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Haas SJ, Zhou X, Machado V, et al. Expression of Tgfβ1 and Inflammatory Markers in the 6-hydroxydopamine Mouse Model of Parkinson's Disease. Front Mol Neurosci. 2016;9:7doi: 10.3389/fnmol.2016.00007.
Haas, S. J., Zhou, X., Machado, V., Wree, A., Krieglstein, K., & Spittau, B. (2016). Expression of Tgfβ1 and Inflammatory Markers in the 6-hydroxydopamine Mouse Model of Parkinson's Disease. Frontiers in molecular neuroscience, 97. https://doi.org/10.3389/fnmol.2016.00007
Haas, Stefan Jean-Pierre, et al. "Expression of Tgfβ1 and Inflammatory Markers in the 6-hydroxydopamine Mouse Model of Parkinson's Disease." Frontiers in molecular neuroscience vol. 9 (2016): 7. doi: https://doi.org/10.3389/fnmol.2016.00007
Haas SJ, Zhou X, Machado V, Wree A, Krieglstein K, Spittau B. Expression of Tgfβ1 and Inflammatory Markers in the 6-hydroxydopamine Mouse Model of Parkinson's Disease. Front Mol Neurosci. 2016 Feb 03;9:7. doi: 10.3389/fnmol.2016.00007. eCollection 2016. PMID: 26869879; PMCID: PMC4737885.
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Front Mol Neurosci. 2016 Feb 03;9:7. doi: 10.3389/fnmol.2016.00007. eCollection 2016.

Expression of Tgfβ1 and Inflammatory Markers in the 6-hydroxydopamine Mouse Model of Parkinson's Disease.

Frontiers in molecular neuroscience

Stefan Jean-Pierre Haas, Xiaolai Zhou, Venissa Machado, Andreas Wree, Kerstin Krieglstein, Björn Spittau

Affiliations

  1. Institute of Anatomy, Rostock University Medical Center Rostock, Germany.
  2. Department of Molecular Embryology, Institute of Anatomy and Cell Biology, Albert-Ludwigs-UniversityFreiburg, Germany; Department of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell UniversityIthaca, NY, USA.
  3. Department of Molecular Embryology, Institute of Anatomy and Cell Biology, Albert-Ludwigs-UniversityFreiburg, Germany; Spemann Graduate School of Biology and Medicine (SGBM), Albert-Ludwigs-UniversityFreiburg, Germany; Faculty of Biology, Albert-Ludwigs-UniversityFreiburg, Germany.
  4. Spemann Graduate School of Biology and Medicine (SGBM), Albert-Ludwigs-University Freiburg, Germany.

PMID: 26869879 PMCID: PMC4737885 DOI: 10.3389/fnmol.2016.00007

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder that is characterized by loss of midbrain dopaminergic (mDA) neurons in the substantia nigra (SN). Microglia-mediated neuroinflammation has been described as a common hallmark of PD and is believed to further trigger the progression of neurodegenerative events. Injections of 6-hydroxydopamine (6-OHDA) are widely used to induce degeneration of mDA neurons in rodents as an attempt to mimic PD and to study neurodegeneration, neuroinflammation as well as potential therapeutic approaches. In the present study, we addressed microglia and astroglia reactivity in the SN and the caudatoputamen (CPu) after 6-OHDA injections into the medial forebrain bundle (MFB), and further analyzed the temporal and spatial expression patterns of pro-inflammatory and anti-inflammatory markers in this mouse model of PD. We provide evidence that activated microglia as well as neurons in the lesioned SN and CPu express Transforming growth factor β1 (Tgfβ1), which overlaps with the downregulation of pro-inflammatory markers Tnfα, and iNos, and upregulation of anti-inflammatory markers Ym1 and Arg1. Taken together, the data presented in this study suggest an important role for Tgfβ1 as a lesion-associated factor that might be involved in regulating microglia activation states in the 6-OHDA mouse model of PD in order to prevent degeneration of uninjured neurons by microglia-mediated release of neurotoxic factors such as Tnfα and nitric oxide (NO).

Keywords: 6-OHDA; Tgfβ1; Tnfα; astrocytes; microglia

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