Extracellular vesicle-driven information mediates the long-term effects of particulate matter exposure on coagulation and inflammation pathways.
Extracellular vesicle-driven information mediates the long-term effects of particulate matter exposure on coagulation and inflammation pathways.
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DOI:
10.1016/j.toxlet.2016.08.002
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发表时间:
2016-09-30
影响因子:
3.5
通讯作者:
Bollati V
中科院分区:
文献类型:
--
作者:
Pavanello S;Bonzini M;Angelici L;Motta V;Pergoli L;Hoxha M;Cantone L;Pesatori AC;Apostoli P;Tripodi A;Baccarelli A;Bollati V
Continuous exposure to particulate air pollution (PM) is a serious worldwide threat to public health as it coherently links with increased morbidity and mortality of cardiorespiratory diseases (CRD), and of type 2 diabetes (T2D). Extracellular vesicles (EVs) are circular plasma membrane fragments released from human cells that transfer microRNAs between tissues. In the present work it was explored the hypothesis that EVs with their encapsulated microRNAs (EVmiRNAs) contents might mediate PM effects by triggering key pathways in CRD and T2D. Expression of EVmiRNAs analyzed by real-time PCR was correlated with oxidative stress, coagulation and inflammation markers, from healthy steel plant workers (n=55) with a well-characterized exposure to PM and PM-associated metals. All p-values were adjusted for multiple comparisons. In-silico Ingenuity Pathway Analysis (IPA) was performed to identify biological pathways regulated by PM-associated EVmiRNAs. Increased expression in 17 EVmiRNAs is associated with PM and metal exposure (p<0.01). Mir-196b that tops the list, being related to 9 different metals, is fundamental in insulin biosynthesis, however three (miR-302b, miR-200c, miR-30d) out of these 17 EVmiRNAs are in turn also related to disruptions (p<0.01) in inflammatory and coagulation markers. The study’s findings support the hypothesis that adverse cardiovascular and metabolic effects stemming from inhalation exposures in particular to PM metallic component may be mediated by EVmiRNAs that target key factors in the inflammation, coagulation and glucose homeostasis pathways.
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影响因子:
3.7
作者:
Eze IC;Schaffner E;Foraster M;Imboden M;von Eckardstein A;Gerbase MW;Rothe T;Rochat T;Künzli N;Schindler C;Probst-Hensch N
通讯作者:
Probst-Hensch N
影响因子:
--
作者:
Lin, Chen-Sung;Wang, Liang-Shun;Wei, Yau-Huei
通讯作者:
Wei, Yau-Huei
影响因子:
3.7
作者:
Hunter, Melissa Piper;Ismail, Noura;Zhang, Xiaoli;Aguda, Baltazar D.;Lee, Eun Joo;Yu, Lianbo;Xiao, Tao;Schafer, Jeffrey;Lee, Mei-Ling Ting;Schmittgen, Thomas D.;Nana-Sinkam, S. Patrick;Jarjoura, David;Marsh, Clay B.
通讯作者:
Marsh, Clay B.
DOI:
10.1111/j.2517-6161.1995.tb02031.x
发表时间:
1995-01-01
影响因子:
5.8
作者:
BENJAMINI, Y;HOCHBERG, Y
通讯作者:
HOCHBERG, Y
影响因子:
0.5
作者:
Agarwal, Neil K.;Sharma, Prerna;Agarwal, Shashi K.
通讯作者:
Agarwal, Shashi K.