posted on 2024-03-02, 16:22authored byYuzhu Zhang, Yao Pei, Yumiao Sun, Xiaoxi Yang, Jiefeng Liang, Zhipeng Yin, Qian S. Liu, Qunfang Zhou, Guibin Jiang
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.