Lack of Alpha-Synuclein Modulates Microglial Phenotype In Vitro
Alpha (α)-synuclein neuronal effects are continually being defined although its role in regulating glial phenotypes remains unclear. An ability to regulate microglial activation was investigated using primary cultures from wild type and α-synuclein deficient mice ( Snca − / − ). Snca − / − microglia...
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Published in | Neurochemical research Vol. 36; no. 6; pp. 994 - 1004 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
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Springer US
01.06.2011
Springer Nature B.V |
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Abstract | Alpha (α)-synuclein neuronal effects are continually being defined although its role in regulating glial phenotypes remains unclear. An ability to regulate microglial activation was investigated using primary cultures from wild type and α-synuclein deficient mice (
Snca
−
/
−
).
Snca
−
/
−
microglia demonstrated increased secretion of the cytokine tumor necrosis factor-alpha (TNF-α), impaired phagocytic ability, elevated prostaglandin levels, and increased protein levels of key enzymes in lipid-mediated signaling events, cytosolic phospholipase (cPLA
2
), cyclooxygenase-2 (Cox-2) and phospholipase D2 (PLD2) when compared to wild type cells. Increased cytokine secretion and cPLA
2
and Cox-2 levels in
Snca
−
/
−
microglia were partially attenuated by inhibiting PLD-dependent signaling with n-butanol treatment. |
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AbstractList | Alpha (α)-synuclein neuronal effects are continually being defined although its role in regulating glial phenotypes remains unclear. An ability to regulate microglial activation was investigated using primary cultures from wild type and α-synuclein deficient mice (Snca-/-). Snca-/- microglia demonstrated increased secretion of the cytokine tumor necrosis factor-alpha (TNF-α), impaired phagocytic ability, elevated prostaglandin levels, and increased protein levels of key enzymes in lipid-mediated signaling events, cytosolic phospholipase (cPLA(2)), cyclooxygenase-2 (Cox-2) and phospholipase D2 (PLD2) when compared to wild type cells. Increased cytokine secretion and cPLA(2) and Cox-2 levels in Snca-/- microglia were partially attenuated by inhibiting PLD-dependent signaling with n-butanol treatment. Alpha (α)-synuclein neuronal effects are continually being defined although its role in regulating glial phenotypes remains unclear. An ability to regulate microglial activation was investigated using primary cultures from wild type and α-synuclein deficient mice (Snca ^sup -/-^). Snca ^sup -/-^ microglia demonstrated increased secretion of the cytokine tumor necrosis factor-alpha (TNF-α), impaired phagocytic ability, elevated prostaglandin levels, and increased protein levels of key enzymes in lipid-mediated signaling events, cytosolic phospholipase (cPLA^sub 2^), cyclooxygenase-2 (Cox-2) and phospholipase D2 (PLD2) when compared to wild type cells. Increased cytokine secretion and cPLA^sub 2^ and Cox-2 levels in Snca ^sup -/-^ microglia were partially attenuated by inhibiting PLD-dependent signaling with n-butanol treatment.[PUBLICATION ABSTRACT] Alpha (α)-synuclein neuronal effects are continually being defined although its role in regulating glial phenotypes remains unclear. An ability to regulate microglial activation was investigated using primary cultures from wild type and α-synuclein deficient mice ( Snca − / − ). Snca − / − microglia demonstrated increased secretion of the cytokine tumor necrosis factor-alpha (TNF-α), impaired phagocytic ability, elevated prostaglandin levels, and increased protein levels of key enzymes in lipid-mediated signaling events, cytosolic phospholipase (cPLA 2 ), cyclooxygenase-2 (Cox-2) and phospholipase D2 (PLD2) when compared to wild type cells. Increased cytokine secretion and cPLA 2 and Cox-2 levels in Snca − / − microglia were partially attenuated by inhibiting PLD-dependent signaling with n-butanol treatment. |
Author | Golovko, Mikhail Y. Murphy, Eric J. Rojanathammanee, Lalida Austin, Susan A. Combs, Colin K. |
Author_xml | – sequence: 1 givenname: Susan A. surname: Austin fullname: Austin, Susan A. organization: Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota, School of Medicine and Health Sciences – sequence: 2 givenname: Lalida surname: Rojanathammanee fullname: Rojanathammanee, Lalida organization: Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota, School of Medicine and Health Sciences – sequence: 3 givenname: Mikhail Y. surname: Golovko fullname: Golovko, Mikhail Y. organization: Department of Pharmacology, Physiology and Therapeutics, University of North Dakota School of Medicine and Health Sciences – sequence: 4 givenname: Eric J. surname: Murphy fullname: Murphy, Eric J. organization: Department of Pharmacology, Physiology and Therapeutics, University of North Dakota School of Medicine and Health Sciences – sequence: 5 givenname: Colin K. surname: Combs fullname: Combs, Colin K. email: ccombs@medicine.nodak.edu organization: Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota, School of Medicine and Health Sciences |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21384098$$D View this record in MEDLINE/PubMed |
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Keywords | α-Synuclein Phagocytosis Parkinson Phospholipase D Cytokine Microglia |
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Snippet | Alpha (α)-synuclein neuronal effects are continually being defined although its role in regulating glial phenotypes remains unclear. An ability to regulate... |
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SubjectTerms | alpha-Synuclein - genetics alpha-Synuclein - physiology Animals Biochemistry Biomedical and Life Sciences Biomedicine Blotting, Western Cell Biology Mice Mice, Knockout Microglia - physiology Neurochemistry Neurology Neurosciences Original Paper |
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Title | Lack of Alpha-Synuclein Modulates Microglial Phenotype In Vitro |
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