Air Pollution Particulate Matter Exposure and Chronic Cerebral Hypoperfusion and Measures of White Matter Injury in a Murine Model

Liu, Qinghai; Shkirkova, Kristina; Lamorie‐Foote, Krista; Connor, Michelle; Patel, Arati; Babadjouni, Robin; Huuskonen, Mikko T; Montagne, Axel; Baertsch, Hans; Zhang, Hongqiao; Chen, Jiu Chiuan; Mack, Wendy J.; Walcott, Brian P.; Zloković, Berislav V.; Sioutas, Constantinos; Morgan, Todd E.; Finch, Caleb E.; Mack, William J.

doi:10.1289/ehp8792

Cited by 26 publications

(38 citation statements)

References 69 publications

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“…Exposure to nPM, even with potentially decreased potency, worsens cerebrovascular dysfunction and white matter injury in the setting of CCH. This indicates an interaction between these exposures that can yield supra-additive effects; a relationship has been demonstrated in Liu et al (16).…”

Section: Discussionsupporting

confidence: 53%

“… Table adapted from Liu et al. These batches of nPM have been reported from prior experiments ( 16 ). PNC, particle number concentration; TOM, total organic matter; PM, particulate matter; IHC, immunohistochemistry; MRI, magnetic resonance imaging.…”

Section: Methodsmentioning

confidence: 99%

“… Table adapted from Liu et al. These batches of nPM have been reported from prior experiments ( 16 ). …”

Section: Methodsmentioning

confidence: 99%

“… Table adapted from Liu et al. These batches of nPM have been reported from prior experiments ( 16 ). Units are ng/μg of PM mass.…”

Section: Methodsmentioning

confidence: 99%

“…The incision was closed, and the mouse recovered in a temperature-controlled environment. For details of the surgeries see Liu et al (16). Briefly, CBF drop right after insertion of microcoils was not different between filter+BCAS (35%) and nPM+BCAS (33%) groups.…”

Section: Bilateral Carotid Artery Stenosis (Bcas) Surgerymentioning

confidence: 99%

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Air Pollution Particulate Matter Amplifies White Matter Vascular Pathology and Demyelination Caused by Hypoperfusion

et al. 2021

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Cerebrovascular pathologies are commonly associated with dementia. Because air pollution increases arterial disease in humans and rodent models, we hypothesized that air pollution would also contribute to brain vascular dysfunction. We examined the effects of exposing mice to nanoparticulate matter (nPM; aerodynamic diameter ≤200 nm) from urban traffic and interactions with cerebral hypoperfusion. C57BL/6 mice were exposed to filtered air or nPM with and without bilateral carotid artery stenosis (BCAS) and analyzed by multiparametric MRI and histochemistry. Exposure to nPM alone did not alter regional cerebral blood flow (CBF) or blood brain barrier (BBB) integrity. However, nPM worsened the white matter hypoperfusion (decreased CBF on DSC-MRI) and exacerbated the BBB permeability (extravascular IgG deposits) resulting from BCAS. White matter MRI diffusion metrics were abnormal in mice subjected to cerebral hypoperfusion and worsened by combined nPM+BCAS. Axonal density was reduced equally in the BCAS cohorts regardless of nPM status, whereas nPM exposure caused demyelination in the white matter with or without cerebral hypoperfusion. In summary, air pollution nPM exacerbates cerebrovascular pathology and demyelination in the setting of cerebral hypoperfusion, suggesting that air pollution exposure can augment underlying cerebrovascular contributions to cognitive loss and dementia in susceptible elderly populations.

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Section: Discussionsupporting

confidence: 53%

Section: Methodsmentioning

confidence: 99%

“… Table adapted from Liu et al. These batches of nPM have been reported from prior experiments ( 16 ). …”

Section: Methodsmentioning

confidence: 99%

“… Table adapted from Liu et al. These batches of nPM have been reported from prior experiments ( 16 ). Units are ng/μg of PM mass.…”

Section: Methodsmentioning

confidence: 99%

Section: Bilateral Carotid Artery Stenosis (Bcas) Surgerymentioning

confidence: 99%

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Air Pollution Particulate Matter Amplifies White Matter Vascular Pathology and Demyelination Caused by Hypoperfusion

et al. 2021

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Particulate matter exposure and chronic cerebral hypoperfusion promote oxidative stress and induce neuronal and oligodendrocyte apoptosis in male mice

Lamorie‐Foote

Liu

Shkirkova

et al. 2022

J of Neuroscience Research

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Chronic cerebral hypoperfusion (CCH) may amplify the neurotoxicity of nanoscale particulate matter (nPM), resulting in white matter injury. This study characterized the joint effects of nPM (diameter ≤ 200 nm) and CCH secondary to bilateral carotid artery stenosis (BCAS) exposure on neuronal and white matter injury in a murine model. nPM was collected near a highway and re‐aerosolized for exposure. Ten‐week‐old C57BL/6 male mice were randomized into four groups: filtered air (FA), nPM, FA + BCAS, and nPM + BCAS. Mice were exposed to FA or nPM for 10 weeks. BCAS surgeries were performed. Markers of inflammation, oxidative stress, and apoptosis were examined. nPM + BCAS exposure increased brain hemisphere TNFα protein compared to FA. iNOS and HNE immunofluorescence were increased in the corpus callosum and cerebral cortex of nPM + BCAS mice compared to FA. While nPM exposure alone did not decrease cortical neuronal cell count, nPM decreased corpus callosum oligodendrocyte cell count. nPM exposure decreased mature oligodendrocyte cell count and increased oligodendrocyte precursor cell count in the corpus callosum. nPM + BCAS mice exhibited a 200% increase in cortical neuronal TUNEL staining and a 700% increase in corpus callosum oligodendrocyte TUNEL staining compared to FA. There was a supra‐additive interaction between nPM and BCAS on cortical neuronal TUNEL staining (2.6× the additive effects of nPM + BCAS). nPM + BCAS exposure increased apoptosis, neuroinflammation, and oxidative stress in the cerebral cortex and corpus callosum. nPM + BCAS exposure increased neuronal apoptosis above the separate responses to each exposure. However, oligodendrocytes in the corpus callosum demonstrated a greater susceptibility to the combined neurotoxic effects of nPM + BCAS exposure.

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Compound from Magnolia officinalis Ameliorates White Matter Injury by Promoting Oligodendrocyte Maturation in Chronic Cerebral Ischemia Models

Zhang¹,

Shu²,

Cao³

et al. 2023

Neurosci. Bull.

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Chronic cerebral hypoperfusion leads to white matter injury (WMI), which subsequently causes neurodegeneration and even cognitive impairment. However, due to the lack of treatment specifically for WMI, novel recognized and effective therapeutic strategies are urgently needed. In this study, we found that honokiol and magnolol, two compounds derived from Magnolia officinalis, significantly facilitated the differentiation of primary oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes, with a more prominent effect of the former compound. Moreover, our results demonstrated that honokiol treatment improved myelin injury, induced mature oligodendrocyte protein expression, attenuated cognitive decline, promoted oligodendrocyte regeneration, and inhibited astrocytic activation in the bilateral carotid artery stenosis model. Mechanistically, honokiol increased the phosphorylation of serine/threonine kinase (Akt) and mammalian target of rapamycin (mTOR) by activating cannabinoid receptor 1 during OPC differentiation. Collectively, our study indicates that honokiol might serve as a potential treatment for WMI in chronic cerebral ischemia.

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Air Pollution Particulate Matter Exposure and Chronic Cerebral Hypoperfusion and Measures of White Matter Injury in a Murine Model

Cited by 26 publications

References 69 publications

Air Pollution Particulate Matter Amplifies White Matter Vascular Pathology and Demyelination Caused by Hypoperfusion

Air Pollution Particulate Matter Amplifies White Matter Vascular Pathology and Demyelination Caused by Hypoperfusion

Particulate matter exposure and chronic cerebral hypoperfusion promote oxidative stress and induce neuronal and oligodendrocyte apoptosis in male mice

Compound from Magnolia officinalis Ameliorates White Matter Injury by Promoting Oligodendrocyte Maturation in Chronic Cerebral Ischemia Models

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