Person:
Motta, Valeria

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Motta

First Name

Valeria

Name

Motta, Valeria
Author's Publications: search.filters.isAuthorOfPublication.cfd49624-f4f9-4517-8725-0ec6e0f07d21

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    Effects of airborne pollutants on mitochondrial DNA Methylation
    (BioMed Central, 2013) Byun, Hyang-Min; Panni, Tommaso; Motta, Valeria; Hou, Lifang; Nordio, Francesco; Apostoli, Pietro; Bertazzi, Pier Alberto; Baccarelli, Andrea
    Background: Mitochondria have small mitochondrial DNA (mtDNA) molecules independent from the nuclear DNA, a separate epigenetic machinery that generates mtDNA methylation, and are primary sources of oxidative-stress generation in response to exogenous environments. However, no study has yet investigated whether mitochondrial DNA methylation is sensitive to pro-oxidant environmental exposures. Methods: We sampled 40 male participants (20 high-, 20 low-exposure) from each of three studies on airborne pollutants, including investigations of steel workers exposed to metal-rich particulate matter (measured as PM1) in Brescia, Italy (Study 1); gas-station attendants exposed to air benzene in Milan, Italy (Study 2); and truck drivers exposed to traffic-derived Elemental Carbon (EC) in Beijing, China (Study 3). We have measured DNA methylation from buffy coats of the participants. We measured methylation by bisulfite-Pyrosequencing in three mtDNA regions, i.e., the transfer RNA phenylalanine (MT-TF), 12S ribosomal RNA (MT-RNR1) gene and “D-loop” control region. All analyses were adjusted for age and smoking. Results: In Study 1, participants with high metal-rich PM1 exposure showed higher MT-TF and MT-RNR1 methylation than low-exposed controls (difference = 1.41, P = 0.002); MT-TF and MT-RNR1 methylation was significantly associated with PM1 exposure (beta = 1.35, P = 0.025); and MT-RNR1 methylation was positively correlated with mtDNA copy number (r = 0.36; P = 0.02). D-loop methylation was not associated with PM1 exposure. We found no effects on mtDNA methylation from air benzene (Study 2) and traffic-derived EC exposure (Study 3). Conclusions: Mitochondrial MT-TF and MT-RNR1 DNA methylation was associated with metal-rich PM1 exposure and mtDNA copy number. Our results suggest that locus-specific mtDNA methylation is correlated to selected exposures and mtDNA damage. Larger studies are needed to validate our observations.
  • Thumbnail Image
    Publication
    Exposure to Metal-rich Particulate Matter Modifies the Expression of Candidate Micrornas in Peripheral Blood Leukocytes
    (National Institute of Environmental Health Sciences, 2010) Bollati, Valentina; Marinelli, Barbara; Apostoli, Pietro; Bonzini, Matteo; Nordio, Francesco; Hoxha, Mirjam; Pegoraro, Valeria; Tarantini, Letizia; Cantone, Laura; Bertazzi, Pier Alberto; Motta, Valeria; Schwartz, Joel; Baccarelli, Andrea
    Background: Altered patterns of gene expression mediate the effects of particulate matter (PM) on human health, but mechanisms through which PM modifies gene expression are largely undetermined. MicroRNAs (miRNAs) are highly conserved, noncoding small RNAs that regulate the expression of broad gene networks at the posttranscriptional level. Objectives: We evaluated the effects of exposure to PM and PM metal components on candidate miRNAs (miR-222, miR-21, and miR-146a) related with oxidative stress and inflammatory processes in 63 workers at an electric-furnace steel plant. Methods: We measured miR-222, miR-21, and miR-146a expression in blood leukocyte RNA on the first day of a workweek (baseline) and after 3 days of work (postexposure). Relative expression of miRNAs was measured by real-time polymerase chain reaction. We measured blood oxidative stress (8-hydroxyguanine) and estimated individual exposures to PM\(_{1}\)PM\(_{1}\) (< 1 μm in aerodynamic diameter), PM\(_{10}\) (< 10 μm in aerodynamic diameter), coarse PM (PM\(_{10}\) minus PM\(_{1}\)), and PM metal components (chromium, lead, cadmium, arsenic, nickel, manganese) between the baseline and postexposure measurements. Results: Expression of miR-222 and miR-21 (using the 2\(^{−ΔΔCT}\) method) was significantly increased in postexposure samples (miR-222: baseline = 0.68 ± 3.41, postexposure = 2.16 ± 2.25, p = 0.002; miR-21: baseline = 4.10 ± 3.04, postexposure = 4.66 ± 2.63, p = 0.05). In postexposure samples, miR-222 expression was positively correlated with lead exposure (β = 0.41, p = 0.02), whereas miR-21 expression was associated with blood 8-hydroxyguanine (β = 0.11, p = 0.03) but not with individual PM size fractions or metal components. Postexposure expression of miR-146a was not significantly different from baseline (baseline = 0.61 ± 2.42, postexposure = 1.90 ± 3.94, p = 0.19) but was negatively correlated with exposure to lead (β = −0.51, p = 0.011) and cadmium (β = −0.42, p = 0.04). Conclusions: Changes in miRNA expression may represent a novel mechanism mediating responses to PM and its metal components.