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Keratan sulfate

About: Keratan sulfate is a research topic. Over the lifetime, 1253 publications have been published within this topic receiving 57984 citations. The topic is also known as: keratan sulfate & KS.


Papers
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Journal ArticleDOI
TL;DR: In vitro experimental comparison of adhesion levels of cancer cells to glycosaminoglycan-modified substrates was performed and results suggest that tissues with higher composition of heparan sulfate chains may be preferential metastatic targets and indicate that the effective use ofheparin as anti-metastatic or anti-inflammatory agent may also depend on glycosamine composition of the affected organs.

7 citations

Journal ArticleDOI
TL;DR: Exogenously added KS totally blocks keratanase sensitive glycosaminoglycan release measured by radiolabeled ligand and KS release is potentially inhibited by its own presence as measured by ELISA, suggesting that KS negatively regulates its own secretion.
Abstract: Keratan sulfate (KS) is one of the major glycosaminoglycans in cartilage matrix proteoglycan. We find that exogenously added KS totally blocks keratanase sensitive glycosaminoglycan release measured by radiolabeled ligand. We also find that KS release is potentially inhibited by its own presence as measured by ELISA. When KS is digested with keratanase before its addition to the medium, its inhibitory effect on KS secretion is partially blocked. Exogenously added KS promotes the accumulation of the KS epitope in the cell layer. These data suggest that KS negatively regulates its own secretion.

7 citations

Journal ArticleDOI
TL;DR: The findings indicate that 5D4+ microglia may play some role in epileptogenesis via pruning of excitatory synapses during the latent period after pilocarpine‐induced status epilepticus (SE).
Abstract: Induction of keratan sulfate in microglia has been found in several animal models of neurological disorders. However, the significance of keratan sulfate-expressing microglia is not fully understood. To address this issue, we analyzed the characteristics of microglia labeled by the 5D4 epitope, a marker of high-sulfated keratan sulfate, in the mouse hippocampus during the latent period after pilocarpine-induced status epilepticus (SE). Only 5D4-negative (5D4- ) microglia were found in the CA1 region of vehicle-treated controls and pilocarpine-treated mice at 1 day after SE onset. A few 5D4+ microglia appeared in the strata oriens and radiatum at 5 days post-SE, and they were distributed into the stratum pyramidale at 14 days post-SE. The expressions of genes related to both anti- and pro-inflammatory cytokines were higher in 5D4+ cells than in 5D4- cells at 5 but not 14 days post-SE. The expressions of genes related to phagocytosis were higher in 5D4+ cells than in 5D4- cells throughout the latent period. The phagocytic activity of microglia, as measured by engulfment of the zymosan bioparticles, was higher in 5D4+ cells than in 5D4- cells. The contact ratios between excitatory synaptic boutons and microglia were also higher in 5D4+ cells than in 5D4- cells at 5 and 14 days post-SE. The excitatory/inhibitory ratios of synaptic boutons within the microglial domain were lower in 5D4+ cells than in 5D4- cells at 14 days post-SE. Our findings indicate that 5D4+ microglia may play some role in epileptogenesis via pruning of excitatory synapses during the latent period after SE.

6 citations

Journal ArticleDOI
TL;DR: The results demonstrate that human epidermis produces at least three different, rapidly metabolized PG, including the 35SO4-labeled epidermal PG and glycosaminoglycans (GAG).

6 citations

Patent
28 Jan 1999
TL;DR: In this article, the problem of obtaining a bone induction promoter which can effectively promote bone induction even when it is administered in a small dosage or in a low concentration by using as the active ingredient a lipid-bonded glycosaminoglycan composed of a glyco-can and a lipid bonded thereto or a pharmacologically acceptable salt thereof is addressed.
Abstract: PROBLEM TO BE SOLVED: To obtain a bone induction promoter which can effectively promote bone induction even when it is administered in a small dosage or in a low concentration by using as the active ingredient a lipidbonded glycosaminoglycan composed of a glycosaminoglycan and a lipid bonded thereto or a pharmacologically acceptable salt thereof. SOLUTION: This promoter is desirably selected from among a bone induction promoter in which the glycosaminoglycan is hyaluronic acid, chondroitin, chondroitin sulfate, chondroitin polysulfate, dermatan sulfate, heparin, keratan sulfate, or keratan polysulfate, a bond induction promoter in which the lipid is a glycerolipid, a bone induction promoter in which the glycerolipid is a phospholipid, a bone induction promoter in which the phospholipid is phosphatidylethanolamine, a bone induction promoter in which the glycosaminoglycan is hyaluronic acid and the lipid is phosphatidylethanolamine, and a bone induction promoter in which the lipid is covalently bonded to the reducing terminal of the glycosaminoglycan.

6 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202310
202222
20217
20209
201912
201812