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

Huang, Xiaoliu; Zhou, Zhitong; Liu, Xinwen; Li, Jue; Zhang, Lijuan

doi:10.21203/rs.3.rs-23189/v2

Cited by 2 publications

(3 citation statements)

References 49 publications

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“…These cytoplasmic vacuoles might indicate the formation of numerous autophagic vacuoles as an adaptive response to the repeated exposure to DEP. This notion could be further confirmed by ultrastructural evaluation of the renal tubules (an issue that has not been addressed herein) as demonstrated by Huang et al 13 who displayed the formation of autophagosomes in electron microscopic studies of renal tubules of particulate matter (PM2.5)-exposed rats rather than filtered airexposed animals.…”

Section: Discussionsupporting

confidence: 63%

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The biomechanistic aspects of renal cortical injury induced by diesel exhaust particles in rats and the renoprotective contribution of quercetin pretreatment: Histological and biochemical study

Morsi

Fouad

Alasmari

et al. 2021

Environmental Toxicology

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Although several studies have reported a toxic effect of diesel exhaust particles (DEP) exposure on the kidney tissues, the involvement of autophagy/NF-kB signaling as encountered mechanisms and the protective effects of a natural flavonoid, quercetin on DEP remains unclear. Thirty-two albino rats were divided as control, quercetintreated (60 mg/kg, oral), DEP-exposed (0.5 mg/kg, intra-tracheal), and quercetin/DEPexposed groups. Specimens of the renal cortex were subjected to histo-biochemical study and immunohistochemical analysis using anti-NF-kB, and anti-LC3β antibodies followed by morphometric and statistical analyses. The expression level of autophagy genes was quantitatively evaluated using RT-PCR, as well. The DEP-exposed rats showed an elevation in the renal tissue levels of MDA and a decrease in the catalase and superoxide dismutase (p < .05). Histologically, there were cytoplasmic vacuolar changes in the lining cells of the renal tubules, glomerular atrophy, and vascular congestion. In addition, renal inflammation was evident as confirmed by the increased NF-kB immunoexpression. Moreover, the gene expression of Becn1, ATG5, and LC3β increased (p <. 0) due to DEP exposure. Conversely, quercetin pretreatment improved these renal histo-biochemical alterations (p < .05) and regulated autophagy/NF-kB pathways. Overall, the study proved the renal toxicity mediated by DEP exposure via precipitating renal inflammation, autophagy activation, and oxidative stress. Quercetin pretreatment could antagonize such machinery to protect the kidney against DEP.

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Section: Discussionsupporting

confidence: 63%

“…11 On the other hand, exaggerated levels of autophagy can initiate cell death, as well. 12 Hence, Huang et al 13 reported a nephrotoxic effect of airborne particulate matter (PM2.5) via activation of the autophagy pathway.…”

mentioning

confidence: 99%

The biomechanistic aspects of renal cortical injury induced by diesel exhaust particles in rats and the renoprotective contribution of quercetin pretreatment: Histological and biochemical study

Morsi

Fouad

Alasmari

et al. 2021

Environmental Toxicology

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“…PM2.5 exposure activates the autophagy markers in the spleen of SD rats, such as ATG5, VSP34, Beclin 1, and LC3 [ 174 ]. PM2.5 exposure induces renal injury and changes autophagy markers, such as p62, Beclin 1, and LC3, in rats and HK-2 cells [ 175 ]. Diesel exhaust particles (DEP) induce the generation of ROS, pro-inflammation, and apoptosis in the HUVEC tube cells [ 176 ].…”

Section: Autophagy-related Responses To Mss and Nss In Animal And Cell Linesmentioning

confidence: 99%

Micro- and Nanosized Substances Cause Different Autophagy-Related Responses

Wang

Zheng

Lee

et al. 2021

IJMS

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With rapid industrialization, humans produce an increasing number of products. The composition of these products is usually decomposed. However, some substances are not easily broken down and gradually become environmental pollutants. In addition, these substances may cause bioaccumulation, since the substances can be fragmented into micro- and nanoparticles. These particles or their interactions with other toxic matter circulate in humans via the food chain or air. Whether these micro- and nanoparticles interfere with extracellular vesicles (EVs) due to their similar sizes is unclear. Micro- and nanoparticles (MSs and NSs) induce several cell responses and are engulfed by cells depending on their size, for example, particulate matter with a diameter ≤2.5 μm (PM2.5). Autophagy is a mechanism by which pathogens are destroyed in cells. Some artificial materials are not easily decomposed in organisms. How do these cells or tissues respond? In addition, autophagy operates through two pathways (increasing cell death or cell survival) in tumorigenesis. Many MSs and NSs have been found that induce autophagy in various cells and tissues. As a result, this review focuses on how these particles interfere with cells and tissues. Here, we review MSs, NSs, and PM2.5, which result in different autophagy-related responses in various tissues or cells.

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

Cited by 2 publications

References 49 publications

The biomechanistic aspects of renal cortical injury induced by diesel exhaust particles in rats and the renoprotective contribution of quercetin pretreatment: Histological and biochemical study

The biomechanistic aspects of renal cortical injury induced by diesel exhaust particles in rats and the renoprotective contribution of quercetin pretreatment: Histological and biochemical study

Micro- and Nanosized Substances Cause Different Autophagy-Related Responses

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