FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2799667091> ?p ?o ?g. }

• W2799667091 abstract "Spinal cord injury (SCI) is a complex clinical and progressive condition characterized by neuronal loss, axonal destruction and demyelination. In the last few years, adenosine receptors have been studied as a target for many diseases, including neurodegenerative conditions. The aim of this study was to investigate the effects of an adenosine receptor agonist, PDRN, in an experimental model of SCI. Moreover, since adenosine receptors stimulation may also activate the Wnt pathway, we wanted to study PDRN effects on Wnt signaling following SCI. Spinal trauma was induced by extradural compression of spinal cord at T5-T8 level in C57BL6/J mice. Animals were randomly assigned to the following groups: Sham (n = 10), SCI (n = 14), SCI+PDRN (8 mg/kg/i.p.; n = 14), SCI+PDRN+DMPX (8 and 10 mg/kg/i.p., respectively; n = 14). DMPX was used as an adenosine receptor antagonist to evaluate whether adenosine receptor block might prevent PDRN effects. PDRN systemically administered 1 h following SCI, protected from tissue damage, demyelination, and reduced motor deficits evaluated after 10 days. PDRN also reduced the release of the pro-inflammatory cytokines TNF-α and IL-1β, reduced BAX expression and preserved Bcl-2. Furthermore, PDRN stimulated Wnt/β-catenin pathway and decreased apoptotic process 24 h following SCI, whereas DMPX administration prevented PDRN effects on Wnt/β-catenin signaling. These results confirm PDRN anti-inflammatory activity and demonstrate that a crosstalk between Wnt/β-catenin signaling is possible by adenosine receptors activation. Moreover, these data let us hypothesize that PDRN might promote neural repair through axonal regeneration and/or neurogenesis." @default.
• W2799667091 created "2018-05-17" @default.
• W2799667091 creator A5000863770 @default.
• W2799667091 creator A5010245193 @default.
• W2799667091 creator A5014523351 @default.
• W2799667091 creator A5026283915 @default.
• W2799667091 creator A5040381615 @default.
• W2799667091 creator A5054687534 @default.
• W2799667091 creator A5059353158 @default.
• W2799667091 creator A5068357190 @default.
• W2799667091 creator A5069889196 @default.
• W2799667091 creator A5070587833 @default.
• W2799667091 creator A5073458708 @default.
• W2799667091 creator A5080680155 @default.
• W2799667091 creator A5086062480 @default.
• W2799667091 date "2018-05-29" @default.
• W2799667091 modified "2023-10-12" @default.
• W2799667091 title "Activation of A2A Receptor by PDRN Reduces Neuronal Damage and Stimulates WNT/β-CATENIN Driven Neurogenesis in Spinal Cord Injury" @default.
• W2799667091 cites W141799690 @default.
• W2799667091 cites W1593555249 @default.
• W2799667091 cites W1827374308 @default.
• W2799667091 cites W1962232533 @default.
• W2799667091 cites W1977782116 @default.
• W2799667091 cites W1987248191 @default.
• W2799667091 cites W1988868629 @default.
• W2799667091 cites W1999160051 @default.
• W2799667091 cites W2006419043 @default.
• W2799667091 cites W2045880711 @default.
• W2799667091 cites W2053488609 @default.
• W2799667091 cites W2054096295 @default.
• W2799667091 cites W2058678069 @default.
• W2799667091 cites W2059829735 @default.
• W2799667091 cites W2061338082 @default.
• W2799667091 cites W2061928399 @default.
• W2799667091 cites W2062344469 @default.
• W2799667091 cites W2064600258 @default.
• W2799667091 cites W2069260718 @default.
• W2799667091 cites W2078619271 @default.
• W2799667091 cites W2092935442 @default.
• W2799667091 cites W2095207160 @default.
• W2799667091 cites W2102291861 @default.
• W2799667091 cites W2103170336 @default.
• W2799667091 cites W2103258137 @default.
• W2799667091 cites W2106544674 @default.
• W2799667091 cites W2107648723 @default.
• W2799667091 cites W2116238347 @default.
• W2799667091 cites W2143122330 @default.
• W2799667091 cites W2146455000 @default.
• W2799667091 cites W2150947082 @default.
• W2799667091 cites W2153104965 @default.
• W2799667091 cites W2153561951 @default.
• W2799667091 cites W2156321901 @default.
• W2799667091 cites W2157228654 @default.
• W2799667091 cites W2158021558 @default.
• W2799667091 cites W2161456562 @default.
• W2799667091 cites W2170645579 @default.
• W2799667091 cites W2184947876 @default.
• W2799667091 cites W2508740119 @default.
• W2799667091 cites W2569062098 @default.
• W2799667091 cites W2606191437 @default.
• W2799667091 cites W2610140566 @default.
• W2799667091 cites W2729745157 @default.
• W2799667091 cites W2751182754 @default.
• W2799667091 cites W331495762 @default.
• W2799667091 cites W621842823 @default.
• W2799667091 doi "https://doi.org/10.3389/fphar.2018.00506" @default.
• W2799667091 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5986913" @default.
• W2799667091 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29896101" @default.
• W2799667091 hasPublicationYear "2018" @default.
• W2799667091 type Work @default.
• W2799667091 sameAs 2799667091 @default.
• W2799667091 citedByCount "32" @default.
• W2799667091 countsByYear W27996670912019 @default.
• W2799667091 countsByYear W27996670912020 @default.
• W2799667091 countsByYear W27996670912021 @default.
• W2799667091 countsByYear W27996670912022 @default.
• W2799667091 countsByYear W27996670912023 @default.
• W2799667091 crossrefType "journal-article" @default.
• W2799667091 hasAuthorship W2799667091A5000863770 @default.
• W2799667091 hasAuthorship W2799667091A5010245193 @default.
• W2799667091 hasAuthorship W2799667091A5014523351 @default.
• W2799667091 hasAuthorship W2799667091A5026283915 @default.
• W2799667091 hasAuthorship W2799667091A5040381615 @default.
• W2799667091 hasAuthorship W2799667091A5054687534 @default.
• W2799667091 hasAuthorship W2799667091A5059353158 @default.
• W2799667091 hasAuthorship W2799667091A5068357190 @default.
• W2799667091 hasAuthorship W2799667091A5069889196 @default.
• W2799667091 hasAuthorship W2799667091A5070587833 @default.
• W2799667091 hasAuthorship W2799667091A5073458708 @default.
• W2799667091 hasAuthorship W2799667091A5080680155 @default.
• W2799667091 hasAuthorship W2799667091A5086062480 @default.
• W2799667091 hasBestOaLocation W27996670911 @default.
• W2799667091 hasConcept C126322002 @default.
• W2799667091 hasConcept C134018914 @default.
• W2799667091 hasConcept C137620995 @default.
• W2799667091 hasConcept C169760540 @default.
• W2799667091 hasConcept C170493617 @default.
• W2799667091 hasConcept C25498285 @default.
• W2799667091 hasConcept C2776991684 @default.
• W2799667091 hasConcept C2778334475 @default.

• next