Disease relevance of Cspg2

• The findings suggested that GHAP-negative astrocytes responding to traumatic injury are permissive for axonal growth and that GHAP-positive astrocytes responding to Wallerian degeneration are not permissive [1].
• Exposure of the cells to hypoxia activated the phosphoglycerate mutase B (PGM-B) gene, resulting in the induction of PGM enzymatic activity, concomitant with elevations of PGM-B mRNA and protein levels [2].

High impact information on Cspg2

• Versican/PG-M isoforms in vascular smooth muscle cells [3].
• In normal rat optic nerve, staining for HA and GHAP ceased abruptly in the region of the lamina cribrosa [4].
• In spinal cord white matter, versican immunoreactivity was already present in 3-day-old rats and preceded the appearance of GHAP, which was first detected on day 13 after the onset of myelination [5].
• In the rat, intracerebral injection of bacterial hyaluronidase resulted in the almost complete disappearance of hyaluronic acid (HA) and glial hyaluronate-binding protein (GHAP) from cerebral hemispheres, brain stem, and cerebellum (but not from optic nerves and chiasm) starting 2-3 hr after the injection [4].
• The extracellular matrix of rat spinal cord: a comparative study on the localization of hyaluronic acid, glial hyaluronate-binding protein, and chondroitin sulfate proteoglycan [6].

Chemical compound and disease context of Cspg2

• Up-regulation of PGM mRNA by hypoxia was obvious after 8 h exposure, reached its peak after 16 h, persisting for 40 h and returned to the basal level after reoxygenation at 20% O2 for 16 h [2].

Biological context of Cspg2

• The similarity of HN with PG-M (V3) suggested that HN found in vivo could be the result of an alternative splicing of a single gene [7].

Anatomical context of Cspg2

• Permissive and non-permissive reactive astrocytes: immunofluorescence study with antibodies to the glial hyaluronate-binding protein [1].
• Conversely, isomorphic glial scars were still GHAP-positive 3 months after dorsal root transection [1].
• The distribution of hyaluronate in adult brain white matter and cerebellar cortex was similar to that previously reported for GHAP [8].
• Conversely, in both dog and rat, GHAP immunoreactivity ceased abruptly in the region of the lamina cribrosa, a sieve-like structure continuous with the sclera through which bundles of optic nerve axons pass [9].
• Little reactivity was observed in rat cerebral cortex with polyclonal GHAP antibodies if the sections were not incubated with GHAP [10].

Associations of Cspg2 with chemical compounds

• Expression of a chondroitin sulfate proteoglycan, versican (PG-M), during development of rat cornea [11].
• Anisomorphic glial scars did not stain with antibodies to the glial hyaluronate-binding protein (GHAP), a structural glycoprotein of white matter extracellular matrix [1].

Analytical, diagnostic and therapeutic context of Cspg2

• Cells were probed with the glial hyaluronate binding protein (GHAP) which was itself then visualized by conventional indirect immunofluorescence [12].
• Glial hyaluronate-binding protein expression in aggregating brain cell cultures [13].

References