Female sex steroids and glia cells: Impact on multiple sclerosis lesion formation and fine tuning of the local neurodegenerative cellular network. (August 2016)

• Record Type: Journal Article
• Authors: Kipp, Markus; Hochstrasser, Tanja; Schmitz, Christoph; Beyer, Cordian
• Is Part Of: Neuroscience and biobehavioral reviews. Volume 67(2016)
• Page Start: 125
• Page End: 136
• Publication Date: 2016-08
• Subjects: Multiple sclerosis -- Astroglia -- Microglia -- Inflammation -- Invasion -- Immune cells -- Estrogen -- Progesterone -- Neuroinflammation -- Neuroprotection; AD Alzheimer's disease -- ADIOL 5-androsten-3ß, 17ß-diol -- AIDT autoimmune thyroid disease -- Akt Serine/threonine kinase -- ALS amyotrophic lateral sclerosis -- ATP adenosine tri-phosphate -- BBB blood–brain barrier -- BDNF brain-derived neurotrophic factor -- CCL chemokine (C-C motif) ligand -- CD cluster of designation -- CIS clinically isolated syndrome -- CNS central nervous system -- CNP 2′, 3′-cyclic nucleotide 3′-phosphodiesterase -- CtBP C-terminal-binding protein 1 -- DAMPs damage-associated molecular pattern -- 25-Dx putative membrane progesterone receptor -- E2 17ß-estradiol -- EAE experimental autoimmune encephalomyelitis -- ER estrogen receptor -- ERK1/2 extracellular signal-regulated kinases 1/2 -- FGF fibroblast growth factor -- GD Graves' disease -- GDNF glial-derived neurotrophic factor -- GFAP glial fibrillary acidic protein -- GPR30 G protein-coupled estrogen receptor 30 -- HT Hashimoto's thyroiditis -- IBA1 ionized calcium-binding adapter molecule 1 -- IFNγ interferon gamma -- IGF1 insulin-like growth factor 1 -- IL interleukin -- LPS lipopolysaccharides -- MBP myelin basic protein -- MCP monocyte chemoattractant protein -- MCT monocarboxylate transporter -- MHC major histocompatibility complex -- MMP matrix metalloproteinase -- mPRα membrane progesterone receptor alpha -- MHV mouse hepatitis virus -- MS multiple sclerosis -- mTOR mechanistic target of rapamycin -- Necl-1 nectin-like 1 -- NLRP NOD-like receptor protein -- NO nitric oxide -- Nrf2 nuclear factor (erythroid-derived 2)-like 2 -- Olig2 oligodendrocyte transcription factor 2 -- OPC oligodendrocyte precursor cell -- P progesterone -- PAMPs pathogen-associated molecular pattern -- PD Parkinson's disease -- PDGFRα platelet-derived growth factor receptor alpha -- Pgrmc1 progesterone receptor membrane component 1 -- PI3K phosphoinositide-3-kinase -- PLP proteolipid protein -- PPMS primary progressive MS -- PR progesterone receptor -- RA rheumatoid arthritis -- ROS reactive oxygen species -- RRMS Relapsing remitting MS -- SLE systemic lupus erythematosus -- SPMS Secondary progressive MS -- SFV Semliki Forest virus -- TBI traumatic brain injury -- TGFß transforming growth factor-beta -- Th cell T helper cell -- TLR Toll-like receptors -- TMEV Theiler's murine encephalomyelitis virus -- tMCAO transient focal middle cerebral artery occlusion -- TNFα tumor necrosis factor alpha -- VCAM-1 vascular cell adhesion molecule 1 -- VLA-4 integrin alpha4beta1 (very late antigen-4); Psychophysiology -- Periodicals; Human behavior -- Periodicals; Animal behavior -- Periodicals; Neurology -- Periodicals; Behavior -- Periodicals; Ethology -- Periodicals; Neurology -- Periodicals; Psychophysiologie -- Périodiques; Comportement humain -- Périodiques; Animaux -- Mœurs et comportement -- Périodiques; Neurologie -- Périodiques; Animal behavior; Human behavior; Neurology; Psychophysiology; Periodicals; Electronic journals; 573.8
• DOI: 10.1016/j.neubiorev.2015.11.016
• Languages: English
• ISSNs: 0149-7634

Abstract

Highlights: Local glia cells regulate immune cell recruitment in multiple sclerosis. Sex hormones are protective in multiple sclerosis. Glia–glia cell communication is pivotal for multiple sclerosis pathology. Abstract: Multiple sclerosis (MS) is a chronic inflammatory and demyelinating disease that shows a female-to-male gender prevalence and alleviation of disease activity during late stage pregnancy. In MS-related animal models, sex steroids ameliorate symptoms and protect from demyelination and neuronal damage. Underlying mechanisms of these protective avenues are continuously discovered, in part by using novel transgenic animal models. In this review article, we highlight the regulation of glia cell function by female sex steroids. We specifically focus on the relevance of glia cells for immune cell recruitment into the central nervous system and show how estrogen and progesterone can modulate these cell-cell communication pathways. Since MS is considered to have a strong neurodegenerative component, principal neuroprotective mechanisms, exerted by sex-steroids will be discussed as well. Activation of steroid receptors might not just act as immunosuppressant but at the same time harmonize brain-intrinsic networks to dampen neurodegeneration and, thus, disease progression in MS.