Short-Term Blood Pressure Responses to Ambient Fine Particulate Matter Exposures at the Extremes of Global Air Pollution Concentrations

Huang, Wei; Wang, Lu; Li, Jianping; Liu, Mochuan; Xu, Hongbing; Liu, Shengcong; Chen, Jie; Zhang, Yi; Morishita, Masako; Bard, Robert L.; Harkema, Jack R.; Rajagopalan, Sanjay; Brook, Robert D.

doi:10.1093/ajh/hpx216

Cited by 54 publications

(18 citation statements)

References 30 publications

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“…PM 2.5 exposure increased the risk of cardiovascular disease (Huang et al, 2018). Vascular endothelial cells are the primary vascular barrier to local damage factors induced by exposure to PM 2.5 , such as in ammatory factors and free radicals, as well as toxic and harmful substances of PM 2.5 (Feng et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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Abstract Background: Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.Results: In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the concentrated PM2.5 (PM2.5) group and the filtered air (FA) group. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure activated the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, activation of P62 and beclin-1. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure. Conclusions: Taken together, our findings indicated that PM2.5-induced renal function impairment via the activation of the autophagic pathway in renal tubular epithelial cells.

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Section: Discussionmentioning

confidence: 99%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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show abstract

“…The global burden of co-existing PM exposure and metabolic dysregulation is significant. Systemic inflammation caused by this co-exposure results in significant end organ compromise [ 82 , 83 ]. Individuals with MetSyn are predisposed to PM-exposure-associated lung injury [ 5 , 8 , 9 , 84 ].…”

Section: Discussionmentioning

confidence: 99%

Synergistic Effect of WTC-Particulate Matter and Lysophosphatidic Acid Exposure and the Role of RAGE: In-Vitro and Translational Assessment

Lam

Haider

Crowley

et al. 2020

IJERPH

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World Trade Center particulate matter (WTC-PM)-exposed firefighters with metabolic syndrome (MetSyn) have a higher risk of WTC lung injury (WTC-LI). Since macrophages are crucial innate pulmonary mediators, we investigated WTC-PM/lysophosphatidic acid (LPA) co-exposure in macrophages. LPA, a low-density lipoprotein metabolite, is a ligand of the advanced glycation end-products receptor (AGER or RAGE). LPA and RAGE are biomarkers of WTC-LI. Human and murine macrophages were exposed to WTC-PM, and/or LPA, and compared to controls. Supernatants were assessed for cytokines/chemokines; cell lysate immunoblots were assessed for signaling intermediates after 24 h. To explore the translatability of our in-vitro findings, we assessed serum cytokines/chemokines and metabolites of symptomatic, never-smoking WTC-exposed firefighters. Agglomerative hierarchical clustering identified phenotypes of WTC-PM-induced inflammation. WTC-PM induced GM-CSF, IL-8, IL-10, and MCP-1 in THP-1-derived macrophages and induced IL-1α, IL-10, TNF-α, and NF-κB in RAW264.7 murine macrophage-like cells. Co-exposure induced synergistic elaboration of IL-10 and MCP-1 in THP-1-derived macrophages. Similarly, co-exposure synergistically induced IL-10 in murine macrophages. Synergistic effects were seen in the context of a downregulation of NF-κB, p-Akt, -STAT3, and -STAT5b. RAGE expression after co-exposure increased in murine macrophages compared to controls. In our integrated analysis, the human cytokine/chemokine biomarker profile of WTC-LI was associated with discriminatory metabolites (fatty acids, sphingolipids, and amino acids). LPA synergistically elaborated WTC-PM’s inflammatory effects in vitro and was partly RAGE-mediated. Further research will focus on the intersection of MetSyn/PM exposure.

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“…PM 2.5 exposure increased the risk of cardiovascular disease (Huang et al, 2018). Vascular endothelial cells are the primary vascular barrier to local damage factors induced by exposure to PM 2.5 , such as inflammatory factors and free radicals, as well as toxic and harmful substances of PM 2.5 (Feng et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

PM2.5 exposure induces renal injury via the activation of the autophagic pathway in rat and HK-2 cell

Huang

2020

Preprint

View full text Add to dashboard Cite

Background Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to the human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro. Results In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the PM2.5 group and FA group during the period of PM2.5 exposure. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure resulted in the activation of the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, P62 and beclin-1 activated. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure. Conclusions Taken together, our findings indicated that PM2.5-induced renal injury via the activation of the autophagic pathway in renal tubular epithelial cells.

show abstract

Short-Term Blood Pressure Responses to Ambient Fine Particulate Matter Exposures at the Extremes of Global Air Pollution Concentrations

Cited by 54 publications

References 30 publications

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Synergistic Effect of WTC-Particulate Matter and Lysophosphatidic Acid Exposure and the Role of RAGE: In-Vitro and Translational Assessment

PM2.5 exposure induces renal injury via the activation of the autophagic pathway in rat and HK-2 cell

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