STAT1 and STAT6 orchestrate Cbs transcription and transsulfur metabolism in microglia and contribute to parkinson’s disease-related neuroinflammation

Microglia-mediated neuroinflammation is implicated in the pathogenesis of Parkinson’s disease (PD). Cystathionine β-synthase (CBS) and transsulfur metabolism modulate neuroinflammation. However, the regulation of Cbs transcription is poorly understood, and it remains unknown whether microglial CBS e...

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Published inCellular and molecular life sciences : CMLS Vol. 82; no. 1; pp. 294 - 20
Main Authors Liu, Yang, Wang, Zhen, Ma, Ya-Ting, Chen, Yu-Xuan, Qian, Xin-Yi, Hou, Xiao-Ou, Wan, Bo, Ren, Hai-Gang, Hu, Li-Fang
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 30.07.2025
Springer Nature B.V
Springer
Subjects
Antibodies
Biochemistry
Biomedical and Life Sciences
Biomedicine
CBS
Cell Biology
Cystathionine b-synthase
DJ-1
Dopamine receptors
Fibrils
Gene regulation
Genetic factors
Homeostasis
Inflammation
Life Sciences
Lipopolysaccharides
Metabolism
Metabolites
Microglia
Movement disorders
Neurodegenerative diseases
Neurotoxicity
Nitric oxide
Original
Original Article
PARK7 protein
Parkinson's disease
Pathogenesis
Penicillin
Proteins
Signal transduction
STAT1
Stat1 protein
STAT6
Stat6 protein
Stimulation
Sulfur
Synuclein
Transcription activation
Transsulfur metabolism
Tumor necrosis factor-TNF
γ-Interferon
United States > US
Switzerland
China
Shanghai China
STAT6
DJ-1
CBS
STAT1
Transsulfur metabolism
Microglia
Online AccessGet full text

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Abstract Microglia-mediated neuroinflammation is implicated in the pathogenesis of Parkinson’s disease (PD). Cystathionine β-synthase (CBS) and transsulfur metabolism modulate neuroinflammation. However, the regulation of Cbs transcription is poorly understood, and it remains unknown whether microglial CBS expression is affected by genetic factors in PD. Here, our in vitro study revealed that microglial CBS expression was downregulated by lipopolysaccharide (LPS)/interferon-γ (IFN-γ) but upregulated by interleukin (IL)-4/IL-13 stimulation. CBS and transsulfur metabolism not only inhibited inflammation but also promoted the anti-inflammatory transition of microglia. The mice with conditional microglial Cbs overexpression conferred resistance to LPS-induced neuroinflammation and dopaminergic neuron damage. A novel regulatory effect of the signal transducer and activator of transcription (STAT) family on Cbs transcription was identified: STAT1 as a suppressor, whereas STAT6 as an enhancer of Cbs transcription. PD-related gene DJ-1 knockdown (KD) decreased Cbs transcription through STAT1 activation in microglia. Moreover, Cbs overexpression alleviated the susceptibility of DJ-1 KD microglia to α-synuclein preformed fibrils (α-Syn PFFs) stimulation and the neurotoxicity to dopaminergic cells. Taken together, our findings reveal novel and opposite regulatory effects of STAT1 and STAT6 on microglial Cbs transcription in response to pro- and anti-inflammatory stimulation and demonstrate that CBS acts downstream of DJ-1, highlighting its role in PD.
AbstractList Microglia-mediated neuroinflammation is implicated in the pathogenesis of Parkinson’s disease (PD). Cystathionine β-synthase (CBS) and transsulfur metabolism modulate neuroinflammation. However, the regulation of Cbs transcription is poorly understood, and it remains unknown whether microglial CBS expression is affected by genetic factors in PD. Here, our in vitro study revealed that microglial CBS expression was downregulated by lipopolysaccharide (LPS)/interferon-γ (IFN-γ) but upregulated by interleukin (IL)-4/IL-13 stimulation. CBS and transsulfur metabolism not only inhibited inflammation but also promoted the anti-inflammatory transition of microglia. The mice with conditional microglial Cbs overexpression conferred resistance to LPS-induced neuroinflammation and dopaminergic neuron damage. A novel regulatory effect of the signal transducer and activator of transcription (STAT) family on Cbs transcription was identified: STAT1 as a suppressor, whereas STAT6 as an enhancer of Cbs transcription. PD-related gene DJ-1 knockdown (KD) decreased Cbs transcription through STAT1 activation in microglia. Moreover, Cbs overexpression alleviated the susceptibility of DJ-1 KD microglia to α-synuclein preformed fibrils (α-Syn PFFs) stimulation and the neurotoxicity to dopaminergic cells. Taken together, our findings reveal novel and opposite regulatory effects of STAT1 and STAT6 on microglial Cbs transcription in response to pro- and anti-inflammatory stimulation and demonstrate that CBS acts downstream of DJ-1, highlighting its role in PD.
Abstract Microglia-mediated neuroinflammation is implicated in the pathogenesis of Parkinson’s disease (PD). Cystathionine β-synthase (CBS) and transsulfur metabolism modulate neuroinflammation. However, the regulation of Cbs transcription is poorly understood, and it remains unknown whether microglial CBS expression is affected by genetic factors in PD. Here, our in vitro study revealed that microglial CBS expression was downregulated by lipopolysaccharide (LPS)/interferon-γ (IFN-γ) but upregulated by interleukin (IL)-4/IL-13 stimulation. CBS and transsulfur metabolism not only inhibited inflammation but also promoted the anti-inflammatory transition of microglia. The mice with conditional microglial Cbs overexpression conferred resistance to LPS-induced neuroinflammation and dopaminergic neuron damage. A novel regulatory effect of the signal transducer and activator of transcription (STAT) family on Cbs transcription was identified: STAT1 as a suppressor, whereas STAT6 as an enhancer of Cbs transcription. PD-related gene DJ-1 knockdown (KD) decreased Cbs transcription through STAT1 activation in microglia. Moreover, Cbs overexpression alleviated the susceptibility of DJ-1 KD microglia to α-synuclein preformed fibrils (α-Syn PFFs) stimulation and the neurotoxicity to dopaminergic cells. Taken together, our findings reveal novel and opposite regulatory effects of STAT1 and STAT6 on microglial Cbs transcription in response to pro- and anti-inflammatory stimulation and demonstrate that CBS acts downstream of DJ-1, highlighting its role in PD.
Microglia-mediated neuroinflammation is implicated in the pathogenesis of Parkinson’s disease (PD). Cystathionine β-synthase (CBS) and transsulfur metabolism modulate neuroinflammation. However, the regulation of Cbs transcription is poorly understood, and it remains unknown whether microglial CBS expression is affected by genetic factors in PD. Here, our in vitro study revealed that microglial CBS expression was downregulated by lipopolysaccharide (LPS)/interferon-γ (IFN-γ) but upregulated by interleukin (IL)-4/IL-13 stimulation. CBS and transsulfur metabolism not only inhibited inflammation but also promoted the anti-inflammatory transition of microglia. The mice with conditional microglial Cbs overexpression conferred resistance to LPS-induced neuroinflammation and dopaminergic neuron damage. A novel regulatory effect of the signal transducer and activator of transcription (STAT) family on Cbs transcription was identified: STAT1 as a suppressor, whereas STAT6 as an enhancer of Cbs transcription. PD-related gene DJ-1 knockdown (KD) decreased Cbs transcription through STAT1 activation in microglia. Moreover, Cbs overexpression alleviated the susceptibility of DJ-1 KD microglia to α-synuclein preformed fibrils (α-Syn PFFs) stimulation and the neurotoxicity to dopaminergic cells. Taken together, our findings reveal novel and opposite regulatory effects of STAT1 and STAT6 on microglial Cbs transcription in response to pro- and anti-inflammatory stimulation and demonstrate that CBS acts downstream of DJ-1, highlighting its role in PD.
ArticleNumber 294
Author Ma, Ya-Ting
Wan, Bo
Chen, Yu-Xuan
Ren, Hai-Gang
Hou, Xiao-Ou
Wang, Zhen
Qian, Xin-Yi
Liu, Yang
Hu, Li-Fang
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Issue 1
Keywords STAT6
DJ-1
CBS
STAT1
Transsulfur metabolism
Microglia
Language English
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Snippet Microglia-mediated neuroinflammation is implicated in the pathogenesis of Parkinson’s disease (PD). Cystathionine β-synthase (CBS) and transsulfur metabolism...
Abstract Microglia-mediated neuroinflammation is implicated in the pathogenesis of Parkinson’s disease (PD). Cystathionine β-synthase (CBS) and transsulfur...
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StartPage 294
SubjectTerms Antibodies
Biochemistry
Biomedical and Life Sciences
Biomedicine
CBS
Cell Biology
Cystathionine b-synthase
DJ-1
Dopamine receptors
Fibrils
Gene regulation
Genetic factors
Homeostasis
Inflammation
Life Sciences
Lipopolysaccharides
Metabolism
Metabolites
Microglia
Movement disorders
Neurodegenerative diseases
Neurotoxicity
Nitric oxide
Original
Original Article
PARK7 protein
Parkinson's disease
Pathogenesis
Penicillin
Proteins
Signal transduction
STAT1
Stat1 protein
STAT6
Stat6 protein
Stimulation
Sulfur
Synuclein
Transcription activation
Transsulfur metabolism
Tumor necrosis factor-TNF
γ-Interferon
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Title STAT1 and STAT6 orchestrate Cbs transcription and transsulfur metabolism in microglia and contribute to parkinson’s disease-related neuroinflammation
URI https://link.springer.com/article/10.1007/s00018-025-05768-9
https://www.ncbi.nlm.nih.gov/pubmed/40736565
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