the vitreous gel these cells of different origin can transform into fibroblast-like or myofibroblast-like cells. They also behave in the same way like fibroblasts or myofibroblasts and cause a kind of excessive wound healing and scar formation in the vitreous cavity. With the use of modern vitreous techniques we could cure nearly 43% of 14 patients with MPP after uncured retinal detachments or after perforating injuries. Because mechanical removal of intravitreal and periretinal membranes alone turned out to be unsuccessful in nearly 60%, methods of medical therapy to suppress this cell-activity seemed to be rather needed. By animal experiment we tried to produce retinal detachments by transplantation of homologue fibroblasts into the vitreous cavity of rabbit eyes, and observed traction detachments in 55% of the eyes. Histologic examination showed a rapid change of loose, round fibroblasts into elongated cells with long nuclei, which formed strands and caused vasoproliferation, especially where the strand reached the rabbit retina. By means of autoradiography the peak of cell activity turned out to be in the 3rd week after cell-transplantation and further examinations of the optic disc showed, that the vascular endothelium cell might be one source of the proliferation. There was no difference between the number of eyes which developed retinal detachment in the aphakic eyes and in the lentectomized and vitrectomized eyes, but we observed the clinical appearance of MPP earlier and more pronounced in the lentectomized and vitrectomized eyes. In the last experiment we tried to inhibit intraocular proliferation with intravitreal dexamethasone alcohol. This leaded to a significant reduce of the number of experimental detachments and vasoproliferations.

Adolescent↗
PubMed1998

Rat messenger RNA for the retinal pigment epithelium-specific protein RPE65 gradually accumulates in two weeks from late embryonic days.

The RPE65 protein appears late during the retinal development. To study the basis for this regulation, the rat RPE65 cDNA was sequenced and the mRNA subsequently quantitated at various stages by competitive RT-PCR. RPE65 mRNA was detected as early as E18 (36 copies/ng of whole eye total RNA). It gradually accumulates up to P12 (27000 copies/ng) at which point it reaches a steady state level. This increase is interrupted for 3 days (P2-P4) during which the levels of mRNA remain stable. This timing and rate of accumulation parallels that of rat and mouse opsin mRNA and suggests that common factors may control the activation of genes in photoreceptors and retinal pigment epithelium cells.

Animals↗
PubMedDate not supplied

Interleukin-2 immunotherapy of murine cytomegalovirus retinitis during MAIDS correlates with increased intraocular CD8+ T-cell infiltration.

AIDS-related human cytomegalovirus retinitis continues to be an important sight-threatening disease in AIDS patients who do not respond to highly active antiretroviral therapy. We have shown previously that systemic cytokine immunotherapy with interleukin-2 (IL-2) will protect against experimental murine cytomegalovirus (MCMV) in mice with a murine retrovirus-induced immunodeficiency syndrome (MAIDS). Since IL-2 serves as a Th1 immunoregulatory cytokine, we hypothesized that IL-2-induced protection against MCMV retinitis during MAIDS would correlate with a measurable increase in the number of natural killer (NK) cells and/or CD8+ T cells that infiltrate the eye in response to MCMV infection of the retina. We therefore performed a study to quantify and compare the number of NK cells and CD8+ T cells that infiltrate MCMV-infected eyes in untreated and IL-2-treated mice with MAIDS at 3 days and 5 days after subretinal MCMV inoculation. Double-label flow cytometric analysis revealed the detection of measurable numbers of both NK cells and CD8+ T cells in MCMV-infected eyes of untreated MAIDS mice destined to develop retinitis. In contrast, IL-2 immunotherapy during MAIDS correlated with a 10-fold increase by day 5 after inoculation in the number of CD8+ T cells in MCMV-infected eyes destined to be resistant to retinitis. However, IL-2 immunotherapy during MAIDS had no appreciable effect on the number of NK cells that infiltrated MCMV-infected eyes. Taken together, our findings suggest that function of cytotoxic lymphocytes that infiltrate the eye may be more important than absolute numbers of cytotoxic lymphocytes that infiltrate the eye when assessing the protective effects of IL-2 immunotherapy on MCMV retinitis during MAIDS.

AIDS-Related Opportunistic Infections↗
PubMed2001

Atrophy of Müller glia and photoreceptor cells in chick retina misexpressing cNSCL2.

PURPOSE: To investigate whether and how the basic helix-loop-helix (bHLH) gene cNSCL2 is involved in retinal development. METHODS: cNSCL2, the chick homologue of human NSCL2, was isolated and sequenced. In situ hybridization was used to examine its spatial and temporal expression pattern in the retina. Replication-competent retrovirus RCAS was used to drive cNSCL2 misexpression in the developing chick retina, and the effect of the misexpression was analyzed. RESULTS: Expression of cNSCL2 in the retina was restricted. Its mRNA was detected in amacrine and horizontal cells, but not in photoreceptor, bipolar, or ganglion cells. Retroviral-driven misexpression of cNSCL2 in the developing chick retina resulted in missing photoreceptor cells and gross deficits in the outer nuclear layer (ONL). These deficits were probably not because of decreased photoreceptor production, in that the ONL appeared normal in early developmental stages. TUNEL+ cells were detected in the ONL, indicating that photoreceptor cells underwent apoptosis in retinas misexpressing cNSCL2. Müller glial cells were far fewer in the experimental retina than in the control, indicating that cNSCL2 also caused Müller glia atrophy. The onset of Müller glia disappearance preceded that of photoreceptor degeneration. CONCLUSIONS: Expression of cNSCL2 in the chick retina was restricted to amacrine and horizontal cells. Misexpression of cNSCL2 caused severe retinal degeneration, and photoreceptor cells and Müller glia were particularly affected.

Animals↗
PubMed1992

Ocular toxoplasmosis in human immunodeficiency virus-infected patients.

The files of 45 human immunodeficiency virus-infected patients with ocular toxoplasmosis were reviewed, with a median follow-up of eight months. The condition was unilateral in 37 of the 45 patients (82%) and was bilateral in eight (18%). Inflammation of the anterior chamber and the vitreous was present in 32 of 53 eyes (60%) and 38 of 53 eyes (72%), respectively. Cytomegalovirus retinitis developed during the follow-up period in nine patients (20%). Cerebral toxoplasmosis was concurrently diagnosed with the ocular toxoplasmosis in 13 patients (29%). The efficacy of the combination of pyrimethamine and sulfadiazine or clindamycin was assessed in 42 patients for the induction therapy and in 38 patients for the maintenance therapy. Induction therapy was always effective within a median period of six weeks. During maintenance treatment, the 24-month relapse rates were 0.20 and 0.18 for the 50-mg/day and 25-mg/day dosage of pyrimethamine, respectively. The overall 12-month survival rate was 0.72. Our results suggested that ocular toxoplasmosis has a better ocular prognosis than cytomegalovirus retinitis, but that it requires appropriate treatment because life-threatening cerebral involvement is often associated.

Adult↗
PubMed2001

Mice devoid of fer protein-tyrosine kinase activity are viable and fertile but display reduced cortactin phosphorylation.

The ubiquitous Fer protein-tyrosine kinase has been proposed to regulate diverse processes such as cell growth, cell adhesion, and neurite outgrowth. To gain insight into the biological function of Fer, we have targeted the fer locus with a kinase-inactivating missense mutation (fer(D743R)). Mice homozygous for this mutation develop normally, have no overt phenotypic differences from wild-type mice, and are fertile. Since these mice lack both Fer and the testis-specific FerT kinase activities, these proteins are clearly not essential for development and survival. No differences were observed in overall cellularity of bone marrow, spleen, or thymus in the absence of Fer activity. While most platelet-derived growth factor (PDGF)-induced tyrosine phosphorylation was unchanged in fer(D743R) homozygous embryonic fibroblasts, cortactin phosphorylation was reduced. However, Fer kinase activity was not required for PDGF-induced Stat3, p120(ctn), or epidermal growth factor (EGF)-induced beta-catenin phosphorylation. Also, no defects were observed in changes to the actin cytoskeleton, adherens junctions, or focal adhesions in PDGF- or EGF-stimulated fer(D743R) homozygous embryonic fibroblasts. Therefore, Fer likely serves a redundant role in regulating cell growth, cell adhesion, retinal development, and spermatogenesis but is required for efficient phosphorylation of cortactin.

Actins↗
PubMedDate not supplied

Human retinoblastoma: a morphological study of apoptotic, leukocytic, and vascular elements.

Retinoblastoma (Rb), derived from retinal neuroepithelial progenitor cells, is the most common intraocular malignancy of childhood. This study examined 10 human Rb biopsy specimens with light and electron microscopy for histopathological features not previously described in detail, including cell death, leukocytic infiltration, and the tumor vasculature. Rb is a solid well-vascularized tumor with regions of viable tumor cells surrounding vessels, interspersed with zones of necrosis; apoptotic cells were seen in all specimens. Mononuclear phagocyte series (MPS) cells and lymphocytes often colocalized, adjacent to tumor vessels, and MPS cells frequently invested the perivascular space. Lymphocytes were rarely seen within areas of viable tumor. Tumor vessels at early stages of formation resembled normal developing retinal vessels. While junctions were often seen between endothelial calls, disruption of these junctions and endothelial fenestrae was sometimes evident. Müller cells and astrocytes extended processes around tumor cells and blood vessels, and contributed to the formation of the vascular glia limitans, which in some mature vessels was disrupted and discontinuous. Overall, this study provides further morphological details of cell death within Rb, particularly apoptotic involution, and describes the presence of a vascular-associated leukocytic infiltration in Rb. Evidence of compromise of the normal blood-retinal barrier (BRB) within the Rb tumor vessels is presented.

Apoptosis↗
PubMed2000

MAP1B is required for axon guidance and Is involved in the development of the central and peripheral nervous system.

Microtubule-associated proteins such as MAP1B have long been suspected to play an important role in neuronal differentiation, but proof has been lacking. Previous MAP1B gene targeting studies yielded contradictory and inconclusive results and did not reveal MAP1B function. In contrast to two earlier efforts, we now describe generation of a complete MAP1B null allele. Mice heterozygous for this MAP1B deletion were not affected. Homozygous mutants were viable but displayed a striking developmental defect in the brain, the selective absence of the corpus callosum, and the concomitant formation of myelinated fiber bundles consisting of misguided cortical axons. In addition, peripheral nerves of MAP1B-deficient mice had a reduced number of large myelinated axons. The myelin sheaths of the remaining axons were of reduced thickness, resulting in a decrease of nerve conduction velocity in the adult sciatic nerve. On the other hand, the anticipated involvement of MAP1B in retinal development and gamma-aminobutyric acid C receptor clustering was not substantiated. Our results demonstrate an essential role of MAP1B in development and function of the nervous system and resolve a previous controversy over its importance.

Animals↗
PubMed1987

Development of somatostatin immunoreactive neurons in rat retina.

Levels of somatostatin-like immunoreactivity (SLI) were measured in the rat retina by radioimmunoassay during prenatal and postnatal development. SLI-containing cells were visualized by immunocytochemistry throughout this time period. SLI is present as early as embryonic day 15 (E15) and by E16 at concentrations 10-fold (4.4 +/- 1.4 pg/micrograms protein) higher than the adult retina, and the SLI is confined to cells in the inner neuroblastic layer. As the inner plexiform layer (IPL) develops (E17-18), the level of SLI falls (2.0 pg/micrograms protein) and distinct SLI neurites are seen throughout the inner neuroblastic layer. At birth (P0), the SLI level continues to decline at a time when cells are migrating. Few immunoreactive cells are seen in the developing ganglion cell layer (GCL), presumably as a result of this migration. At postnatal day 4 (P4), the amount of SLI continues to decline, and very few immunoreactive cells are noted. At P8, distinct cells contain SLI both in the GCL and inner nuclear layer (INL). SLI then increases as the retina matures postnatally. After eye opening, the amount of SLI approaches adult levels and the immunocytochemical pattern is similar to that reported for the adult rat retina; i.e. SLI is confined to two subpopulations of cells, one in the INL and one in the GCL. The early prenatal appearance of SLI suggests that it may play a role in retinal development.

Animals↗
PubMed2006

Nucleosome regulator Xhmgb3 is required for cell proliferation of the eye and brain as a downstream target of Xenopus rax/Rx1.

Rax/Rx is a paired-type homeodomain-containing transcription factor that is essential for cell proliferation in the developing eye and brain. The molecular mechanisms that regulate cell proliferation by rax, however, are largely unknown. Here, we identify the high mobility group B3 gene (hmgb3) as a downstream target of Xenopus rax (Xrax/XRx1). Overexpression of Xhmgb3 results in an increase in eye and brain sizes due to promoted cell proliferation, while morpholino-oligo-mediated knock down of Xhmgb3 reduces eye and brain sizes. In addition, ChIP assays showed that Xhmgb3 is recruited around the promoter region of c-myc to enhance c-myc transcription. We also found that XOptx2 requires rax for its initial expression. Furthermore, we show that Xhmgb3 and XOptx2 are required for retinal development mainly at different developmental stages. Our findings reveal a novel aspect of progenitor cell proliferation during embryonic central nervous system (CNS) development.

Animals↗
PubMed1999

Heparan sulfate in the inner limiting membrane of embryonic chicken retina binds basic fibroblast growth factor to promote axonal outgrowth.

During neural development retinal ganglion cell axons migrate over the retinal basal lamina (inner limiting membrane, ILM) in directed growth toward the optic nerve. We found that both growth rate and distribution density of the ganglion cell axons on isolated cell-free ILM was greatly inhibited by pretreatment with heparitinase but not with chondroitinase ABC. The persistence of radioactively labeled proteoglycans added to the culture medium eliminated residual heparitinase as an explanation for the inhibition. A cell binding assay showed that heparitinase acted on the ILM to influence axonal behavior without apparent inhibition of cell adhesion. These results indicated that the neurite outgrowth promoting activity of the ILM depended on the heparan sulfate (HS) side chains of its proteoglycans. Basic fibroblast growth factor (bFGF) stimulated additional neuronal sprouting and neurite elongation on the ILM. This neurotropic activity of bFGF was inhibited by heparitinase pretreatment of the ILM, suggesting that bFGF bound to HS on the ILM. The activity of bFGF was enhanced by exogenous heparin added to the culture medium; although heparin alone failed to stimulate either neurite extension or neuronal cell sprouting. These results demonstrate that HS in the ILM possesses neurotropic activity for axons of the ganglion cells by binding bFGF for presentation to cell-surface receptors and may, therefore, play a significant role in stimulating axonal outgrowth during development.

Animals↗
PubMed1996

Development of nitric oxide synthase in the avian retina.

Nitric oxide is an important intercellular messenger in the central nervous system. Our previous work showed the presence of NADPH-diaphorase activity, that partially corresponded to nitric oxide synthase, in the chick embryo retina. In the present study, we have demonstrated the presence of nitric oxide synthase in the chick retina measuring the conversion of 3(H)arginine to 3(H)citrulline. We found that the enzyme is dependent on the presence of calcium, calmodulin and NADPH and is inhibited by the arginine analog L-NG-nitroarginine. The enzyme activity was higher at 8-day-old embryonic retinas, decreased at 13-14 days and attained minimal levels at 15 days up to the post-hatching period. Glutamate stimulated nitric oxide synthase activity approximately 4 fold, an effect that was blocked by the NMDA antagonist MK-801. The results indicate that the glutamate/nitric oxide system has important functions during retinal development.

Animals↗
PubMed1989

New and previously unidentified retinal breaks in eyes with recurrent retinal detachment with proliferative vitreoretinopathy.

The location of retinal breaks found on preoperative examination was studied in 68 eyes of 68 patients with recurrent retinal detachment and proliferative vitreoretinopathy. Twelve eyes had 23 open breaks that were known to exist previously, no open break was detected in 18 eyes, and 72 new or previously unidentified breaks were found in 41 eyes. Forty-seven (65.3%) of the 72 breaks were located on previous buckles, and 31 of these were on the posterior slope of the buckle. Twenty-nine (40.2%) of all new or previously unidentified breaks were on the border of a cryopexy-induced chorioretinal scar, and of these, 25 breaks (86%) were on the posterior slope of the buckle. Our results indicate that the retina that borders chorioretinal scars is vulnerable and prone to develop retinal tears secondary to traction from preretinal membranes. The vicinity of cryopexy-induced scars should be closely observed for retinal breaks in cases of recurrent retinal detachment with proliferative vitreoretinopathy.

Choroid↗
PubMed2002

Eye defects in receptor protein-tyrosine phosphatase alpha knock-down zebrafish.

Receptor protein-tyrosine phosphatase alpha (RPTP alpha) is highly expressed in the developing retina of different species, but little is known about its function there. Here, we report that injection of antisense morpholinos in zebrafish embryos reduced RPTP alpha expression to almost nondetectable levels up to 3 days postfertilization (dpf). RPTP alpha was detectable again from 4 dpf onward. RPTP alpha knock-down resulted in smaller eyes. Examination of sections of the retina at different developmental stages demonstrated that already at 28 hours postfertilization (hpf) fewer cells were present in the retina of RPTP alpha-morpholino-injected embryos. At 3 dpf, the layered organization of the retina was absent. In addition, the morphology and labeling with an axon specific antibody, acetylated tubulin, demonstrated that most cells appeared to be undifferentiated. Strikingly, at 5 dpf the lamination of the retina was partially restored, concomitant with re-expression of RPTP alpha protein. Although cells in the retina were now differentiated, the layering of the retina remained disrupted and significant gaps were observed in the amacrine cell layer. Therefore, knock-down of RPTP alpha protein provides evidence that RPTP alpha is essential for normal retinal development.

Animals↗
PubMed1999

Serotonergic neurons and processes in the adult and developing retina of Ichthyophis kohtaoensis (Amphibia; Gymnophiona).

Ichthyophis kohtaoensis is a tropical, limbless amphibian species with extremely small eyes (540 microm in adults). Adapted to a subterranean, burrowing mode of life, orientation and prey capture are predominantly guided by olfaction. The only visually guided behavior seems to be negative phototaxis. As electrophysiological single cell recordings have so far failed, immunohistochemical transmitter studies are a starting-point for a functional investigation of the visual system of this group of amphibians. In the present study, the organization and development of the serotonergic system have been examined in the retinae of embryonic, larval and adult I. kohtaoensis, using an antiserum against serotonin. Labeled somata are situated in the inner nuclear layer, presumably representing amacrine cells, and in the ganglion cell layer. However, some immunoreactive cells are located in the middle of the inner nuclear layer that send processes to both plexiform layers, probably representing bipolar cells. An additional type of immunoreactive soma, situated in the inner plexiform layer, have been found only in retinae of embryonic stages. Varicose serotonergic fibers form a diffuse plexus that covers the whole inner plexiform layer. Immunolabeled fibers can occasionally be demonstrated in the optic nerve head. During retinal development, the distribution and number of transmitter-expressing cells changes but no general reduction of the visual system is detectable. Adult stages still have a serotonergic system comparable to amphibians with a well-developed visually guided behavior indicating that the eyes of I. kohtaoensis although being of minor importance in a subterranean habitat, retain all the elements of functioning sense organs.

Amphibians↗
PubMed1999

Neovascularization of the optic disc after highly active antiretroviral therapy in an AIDS patient with cytomegalovirus retinitis--A new immune recovery-related ocular disorder?

A patient with AIDS and cytomegalovirus (CMV) retinitis developed a massive bilateral peripheral occlusive vasculopathy with a bilateral neovascularization of the optic disc five weeks after the introduction of highly active antiretroviral therapy (HAART). No associate cause of occlusive vasculopathy was found. Occlusive vasculopathy and optic disc neovascularization may be an immune recovery-related ocular disorder.

Acquired Immunodeficiency Syndrome↗
PubMed2007

Visual outcomes and associated risk factors of cataract surgeries in highly myopic Taiwanese.

AIMS: The purposes of this study are to describe the visual outcome of highly myopic eyes undergoing cataract surgery, to investigate associated risk factors for poor postoperative vision and to assess the postoperative complication frequency among the myopic Taiwanese population. METHODS: We conducted a retrospective, noncomparative case series study at the Department of Ophthalmology, Zhongxing Branch, Taipei City Hospital, Taiwan. High myopia was defined as axial length > or =26.0 mm. The main study outcomes were visual acuity for the initial 6-month postoperative period (including visual acuities and improvement of postoperative vision) and postoperative complications (including subsequent cataract formation and postoperative retinal detachment). RESULTS: Fifty-two highly myopic eyes were enrolled between January 2002 and December 2004. The mean follow-up interval was 43.3 +/- 20.2 weeks (range 25-103). Thirty-two eyes (61.5%) had good postoperative visual improvement (> or =4 lines of Snellen chart). Thirty-seven eyes (71.2%) achieved good postoperative vision (20/40 or better). Fifteen eyes (28.8%) demonstrated poor postoperative vision. Pre-existing maculopathy was an independent risk factor for failure to achieve good postoperative vision [odds ratio (OR): 6.84, 95% confidence interval (CI): 1.12-41.8] and improvement (OR: 16.1, 95% CI: 2.2-119.9). Diabetic history was considered another independent risk factor for poor postoperative vision (OR: 15.6, 95% CI: 0.97-267.6). Six eyes (11.5%) developed subsequent posterior capsular opacification requiring Nd:YAG laser capsulotomy. Two eyes (3.8%) developed retinal detachment during follow-up. CONCLUSIONS: Most highly myopic eyes achieved good visual improvement and good postoperative visual acuity after cataract surgery. Pre-existing maculopathy was an independent risk factor of postoperative visual improvement and status. It is crucial to examine retinal status prior to cataract surgery to prevent poor vision improvement, poor postoperative vision or retinal complications.

Adult↗
PubMed1992

Immunohistological Localization of Tenascin in the Developing and Lesioned Adult Mouse Optic Nerve.

To gain insight into the morphogenetic functions of the recognition molecule tenascin in the central nervous system, we have studied its localization in the developing and lesioned adult mouse optic nerve using light and electron microscopic immunocytochemistry. Since tenascin is a secreted molecule, we have analysed the tenascin-synthesizing cells in tissue sections of retinae and optic nerves by in situ hybridization. A weak and homogeneous tenascin immunoreactivity was detectable in the developing retinal nerve fibre layer and optic nerve of 14-day-old mouse embryos, the earliest developmental age investigated. In the optic nerve of neonatal and 1-week-old animals, a high number of tenascin messenger RNA (mRNA)-containing cells were present, and antibodies to tenascin labelled the surfaces of astrocytes and unmyelinated retinal ganglion cell axons. With increasing age, expression of tenascin in the optic nerve was down-regulated at the mRNA and protein levels. At the fourth postnatal week, blood vessels in the optic nerve and collagen fibrils in the vicinity of meningeal fibroblast-like cells still showed significant immunoreactivity, but the optic nerve tissue proper no longer did so. In adult animals, tenascin was no longer detectable in association with blood vessels located in the myelinated part of the optic nerve, and meninges were only weakly immunoreactive. Also, tenascin mRNA-containing cells were no longer detectable in the myelinated part of the adult mouse optic nerve and few labelled cells were found in the meninges. In the retina, ganglion cells contained no detectable levels of tenascin mRNA at any of the developmental ages analysed. No significant up-regulation of tenascin expression was seen in the nerve tissue proper of transected proximal (i.e. retinal) and distal (i.e. cranial) optic nerve stumps of adult mice during the first 4 weeks after lesioning, the time period studied. However, collagen fibrils associated with meningeal fibroblast-like cells and located near the lesion site became strongly tenascin-immunoreactive 2 days after lesioning. Also, some blood vessels at the lesion site became immunoreactive. We conclude that tenascin in the optic nerve is synthesized by glial cells and not by retinal ganglion cells. The detectability of tenascin at embryonic ages suggests that it may mediate neurite growth in vivo. The absence of a strong, lesion-induced up-regulation of tenascin expression in the regeneration-prohibitive mouse optic nerve contrasts with the lesion-induced pronounced up-regulation in the regeneration-permissive peripheral nervous system, and may indicate a functional involvement of tenascin in regenerative processes. The high tenascin positivity of collagen fibrils at early postnatal ages and after lesioning suggests that tenascin expression may be correlated with mitotic activity of the associated meningeal fibroblast-like cells. Finally, tenascin may be involved in the process of vascularization, since the molecule is associated with blood vessels in developing and adult lesioned, but not intact adult, optic nerves.

Journal Article↗