Glycosaminoglycans of the trabecular meshwork of the eye in primary juvenile glaucoma

Kuleshova, O. N.; Зайдман, А. М.; Korel, A. V.

doi:10.1007/s10517-007-0117-8

Cited by 8 publications

(12 citation statements)

References 5 publications

(5 reference statements)

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“…Significant changes in the qualitative and quantitative composition of glycosaminoglycans were detected in PJG presenting as a trend to reduction of the content of sulfated glycosaminoglycans, diffuse proteoglycans, and a significant increase in the content of collagen-bound proteoglycans, indicating collagenogenesis intensification in the juxtacanalicular tissue and deep layers of the sclera [1], which was confirmed by the results of ultrastructural analysis of the operation material.…”

Section: Resultssupporting

confidence: 61%

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Ultrastructure of connective tissue of eye drainage system in ophthalmic hypertension associated with primary juvenile glaucoma

2008

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In primary juvenile glaucoma, the connective tissue of the juxtacanalicular zone and sclera undergo constant reorganization because of incessant synthesis and degradation of extracellular matrix components with pronounced fluctuations of electron density of collagen fibrils. Destructive changes in the perivascular nerve trunks were detected at all stages of the glaucoma process, including the initial stages: numerous large foci of cytoplasmic organelle destruction with the formation of autophagosomes and residual bodies predominated in the cytoplasm of myelinated axons of nerve cells.

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Section: Resultssupporting

confidence: 61%

“…For example, significant changes in qualitative and quantitative composition of glycosaminoglycans of the trabecular networks of the eye and intervertebral disc were demonstrated in PJG [1,2].…”

mentioning

confidence: 99%

Ultrastructure of connective tissue of eye drainage system in ophthalmic hypertension associated with primary juvenile glaucoma

2008

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“…It has also been reported that there are elevated concentrations of TGF-β 2 in the aqueous humor of eyes with POAG (59-61) and in developmental glaucoma (61). The trabecular tissue in developmental glaucoma is associated with an abnormal distribution of HS that exhibits an abnormal accumulation (29) or a significant loss (31). These findings may indicate that improper expression of TGF-β 2 and HS can promote the immaturity of the anterior chamber angle in developmental glaucoma or cause impaired cellular function in the trabecular meshwork and Schlemm canal of POAG.…”

Section: Discussionmentioning

confidence: 97%

“…Both the accumulation and changes of the component in the human trabecular meshwork are thought to affect the aqueous outflow resistance. Abnormal expression of glycosaminoglycans and their glycoproteins, along with proteoglycans in the trabecular meshwork, have been found in human glaucoma (29)(30)(31). Heparan sulfate (HS) is a glycosaminoglycan component of the proteoglycans that is expressed in the extracellular matrix of the iridocorneal angle and on cell surfaces of the trabecular meshwork cells (32,33).…”

Section: Introductionmentioning

confidence: 99%

Heparan sulfate deficiency leads to Peters anomaly in mice by disturbing neural crest TGF-β2 signaling

Iwao

Inatani²,

Matsumoto

et al. 2009

J. Clin. Invest.

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During human embryogenesis, neural crest cells migrate to the anterior chamber of the eye and then differentiate into the inner layers of the cornea, the iridocorneal angle, and the anterior portion of the iris. When proper development does not occur, this causes iridocorneal angle dysgenesis and intraocular pressure (IOP) elevation, which ultimately results in developmental glaucoma. Here, we show that heparan sulfate (HS) deficiency in mouse neural crest cells causes anterior chamber dysgenesis, including corneal endothelium defects, corneal stroma hypoplasia, and iridocorneal angle dysgenesis. These dysfunctions are phenotypes of the human developmental glaucoma, Peters anomaly. In the neural crest cells of mice embryos, disruption of the gene encoding exostosin 1 (Ext1), which is an indispensable enzyme for HS synthesis, resulted in disturbed TGF-β 2 signaling. This led to reduced phosphorylation of Smad2 and downregulated expression of forkhead box C1 (Foxc1) and paired-like homeodomain transcription factor 2 (Pitx2), transcription factors that have been identified as the causative genes for developmental glaucoma. Furthermore, impaired interactions between HS and TGF-β 2 induced developmental glaucoma, which was manifested as an IOP elevation caused by iridocorneal angle dysgenesis. These findings suggest that HS is necessary for neural crest cells to form the anterior chamber via TGF-β 2 signaling. Disturbances of HS synthesis might therefore contribute to the pathology of developmental glaucoma.

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“…This balance is one of the components of PJG pathogenesis, including also genetically determined qualitative and quantitative changes in the connective tissue glycosaminoglycans [3].…”

Section: Resultsmentioning

confidence: 99%

Ultrastructure of the endothelium of the drainage system of the eye

et al. 2008

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The endothelium of the ocular drainage system (Schlemm's canal, collector tubules, and aqueous veins) in primary juvenile glaucoma undergoes degenerative dystrophic changes with compensatory hypertrophy and proliferation at the initial stages of the glaucomatous process and atrophy and desquamation at advanced and terminal stages. Progressive decrease in the pinocytous function of endotheliocytes, reduction of the protein-synthesizing and mitochondrial compartments of the cytoplasm, and formation of autophagosomes reflect the process of endotheliocyte degeneration in general.

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Glycosaminoglycans of the trabecular meshwork of the eye in primary juvenile glaucoma

Cited by 8 publications

References 5 publications

Ultrastructure of connective tissue of eye drainage system in ophthalmic hypertension associated with primary juvenile glaucoma

Ultrastructure of connective tissue of eye drainage system in ophthalmic hypertension associated with primary juvenile glaucoma

Heparan sulfate deficiency leads to Peters anomaly in mice by disturbing neural crest TGF-β2 signaling

Ultrastructure of the endothelium of the drainage system of the eye

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