Locatelli, Giuseppe ORCID: 0000-0002-2179-4407, Marques-Ferreira, Filipa, Katsoulas, Antonis, Kalaitzaki, Vasileia ORCID: 0000-0002-4158-2321, Krueger, Martin, Ingold-Heppner, Barbara, Walthert, Sabrina, Sankowski, Roman, da Costa, Olivia Prazeres, Dolga, Amalia ORCID: 0000-0001-5400-5614, Huber, Magdalena, Gold, Maike, Culmsee, Carsten, Waisman, Ari, Bechmann, Ingo, Milchevskaya, Vladislava, Prinz, Marco, Tresch, Achim, Becher, Burkhard ORCID: 0000-0002-1541-7867 and Buch, Thorsten ORCID: 0000-0002-2236-9074 . IGF1R expression by adult oligodendrocytes is not required in the steady-state but supports neuroinflammation. Glia. HOBOKEN: WILEY. ISSN 1098-1136

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Abstract

In the central nervous system (CNS), insulin-like growth factor 1 (IGF-1) regulates myelination by oligodendrocyte (ODC) precursor cells and shows anti-apoptotic properties in neuronal cells in different in vitro and in vivo systems. Previous work also suggests that IGF-1 protects ODCs from cell death and enhances remyelination in models of toxin-induced and autoimmune demyelination. However, since evidence remains controversial, the therapeutic potential of IGF-1 in demyelinating CNS conditions is unclear. To finally shed light on the function of IGF1-signaling for ODCs, we deleted insulin-like growth factor 1 receptor (IGF1R) specifically in mature ODCs of the mouse. We found that ODC survival and myelin status were unaffected by the absence of IGF1R until 15 months of age, indicating that IGF-1 signaling does not play a major role in post-mitotic ODCs during homeostasis. Notably, the absence of IGF1R did neither affect ODC survival nor myelin status upon cuprizone intoxication or induction of experimental autoimmune encephalomyelitis (EAE), models for toxic and autoimmune demyelination, respectively. Surprisingly, however, the absence of IGF1R from ODCs protected against clinical neuroinflammation in the EAE model. Together, our data indicate that IGF-1 signaling is not required for the function and survival of mature ODCs in steady-state and disease.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Locatelli, GiuseppeUNSPECIFIEDorcid.org/0000-0002-2179-4407UNSPECIFIED
Marques-Ferreira, FilipaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Katsoulas, AntonisUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Kalaitzaki, VasileiaUNSPECIFIEDorcid.org/0000-0002-4158-2321UNSPECIFIED
Krueger, MartinUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ingold-Heppner, BarbaraUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Walthert, SabrinaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Sankowski, RomanUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
da Costa, Olivia PrazeresUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Dolga, AmaliaUNSPECIFIEDorcid.org/0000-0001-5400-5614UNSPECIFIED
Huber, MagdalenaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Gold, MaikeUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Culmsee, CarstenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Waisman, AriUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Bechmann, IngoUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Milchevskaya, VladislavaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Prinz, MarcoUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Tresch, AchimUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Becher, BurkhardUNSPECIFIEDorcid.org/0000-0002-1541-7867UNSPECIFIED
Buch, ThorstenUNSPECIFIEDorcid.org/0000-0002-2236-9074UNSPECIFIED
URN: urn:nbn:de:hbz:38-692469
DOI: 10.1002/glia.24299
Journal or Publication Title: Glia
Publisher: WILEY
Place of Publication: HOBOKEN
ISSN: 1098-1136
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
GROWTH-FACTOR-I; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS; BRAIN; IGF-1; MYELIN; CELLS; DEMYELINATION; ACTIVATION; CONTRIBUTEMultiple languages
NeurosciencesMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/69246

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