Taurine protects dopaminergic neurons in a mouse Parkinson’s disease model through inhibition of microglial M1 polarization

Che, Yuning; Hou, Liyan; Sun, Fuqiang; Zhang, Cong; Liu, Xiaofang; Piao, Fengyuan; Zhang, Dan; Li, Huihua; Wang, Qingshan

doi:10.1038/s41419-018-0468-2

Cited by 116 publications

(78 citation statements)

References 55 publications

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“…Taurine is the single most abundantly free amino acid found in leukocyte cytosol (20-50 nM) [148], which exerts antioxidant effects by scavenging reactive oxygen species (ROS), such as hypohalous acids [149]. Hypobromous acid (HOBr) is a ROS generated by activated neutrophils and eosinophils at sites of inflammation through enzymatic activity of neutrophil myeloperoxidase (MPO) [150] and eosinophil peroxidase [151].…”

Section: Therapeutic Aspects Of Taurine-bromaminementioning

confidence: 99%

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease

et al. 2020

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Taurine is a non-protein amino acid that is expressed in the majority of animal tissues. With its unique sulfonic acid makeup, taurine influences cellular functions, including osmoregulation, antioxidation, ion movement modulation, and conjugation of bile acids. Taurine exerts anti-inflammatory effects that improve diabetes and has shown benefits to the cardiovascular system, possibly by inhibition of the renin angiotensin system. The beneficial effects of taurine are reviewed.

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Section: Therapeutic Aspects Of Taurine-bromaminementioning

confidence: 99%

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease

et al. 2020

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“…And several studies have approach NF-κB and NOX2 cascade to decrease neurodegeneration. Taurine, a major intracellular free β-amino acid in mammalian tissues, was neuroprotective in mice injected with paraquat and maneb ( Che et al, 2018 ). Taurine interfered with the NF-κB pathway and the membrane translocation of p47 phox (thus NOX2 activation), and it supressed paraquat and maneb-induced microglial M1 polarization.…”

Section: Neuroprotective Strategies Based On Immunomodulationmentioning

confidence: 99%

“…Taurine interfered with the NF-κB pathway and the membrane translocation of p47 phox (thus NOX2 activation), and it supressed paraquat and maneb-induced microglial M1 polarization. This resulted in decreased dopaminergic neurodegeneration and a-syn aggregation ( Che et al, 2018 ). Equally α-mangostin, a polyphenolicxanthone from mangosteen, also inhibited NOX2 and NF-κB signaling induced by a-syn in culture, thus supressing microglial release of pro-inflammatory cytokines, iNOS and ROS production ( Hu et al, 2016 ).…”

Section: Neuroprotective Strategies Based On Immunomodulationmentioning

confidence: 99%

Microglia Response During Parkinson’s Disease: Alpha-Synuclein Intervention

Ferreira

Romero‐Ramos

2018

Front. Cell. Neurosci.

165

138

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The discovery of the central role played by the protein alpha-synuclein in Parkinson’s disease and other Lewy body brain disorders has had a great relevance in the understanding of the degenerative process occurring in these diseases. In addition, during the last two decades, the evidence suggesting an immune response in Parkinson’s disease patients have multiplied. The role of the immune system in the disease is supported by data from genetic studies and patients, as well as from laboratory animal models and cell cultures. In the immune response, the microglia, the immune cell of the brain, will have a determinant role. Interestingly, alpha-synuclein is suggested to have a central function not only in the neuronal events occurring in Parkinson’s disease, but also in the immune response during the disease. Numerous studies have shown that alpha-synuclein can act directly on immune cells, such as microglia in brain, initiating a sterile response that will have consequences for the neuronal health and that could also translate in a peripheral immune response. In parallel, microglia should also act clearing alpha-synuclein thus avoiding an overabundance of the protein, which is crucial to the disease progression. Therefore, the microglia response in each moment will have significant consequences for the neuronal fate. Here we will review the literature addressing the microglia response in Parkinson’s disease with an especial focus on the protein alpha-synuclein. We will also reflect upon the limitations of the studies carried so far and in the therapeutic possibilities opened based on these recent findings.

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“…In response to neuronal injury, these two phenotypes have distinct characteristics. Upon the M1 activation state, microglia can release various proinflammatory cytokines, such as: IL-1β, TNF-α and IL-6, IL-12, IL-17 and IL-23; chemokines that include chemokine (C-C motif) ligand 2 (CCL2) and C-X-C motif chemokine 10 (CXCL10); express markers, cluster of differentiation 86 (CD86) and cluster of differentiation 16/32 (CD16/32); and free radicals through the NF-κB pathway that will adversely affect neuronal repair and regeneration (Mahad and Ransohoff, 2003 ; Kawanokuchi et al, 2006 ; Mosser and Edwards, 2008 ; Chhor et al, 2013 ; Davis et al, 2013 ; Franco and Fernández-Suárez, 2015 ; Subramaniam and Federoff, 2017 ; Che et al, 2018 ). Meanwhile, the M2 phenotype can act conversely by improving the brain’s repairing or regeneration processes by attenuating neuroinflammation.…”

Section: Microglial Activation and Neurodegenerationmentioning

confidence: 99%

Importance of GPCR-Mediated Microglial Activation in Alzheimer’s Disease

Haque

Kim

Jakaria

et al. 2018

Front. Cell. Neurosci.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder associated with impairment of cognition, memory deficits and behavioral abnormalities. Accumulation of amyloid beta (Aβ) is a characteristic hallmark of AD. Microglia express several GPCRs, which, upon activation by modulators, mediate microglial activation and polarization phenotype. This GPCR-mediated microglial activation has both protective and detrimental effects. Microglial GPCRs are involved in amyloid precursor protein (APP) cleavage and Aβ generation. In addition, microglial GPCRs are featured in the regulation of Aβ degradation and clearance through microglial phagocytosis and chemotaxis. Moreover, in response to Aβ binding on microglial Aβ receptors, they can trigger multiple inflammatory pathways. However, there is still a lack of insight into the mechanistic link between GPCR-mediated microglial activation and its pathological consequences in AD. Currently, the available drugs for the treatment of AD are mostly symptomatic and dominated by acetylcholinesterase inhibitors (AchEI). The selection of a specific microglial GPCR that is highly expressed in the AD brain and capable of modulating AD progression through Aβ generation, degradation and clearance will be a potential source of therapeutic intervention. Here, we have highlighted the expression and distribution of various GPCRs connected to microglial activation in the AD brain and their potential to serve as therapeutic targets of AD.

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Taurine protects dopaminergic neurons in a mouse Parkinson’s disease model through inhibition of microglial M1 polarization

Cited by 116 publications

References 55 publications

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease

Microglia Response During Parkinson’s Disease: Alpha-Synuclein Intervention

Importance of GPCR-Mediated Microglial Activation in Alzheimer’s Disease

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