FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2108438047> ?p ?o ?g. }

• W2108438047 endingPage "408" @default.
• W2108438047 startingPage "404" @default.
• W2108438047 abstract "Regeneration and plasticity after spinal cord injury are limited by inhibitory proteoglycans; here, modulation of a receptor for proteoglycans in rats is shown to lead to functional recovery after injury. Functional recovery following severe spinal cord injury is often modest due to inhibited neural and axonal regeneration at the scar location. Glia-produced extracellular matrix components may be responsible for this reduced regeneration potential. Using an in vitro model of the inhibitory extracellular matrix that forms after spinal cord injury, Jerry Silver and colleagues identify a component on axons — protein tyrosine phosphatase σ (PTPσ) — that permanently adheres axonal growth cones to these inhibitory extracellular matrix molecules, rendering the axons unable to regrow. In rodent model studies, a peptide mimic of PTPσ can block the proteoglycan sites in the matrix, allowing axons to pass through the injured area and regrow, leading to functional recovery in both the locomotor and urinary systems. Contusive spinal cord injury leads to a variety of disabilities owing to limited neuronal regeneration and functional plasticity. It is well established that an upregulation of glial-derived chondroitin sulphate proteoglycans (CSPGs) within the glial scar and perineuronal net creates a barrier to axonal regrowth and sprouting1,2,3,4,5. Protein tyrosine phosphatase σ (PTPσ), along with its sister phosphatase leukocyte common antigen-related (LAR) and the nogo receptors 1 and 3 (NgR), have recently been identified as receptors for the inhibitory glycosylated side chains of CSPGs6,7,8. Here we find in rats that PTPσ has a critical role in converting growth cones into a dystrophic state by tightly stabilizing them within CSPG-rich substrates. We generated a membrane-permeable peptide mimetic of the PTPσ wedge domain that binds to PTPσ and relieves CSPG-mediated inhibition. Systemic delivery of this peptide over weeks restored substantial serotonergic innervation to the spinal cord below the level of injury and facilitated functional recovery of both locomotor and urinary systems. Our results add a new layer of understanding to the critical role of PTPσ in mediating the growth-inhibited state of neurons due to CSPGs within the injured adult spinal cord." @default.
• W2108438047 created "2016-06-24" @default.
• W2108438047 creator A5001997941 @default.
• W2108438047 creator A5002038417 @default.
• W2108438047 creator A5005496611 @default.
• W2108438047 creator A5009011088 @default.
• W2108438047 creator A5014518319 @default.
• W2108438047 creator A5041831733 @default.
• W2108438047 creator A5042836257 @default.
• W2108438047 creator A5043396522 @default.
• W2108438047 creator A5067962243 @default.
• W2108438047 creator A5068036561 @default.
• W2108438047 creator A5078658086 @default.
• W2108438047 creator A5084010307 @default.
• W2108438047 creator A5084510530 @default.
• W2108438047 creator A5090134535 @default.
• W2108438047 date "2014-12-03" @default.
• W2108438047 modified "2023-10-09" @default.
• W2108438047 title "Modulation of the proteoglycan receptor PTPσ promotes recovery after spinal cord injury" @default.
• W2108438047 cites W1527739697 @default.
• W2108438047 cites W1829071486 @default.
• W2108438047 cites W1837528440 @default.
• W2108438047 cites W1966007526 @default.
• W2108438047 cites W1990277219 @default.
• W2108438047 cites W1990388392 @default.
• W2108438047 cites W2002406661 @default.
• W2108438047 cites W2012928251 @default.
• W2108438047 cites W2014007136 @default.
• W2108438047 cites W2025339136 @default.
• W2108438047 cites W2031868699 @default.
• W2108438047 cites W2043930451 @default.
• W2108438047 cites W2062999076 @default.
• W2108438047 cites W2064423627 @default.
• W2108438047 cites W2077636669 @default.
• W2108438047 cites W2086085796 @default.
• W2108438047 cites W2089263292 @default.
• W2108438047 cites W2090423201 @default.
• W2108438047 cites W2091187766 @default.
• W2108438047 cites W2091998173 @default.
• W2108438047 cites W2092811972 @default.
• W2108438047 cites W2095263564 @default.
• W2108438047 cites W2107057334 @default.
• W2108438047 cites W2110466351 @default.
• W2108438047 cites W2110674840 @default.
• W2108438047 cites W2112961986 @default.
• W2108438047 cites W2113390309 @default.
• W2108438047 cites W2114816633 @default.
• W2108438047 cites W2154415966 @default.
• W2108438047 cites W2157650341 @default.
• W2108438047 cites W2161475511 @default.
• W2108438047 cites W2162066460 @default.
• W2108438047 cites W2170645579 @default.
• W2108438047 cites W2493393615 @default.
• W2108438047 doi "https://doi.org/10.1038/nature13974" @default.
• W2108438047 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4336236" @default.
• W2108438047 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25470046" @default.
• W2108438047 hasPublicationYear "2014" @default.
• W2108438047 type Work @default.
• W2108438047 sameAs 2108438047 @default.
• W2108438047 citedByCount "348" @default.
• W2108438047 countsByYear W21084380472015 @default.
• W2108438047 countsByYear W21084380472016 @default.
• W2108438047 countsByYear W21084380472017 @default.
• W2108438047 countsByYear W21084380472018 @default.
• W2108438047 countsByYear W21084380472019 @default.
• W2108438047 countsByYear W21084380472020 @default.
• W2108438047 countsByYear W21084380472021 @default.
• W2108438047 countsByYear W21084380472022 @default.
• W2108438047 countsByYear W21084380472023 @default.
• W2108438047 crossrefType "journal-article" @default.
• W2108438047 hasAuthorship W2108438047A5001997941 @default.
• W2108438047 hasAuthorship W2108438047A5002038417 @default.
• W2108438047 hasAuthorship W2108438047A5005496611 @default.
• W2108438047 hasAuthorship W2108438047A5009011088 @default.
• W2108438047 hasAuthorship W2108438047A5014518319 @default.
• W2108438047 hasAuthorship W2108438047A5041831733 @default.
• W2108438047 hasAuthorship W2108438047A5042836257 @default.
• W2108438047 hasAuthorship W2108438047A5043396522 @default.
• W2108438047 hasAuthorship W2108438047A5067962243 @default.
• W2108438047 hasAuthorship W2108438047A5068036561 @default.
• W2108438047 hasAuthorship W2108438047A5078658086 @default.
• W2108438047 hasAuthorship W2108438047A5084010307 @default.
• W2108438047 hasAuthorship W2108438047A5084510530 @default.
• W2108438047 hasAuthorship W2108438047A5090134535 @default.
• W2108438047 hasBestOaLocation W21084380472 @default.
• W2108438047 hasConcept C129987498 @default.
• W2108438047 hasConcept C169760540 @default.
• W2108438047 hasConcept C170493617 @default.
• W2108438047 hasConcept C171056886 @default.
• W2108438047 hasConcept C185592680 @default.
• W2108438047 hasConcept C189165786 @default.
• W2108438047 hasConcept C2775895372 @default.
• W2108438047 hasConcept C2777594495 @default.
• W2108438047 hasConcept C2778334475 @default.
• W2108438047 hasConcept C2779024559 @default.
• W2108438047 hasConcept C2779335624 @default.
• W2108438047 hasConcept C2779530196 @default.
• W2108438047 hasConcept C2780775167 @default.

• next