Cited by 13Neuroinflammation and Neurodegeneration MechanismsMultiple Sclerosis Research StudiesNeuroscience and Neuropharmacology Research

Interferon-Beta Induces Major Histocompatibility Complex of Class I (MHC-I) Expression and a Proinflammatory Phenotype in Cultivated Human Astrocytes

Ignarro, Raffaela Silvestre, Bombeiro, André Luis, Chiarotto, Gabriela Bortolança, Cartarozzi, Luciana Politti, Coser, Lilian de Oliveira, Ghizoni, Enrico, Tedeschi, Helder, Cendes, Fernando +3 more·2022·Differentiation

Abstract

Major histocompatibility complex class I (MHC-I) has been implicated in several types of neuroplasticity phenomena. Interferon beta-1b (IFN-β) increases MHC-I expression by motoneurons after sciatic nerve crush in mice, improving axonal growth and functional recovery. Additionally, IFN-β induces glial hypertrophy associated with upregulation of glial fibrillary acidic protein (GFAP) and MHC-I in murine astrocytes in vitro. As knowledge about MHC-I and its role in synaptic plasticity in human astrocytes (HAs) is scarce, we investigated these aspects in mature HAs obtained from the neocortex of patients undergoing surgery due to hippocampal sclerosis. Cells were exposed to media in the absence (0 IU/ml) or presence of IFN-β for 5 days (500 IU/ml). Beta-2 microglobulin (β2m), a component of the MHC-I, GFAP and vimentin proteins, was quantified by flow cytometry (FC) and increased by 100%, 60% and 46%, respectively, after IFN-β exposure. We also performed qRT-PCR gene expression analyses for β2m, GFAP, vimentin, and pro- and anti-inflammatory cytokines. Our data showed that IFN-β-treated astrocytes displayed β2m and GFAP gene upregulation. Additionally, they presented a proinflammatory profile with increase in the IL-6 and IL-1β genes and a tendency to upregulate TNF-α. Moreover, we evaluated the effect of HAs conditioned medium (CM) on the formation/maintenance of neurites/synapses by the PC12 lineage. Synaptophysin protein expression was quantified by FC. The CM of IFN-β-activa…

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Crossref · 10.1016/j.diff.2022.10.004

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Authors
Ignarro, R. S., Bombeiro, A. L., Chiarotto, G. B., Cartarozzi, L. P., Coser, L. D. O., Ghizoni, E., Tedeschi, H., Cendes, F., Lopes-Cendes, I., Rogerio, F., & Oliveira, A. L. R. D.
Affiliations
Universidade Estadual de Campinas (UNICAMP) (BR)
Corresponding author
Oliveira, Alexandre Leite Rodrigues de
Venue
Differentiation
Publisher
Elsevier BV
Published
2022-11
Volume
128
Pages
43-56
ISSN
0301-4681 (ISSN-L)
OpenAlex
W4306318690
Cited by
13
References
7
Citations by year
2026: 3 · 2025: 3 · 2024: 5 · 2023: 1 · 2022: 1
FWCI
0.88
Type
journal article
Language
en
Open access
closed
Locations
  • Differentiation (publishedVersion)
  • PubMed (publishedVersion)
Funders
Fundação de Amparo à Pesquisa do Estado de São Paulo (2018/05006\u20130, 2013/07559\u20133, 2017/03619\u20132, 2285/17)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
interferon-beta, MHC class I, human astrocytes, beta2-microglobulin, glial fibrillary acidic protein, vimentin, astrocyte activation, inflammatory cytokines, interleukin-6, IL-1β, TNF-α, conditioned medium, synaptophysin, neurite outgrowth, hippocampal sclerosis, neuroplasticity
MeSH terms
Animals, Astrocytes, Humans, Major Histocompatibility Complex, Phenotype, Vimentin, Histocompatibility Antigens Class I, Synaptophysin, Interferon-beta, Mice

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