Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM2.5 in human myocardial cells

Lin, Feng; Yang, Xiaozhe; Asweto, Collins Otieno; Wu, Jing; Zhang, Yannan; Hu, Hejing; Shi, Yanfeng; Duan, Junchao; Sun, Zhiwei

doi:10.1007/s11356-017-8773-3

Cited by 28 publications

(11 citation statements)

References 35 publications

(30 reference statements)

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“…Our results demonstrated that cell differentiation and maturation, cell-cell signaling, and signal transduction involved in the immune response were the main molecular and cellular functions of genes, which were enriched in the AP group. The findings from the present study also confirm the findings of several other reports, which have suggested that TGF-β signaling was regulated after exposure to PM2.5 18 – 20 .…”

Section: Discussionsupporting

confidence: 92%

Changes in gene expression in chronic allergy mouse model exposed to natural environmental PM2.5-rich ambient air pollution

Ouyang

Fan

et al. 2018

Sci Rep

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Particulate matter (PM) air pollution has been associated with an increase in the incidence of chronic allergic diseases; however, the mechanisms underlying the effect of exposure to natural ambient air pollution in chronic allergic diseases have not been fully elucidated. In the present study, we aimed to investigate the cellular responses induced by exposure to natural ambient air pollution, employing a mouse model of chronic allergy. The results indicated that exposure to ambient air pollution significantly increased the number of eosinophils in the nasal mucosa. The modulation of gene expression profile identified a set of regulated genes, and the Triggering Receptor Expressed on Myeloid cells1(TREM1) signaling canonical pathway was increased after exposure to ambient air pollution. In vitro, PM2.5 increased Nucleotide-binding oligomerization domain-containing protein 1 (Nod1) and nuclear factor (NF)-κB signaling pathway activation in A549 and HEK293 cell cultures. These results suggest a novel mechanism by which, PM2.5 in ambient air pollution may stimulate the innate immune system through the PM2.5-Nod1-NF-κB axis in chronic allergic disease.

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Section: Discussionsupporting

confidence: 92%

Changes in gene expression in chronic allergy mouse model exposed to natural environmental PM2.5-rich ambient air pollution

Ouyang

Fan

et al. 2018

Sci Rep

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“…Eukaryotic translation initiation factor 5B, or Eif5b , has been previously studied in the area of toxicity. Human myocardial cells which underwent PM2.5‐induced myocardial‐related toxicity showed a confirmed decrease in Eif5b expression (Feng et al, 2017). This may also support the severity of the disease manifestation in females.…”

Section: Discussionmentioning

confidence: 99%

Sexual dimorphism in cardiac transcriptome associated with a troponin C murine model of hypertrophic cardiomyopathy

et al. 2020

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Heart disease remains the number one killer of women in the US. Nonetheless, studies in women and female animal models continue to be underrepresented in cardiac research. Hypertrophic cardiomyopathy (HCM), the most commonly inherited cardiac disorder, has been tied to sarcomeric protein variants in both sexes. Among the susceptible genes, TNNC1—encoding cardiac troponin C (cTnC)—causes a substantial HCM phenotype in mice. Mice bearing an HCM‐associated cTnC‐A8V point mutation exhibited a significant decrease in stroke volume and left ventricular diameter and volume. Importantly, isovolumetric contraction time was significantly higher for female HCM mice. We utilized a transcriptomic approach to investigate the basis underlying the sexual dimorphism observed in the cardiac physiology of adult male and female HCM mice. RNA sequencing revealed several altered canonical pathways within the HCM mice versus WT groups including an increase in eukaryotic initiation factor 2 signaling, integrin‐linked kinase signaling, actin nucleation by actin‐related protein‐Wiskott‐Aldrich syndrome family protein complex, regulation of actin‐based motility by Rho kinase, vitamin D receptor/retinoid X receptor activation, and glutathione redox reaction pathways. In contrast, valine degradation, tricarboxylic acid cycle II, methionine degradation, and inositol phosphate compound pathways were notably down‐regulated in HCM mice. These down‐regulated pathways may be reduced in response to altered energetics in the hypertrophied hearts and may represent conservation of energy as the heart is compensating to meet increased contractile demands. HCM male versus female mice followed similar trends of the canonical pathways altered between HCM and WT. In addition, seven of the differentially expressed genes in both WT and HCM male versus female comparisons swapped directions in fold‐change between the sexes. These findings suggest a sexually‐dimorphic HCM phenotype due to a sarcomeric mutation and pinpoint several key targetable pathways and genes that may provide the means to alleviate the more severe decline in female cardiac function.

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“…Another significant site located 0.3 kb downstream of the BRIX1 (Biogenesis of ribosomes BRX1) gene on the Z chromosome was found. BRIX1 (ribosomal biogenesis protein BRX1) is a protein-coding gene associated with the gastric cancer network pathway and neural development of the chicken brain [37].…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Association Study of H/L Traits in Chicken

Zhu

Liu

et al. 2019

Animals

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Presently, the heterophil-to-lymphocyte (H/L) ratio is being studied extensively as a disease resistance trait. Through intricate mechanisms to identify and destroy pathogenic microorganisms, heterophils play a pivotal role in the immune defense systems of avian species. To reveal the genetic basis and molecular mechanisms affecting the H/L ratio, phenotypic and H/L data from 1650 white feather chicken broilers were used in performing a genome-wide association study. A self-developed, chicken-specific 55K chip was used for heterophils, lymphocytes, and H/L classification, according to individual genomic DNA profiles. We identified five significant single nucleotide polymorphisms (SNPs) when the genome-wide significance threshold was set to 5% (p < 2.42 × 10−6). A total of 15 SNPs obtained seemingly significant levels (p < 4.84 × 10−5). Gene annotation indicated that CARD11 (Caspase recruitment domain family member 11), BRIX1 (Biogenesis of ribosomes BRX1), and BANP (BTG3 associated nuclear protein) play a role in H/L-associated cell regulation and potentially constitute candidate gene regions for cellular functions dependent on H/L ratios. These results lay the foundation for revealing the genetic basis of disease resistance and future marker-assisted selection for disease resistance.

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Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM2.5 in human myocardial cells

Cited by 28 publications

References 35 publications

Changes in gene expression in chronic allergy mouse model exposed to natural environmental PM2.5-rich ambient air pollution

Changes in gene expression in chronic allergy mouse model exposed to natural environmental PM2.5-rich ambient air pollution

Sexual dimorphism in cardiac transcriptome associated with a troponin C murine model of hypertrophic cardiomyopathy

Genome-Wide Association Study of H/L Traits in Chicken

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