Role of CXCR1 and Interleukin-8 in Methamphetamine-Induced Neuronal Apoptosis

Du, Songlin; Zhang, Wei; Xia, Yunlong; Luo, Xiangjian; Tan, Xiaoxue; Liu, Chao; Qiao, Dongfang; Wang, Huijun

doi:10.3389/fncel.2018.00230

Cited by 28 publications

(41 citation statements)

References 58 publications

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“…In this study, we found that the expression of the apoptosis‐related proteins Cleaved Caspase‐3 and Cleaved PARP was increased significantly after METH exposure, which indicated that apoptosis was increased by METH. These results are consistent with previous studies (Du et al, ; Xu et al, ).…”

Section: Discussionsupporting

confidence: 94%

“…METH is toxic to all systems of the body, especially the central nervous system (Yang et al, ). Accumulating evidence shows that METH induces apoptosis, oxidative stress, and mitochondrial dysfunction in vivo and in vitro (Du et al, ; Foroughi, Khaksari, Rahmati, Bitaraf, & Shayannia, ; Shin et al, ; Xu et al, ). Furthermore, METH can lead to the damage of dopaminergic neurons and Parkinson‐like pathology (Biagioni et al, ; Li et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Effect of Parkin on methamphetamine‐induced α‐synuclein degradation dysfunction in vitro and in vivo

et al. 2020

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Introduction Methamphetamine (METH) is a psychostimulant drug with complicated neurotoxicity, and abuse of METH is very common. Studies have shown that METH exposure causes alpha‐synuclein (α‐syn) accumulation. However, the mechanism of α‐syn accumulation has not been determined. Methods In this study, we established cell and animal models of METH intoxication to evaluate how METH affects α‐syn expression. In addition, to explore METH‐induced neurotoxicity, we measured the level of Parkin and the phosphorylation levels of α‐syn, Polo‐like kinase 2 (PLK2), the proteasome activity marker CD3δ, and the apoptosis‐related proteins Caspase‐3 and PARP. Parkin is a key enzyme in the ubiquitin–proteasome system. In addition, the effect of Parkin on METH‐induced neurotoxicity was investigated by overexpressing it in vitro and in vivo. Results METH exposure increased polyubiquitin and α‐syn expression, as did MG132. Furthermore, the level of Parkin and the interaction between Parkin and α‐syn decreased after METH exposure. Importantly, the increases in α‐syn expression and neurotoxicity were relieved by Parkin overexpression. Conclusions By establishing stable cell lines and animal models that overexpress Parkin, we confirmed Parkin as an important factor in METH‐induced α‐syn degradation dysfunction in vitro and in vivo. Parkin may be a promising target for the treatment of METH‐induced neurotoxicity.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Effect of Parkin on methamphetamine‐induced α‐synuclein degradation dysfunction in vitro and in vivo

et al. 2020

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“…In all, these data confirm that METH treatment elicits gliosis and neuroinflammation within cerebral organoids as indicated by enhanced IL-6 expression, overexpression of GFAP and NLRP-1. Consistent with our findings, it was recently found that neuroinflammation was induced in primary mice astrocytes and astrocytic cell lines treated with METH through the involvement of Toll-Like Receptor 4, caspase 11, and nuclear factor-Kappa B [42][43][44]. The induction of neuroinflammation resulted in neurotoxicity by upregulating cytokines IL-6 and IL-8 levels [42,44].…”

Section: Discussionsupporting

confidence: 92%

Glial cell diversity and methamphetamine-induced neuroinflammation in human cerebral organoids

et al. 2020

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Methamphetamine (METH) is a potent stimulant that induces a euphoric state but also causes cognitive impairment, neurotoxicity and neurodevelopmental deficits. Yet, the molecular mechanisms by which METH causes neurodevelopmental defects have remained elusive. Here we utilized human cerebral organoids and single-cell RNA sequencing (scRNA-seq) to study the effects of prenatal METH exposure on fetal brain development. We analyzed 20,758 cells from eight untreated and six METH-treated cerebral organoids and found that the organoids developed from embryonic stem cells contained a diverse array of glial and neuronal cell types. We further identified transcriptionally distinct populations of astrocytes and oligodendrocytes within cerebral organoids. Treatment of organoids with METH-induced marked changes in transcription in multiple cell types, including astrocytes and neural progenitor cells. METH also elicited novel astrocyte-specific gene expression networks regulating responses to cytokines, and inflammasome. Moreover, upregulation of immediate early genes, complement factors, apoptosis, and immune response genes suggests a neuroinflammatory program induced by METH regulating neural stem cell proliferation, differentiation, and cell death. Finally, we observed marked METH-induced changes in neuroinflammatory and cytokine gene expression at the RNA and protein levels. Our data suggest that human cerebral organoids represent a model system to study drug-induced neuroinflammation at single-cell resolution.

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“…The results of this study indicated that (1) serum levels of IL-6 and IL-8 were increased in MAP patients; (2) IL-2R levels had a negative correlation with the intensity of positive psychotic symptoms, but IL-6 and IL-8 levels did not; (3) cognitive dysfunction was present in the MAP patients (MOCA total scores of 26 and higher are generally considered normal); and (4) the severity of different types of cognitive impairment was positively correlated with IL-6, IL-8, and IL-10 levels. These results agree with the aforementioned findings indicating altered immune response activity in MAP patients (14)(15)(16)(17)(18).…”

Section: Discussionsupporting

confidence: 93%

The Relationship Between Serum Cytokine Levels and the Degree of Psychosis and Cognitive Impairment in Patients With Methamphetamine-Associated Psychosis in Chinese Patients

et al. 2020

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Background: Cytokine levels can be changed in methamphetamine (METH) use disorders (MUDs) and primary psychosis. The present study assessed serum levels of some kinds of interleukins (ILs) in METH-associated psychosis (MAP) and their relationships with psychotic symptoms and cognitive dysfunction.Methods: Serum IL-2R, IL-6, IL-8, and IL-10 levels were examined by chemiluminescence assays in MAP patients (n = 119) and healthy controls (n = 108). The Positive and Negative Syndrome Scale (PANSS) and Montreal Cognitive Assessment (MOCA) were administered.Results: Serum levels of IL-6 and IL-8 were significantly increased in MAP patients (all p < 0.05). There was a negative relationship between IL-2R levels and PANSS positive (P) subscale scores (r = −0.193, p = 0.035). IL-6, IL-8 and IL-10 levels were all negatively correlated with the naming, delayed recall and orientation subscores on the MOCA (r = −0.209, p = 0.022; r = −0.245, p = 0.007; r = −0.505, p < 0.001, respectively).Conclusions: Our results indicate that immune disturbances are related to MAP and that IL-2R, IL-6, IL-8, and IL-10 are associated with the severity of psychotic symptoms and cognitive function impairment.

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Role of CXCR1 and Interleukin-8 in Methamphetamine-Induced Neuronal Apoptosis

Cited by 28 publications

References 58 publications

Effect of Parkin on methamphetamine‐induced α‐synuclein degradation dysfunction in vitro and in vivo

Effect of Parkin on methamphetamine‐induced α‐synuclein degradation dysfunction in vitro and in vivo

Glial cell diversity and methamphetamine-induced neuroinflammation in human cerebral organoids

The Relationship Between Serum Cytokine Levels and the Degree of Psychosis and Cognitive Impairment in Patients With Methamphetamine-Associated Psychosis in Chinese Patients

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