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  • Sutinen, Elina M. (författare)

Interleukin-18 alters protein expressions of neurodegenerative diseases-linked proteins in human SH-SY5Y neuron-like cells

  • Artikel/kapitelEngelska2014

Förlag, utgivningsår, omfång ...

  • 2014-08-07
  • Frontiers Media SA,2014
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:uu-230949
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-230949URI
  • https://doi.org/10.3389/fncel.2014.00214DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Chronic inflammation and oxidative stress (OS) are present in Alzheimer's disease (AD) brains in addition to neuronal loss, Amyloid-beta (A beta) plaques and hyperphosphorylated tau-protein neurofibrillary tangles (NFTs). Previously we showed that levels of the pro-inflammatory cytokine, interleukin-18 (IL-18), are elevated in post-mortem AD brains. IL-18 can modulate the tau kinases, Cdk5 and GSK3?, as well as A beta-production. IL-18 levels are also increased in AD risk diseases, including type-2 diabetes and obesity. Here, we explored other IL-18 regulated proteins in neuron-like SH-SY5Y cells. Differentiated SH-SY5Y cells, incubated with IL-18 for 24, 48, or 72 h, were analyzed by two-dimensional gel electrophoresis (2D-DIGE). Specific altered protein spots were chosen and identified with mass spectrometry (MS) and verified by western immunoblotting (WIB). IL-18 had time-dependent effects on the SH-SY5Y proteome, modulating numerous protein levels/modifications. We concentrated on those related to OS (DDAH2, peroxiredoxins 2, 3, and 6, DJ-1, BLVRA), A beta-degradation (MMP14, TIMP2), A beta-aggregation (Septin-2), and modifications of axon growth and guidance associated, collapsin response mediator protein 2 (CRMP2). IL-18 significantly increased antioxidative enzymes, indicative of OS, and altered levels of glycolytic beta- and alpha-enolase and multifunctional 14-3-3 beta and -beta, commonly affected in neurodegenerative diseases. MMP14, TIMP2, alpha-enolase and 14-3-3 beta, indirectly involved in A? metabolism, as well as Septin-2 showed changes that increase A? levels. Increased 14-3-3 beta may contribute to GSK3 beta driven tau hyperphosphorylation and CRMP2 Thr514 and Ser522 phosphorylation with the Thr555-site, a target for Rho kinase, showing time-dependent changes. IL-18 also increased caspase-1 levels and vacuolization of the cells. Although our SH-SY5Y cells were not aged, as neurons in AD, our work suggests that heightened or prolonged IL-18 levels can drive protein changes of known relevance to AD pathogenesis.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Korolainen, Minna A. (författare)
  • Hayrinen, Jukka (författare)
  • Alafuzoff, IrinaUppsala universitet,Molekylär och morfologisk patologi(Swepub:uu)irial548 (författare)
  • Petratos, Steven (författare)
  • Salminen, Antero (författare)
  • Soininen, Hilkka (författare)
  • Pirttila, Tuula (författare)
  • Ojala, Johanna O. (författare)
  • Uppsala universitetMolekylär och morfologisk patologi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Frontiers in Cellular Neuroscience: Frontiers Media SA8, s. 214-1662-5102

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