The role of reactive astrocytes in neurotoxicity induced by ultrafine particulate matter

Li, Ben; Chang, Xiaohan; Liang, Xiaomin; Liu, Ting; Shen, Yongmei; Zhang, Qianwen; Yang, Xiaohui; Lyu, Yi; Liu, Liangpo; Guo, Jian; Wu, Meiqiong; Gao, Yubin; Yan, Xiaoyan; Wang, Tong; Zhang, Wenping; Qiu, Yulan

doi:10.1016/j.scitotenv.2023.161416

Cited by 9 publications

(3 citation statements)

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“…By testing Fkbp5 , a regulator gene of glucocorticoid receptor activity and specific for A1 astrocytes, the exposure concentration-dependent elevation in the mRNA level of this biomarker was observed for SRM1648a treatments (Figure S2A), revealing the induction of astrocytic A1 activation. This result was consistent with the previous finding that ultrafine PM could cause inflammatory reactions through inducing A1 reactive astrocytes. , …”

Section: Discussionmentioning

confidence: 95%

“…23 The mixed cell population with two distinct states are important for the initiation and progression of various neurological disorders. 24 Though ultrafine PM was considered to induce neuroinflammation through dominantly triggering the astrocytic A1 activation, a previous research showed that PM 0.2 exposure concomitantly upregulated some of the A2 specific transcripts, 25 showing the intricate mediation of atmospheric PM on the dichotomy of the A1/A2 astrocytic phenotypes.…”

Section: Discussionmentioning

confidence: 99%

“…This result was consistent with the previous finding that ultrafine PM could cause inflammatory reactions through inducing A1 reactive astrocytes. 12,25 As the commonly used markers specific for A2 astrocytes, S100a10 and Sphk1 regulate toll-like receptor (TLR)-triggered downstream signaling and microglial phagocytosis, respectively. 27,28 Specifically, S100A10 suppresses the inflammatory responses through interfering with the recruitment and activation of the receptor-proximal signaling components.…”

Section: Discussionmentioning

confidence: 99%

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AhR Agonistic Components in Urban Particulate Matter Regulate Astrocytic Activation and Function

Zhang,

Pei,

Sun

et al. 2024

Environ. Sci. Technol.

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Exposure to atmospheric particulate matter (PM) has been found to accelerate the onset of neurological disorders via the induction of detrimental neuroinflammatory responses. To reveal how astrocytes respond to urban atmospheric PM stimulation, a commercially available standard reference material (SRM1648a) was tested in this study on the activation of rat cortical astrocytes. The results showed that SRM1648a stimulation induced both A1 and A2 phenotypes in astrocytes, as characterized by the exposure concentration-dependent increases in Fkbp5, Sphk1, S100a10, and Il6 mRNA levels. Studying the functional alterations of astrocytes indicated that the neurotrophic factors of Gdnf and Ngf were transcriptionally upregulated due to astrocytic A2-type activation. SRM1648a also promoted autonomous motility of astrocytes and elevated the expressions of chemokines. The aryl hydrocarbon receptor (AhR) agonistic components, such as polycyclic aromatic hydrocarbons (PAHs), were recognized to greatly contribute to SRM1648a-induced effects on astrocytes, which was confirmed by the attenuation of PM-disturbed astrocytic effects via AhR blockage. This study, for the first time, uncovered the direct regulation of urban atmospheric PM on astrocytic activation and function and traced the containing bioactive components (e.g., PAHs) with AhR agonistic activity. The findings provided new knowledge on understanding the ambiguous neurological disturbance from ambient fine PM pollution.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%