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

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Sutinen, Elina M. (author)

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

Article/chapterEnglish2014

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2014-08-07
Frontiers Media SA,2014
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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

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Language:English
Summary in:English

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Subject category:art swepub-publicationtype

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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.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Neurologi hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Neurology hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Neurovetenskaper hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Neurosciences hsv//eng
Interleukin-18
inflammation
neurodegenerative diseases
proteomics
oxidative stress related proteins
CRMP2
DDAH
MMP14

Added entries (persons, corporate bodies, meetings, titles ...)

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

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In:Frontiers in Cellular Neuroscience: Frontiers Media SA8, s. 214-1662-5102

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MEDICAL AND HEALTH SCIENCES: MEDICAL AND HEAL ...; and Clinical Medicin ...; and Neurology

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