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      The dark side of circulating nucleic acids

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      Author(s): 1 , 3 , , 2 , 1 ,
      Publication date (Electronic):
      Journal: Aging Cell
      Publisher: John Wiley and Sons Inc.
      Keywords: aging, cell‐free DNA, DNA damage, mutagenesis

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          Summary

          Free circulating or cell‐free DNA (cf DNA), possibly from dying cells that release their contents into the blood as they break down, have become of major interest as a source for noninvasive diagnostics. Recent work demonstrated the uptake of human cf DNA in mouse cells in vitro and in vivo, accompanied by the activation of a cellular DNA damage response ( DDR) and the appearance of apoptotic proteins in the host cells. By acting as a source of mobile genetic elements, cf DNA could be a continuous source of DNA mutagenesis of healthy cells in the body throughout life, promoting progressive cellular aging in vivo. As such, cf DNA may causally contribute to multiple aging‐related diseases, such as cancer, diabetes, and Alzheimer's disease.

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          Transposable elements become active and mobile in the genomes of aging mammalian somatic tissues

          Marco De Cecco, Steven W Criscione, Abigail Peterson … (2013)
          Transposable elements (TEs) were discovered by Barbara McClintock in maize and have since been found to be ubiquitous in all living organisms. Transposition is mutagenic and organisms have evolved mechanisms to repress the activity of their endogenous TEs. Transposition in somatic cells is very low, but recent evidence suggests that it may be derepressed in some cases, such as cancer development. We have found that during normal aging several families of retrotransposable elements (RTEs) start being transcribed in mouse tissues. In advanced age the expression culminates in active transposition. These processes are counteracted by calorie restriction (CR), an intervention that slows down aging. Retrotransposition is also activated in age-associated, naturally occurring cancers in the mouse. We suggest that somatic retrotransposition is a hitherto unappreciated aging process. Mobilization of RTEs is likely to be an important contributor to the progressive dysfunction of aging cells.
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            Cell-free nucleic acids circulating in the plasma of colorectal cancer patients induce the oncogenic transformation of susceptible cultured cells.

            Dolores C García-Olmo, Carolina Dominguez, Mariano Garcia-Arranz … (2010)
            It has been proposed that cell-free nucleic acids in the plasma participate in tumorigenesis and the development of metastases via transfection-like uptake of such nucleic acids by susceptible cells. This putative phenomenon is tentatively referred to as "genometastasis." In the present study, we examined the effects on cultured cells of plasma from healthy individuals and from patients with colon cancer. Cultures of NIH-3T3 cells and human adipose-derived stem cells (hASC) were supplemented with samples of plasma from patients with K-ras-mutated colorectal tumors or from healthy subjects using two different protocols: direct addition of plasma to cultures in standard plates and addition in the absence of contact between plasma and cells, which were separated by a membrane with 0.4-mum pores. In plasma-treated hASCs, no K-ras-mutated sequences were detected by real-time PCR. In contrast, in most cultures of plasma-treated NIH-3T3 cells (murine cells), the transfer of human DNA occurred, as verified by the detection of human K-ras sequences, p53 sequences, and beta-globin-encoding sequences. Moreover, NIH-3T3 cells that had been cultured with plasma from patients with colon cancer were oncogenically transformed, as shown by the development of carcinomas in nonobese diabetic-severe combined immunodeficient mice after the injection of such cells. Microscopic analysis of membranes that had separated plasma from cultured cells confirmed the complete absence of cells in the plasma. We only observed noncell particles, having diameters of <0.4 mum. Our results indicate that plasma from cancer patients is able to transform cultured cells oncogenically, supporting the previously proposed hypothesis of genometastasis.
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              Elevated Levels of Circulating DNA in Cardiovascular Disease Patients: Metagenomic Profiling of Microbiome in the Circulation

              Vasudevan Dinakaran, Andiappan Rathinavel, Muthuirulan Pushpanathan … (2014)
              Cardiovascular diseases (CVDs) are the leading cause of death worldwide. An expanding body of evidence supports the role of human microbiome in the establishment of CVDs and, this has gained much attention recently. This work was aimed to study the circulating human microbiome in CVD patients and healthy subjects. The levels of circulating cell free DNA (circDNA) was higher in CVD patients (n = 80) than in healthy controls (n = 40). More specifically, the relative levels of circulating bacterial DNA and the ratio of 16S rRNA/β-globin gene copy numbers were higher in the circulation of CVD patients than healthy individuals. In addition, we found a higher circulating microbial diversity in CVD patients (n = 3) in comparison to healthy individuals (n = 3) by deep shotgun sequencing. At the phylum level, we observed a dominance of Actinobacteria in CVD patients, followed by Proteobacteria, in contrast to that in healthy controls, where Proteobacteria was predominantly enriched, followed by Actinobacteria. The circulating virome in CVD patients was enriched with bacteriophages with a preponderance of Propionibacterium phages, followed by Pseudomonas phages and Rhizobium phages in contrast to that in healthy individuals, where a relatively greater abundance of eukaryotic viruses dominated by Lymphocystis virus (LCV) and Torque Teno viruses (TTV) was observed. Thus, the release of bacterial and viral DNA elements in the circulation could play a major role leading to elevated circDNA levels in CVD patients. The increased circDNA levels could be either the cause or consequence of CVD incidence, which needs to be explored further.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Aging Cell
                Journal ID (iso-abbrev): Aging Cell
                Journal ID (doi): 10.1111/(ISSN)1474-9726
                Journal ID (publisher-id): ACEL
                Title: Aging Cell
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1474-9718
                ISSN (Electronic): 1474-9726
                Publication date (Electronic): 22 February 2016
                Publication date (Print): June 2016
                Volume: 15
                Issue: 3 ( doiID: 10.1111/acel.2016.15.issue-3 )
                Pages: 398-399
                Affiliations
                [ 1 ] Department of GeneticsAlbert Einstein College of Medicine Bronx NY 10461USA
                [ 2 ] Department of Molecular Biology, Cell Biology and BiochemistryBrown University Providence RI 02912USA
                [ 3 ]Present address: Illumina, Inc. San Diego CA 92122
                Author notes
                [*] [* ] Correspondence

                Silvia Gravina, PhD, Department of Genetics, Albert Einstein College of Medicine, Michael F. Price Center, 1301 Morris Park Avenue, Bronx, NY 10461, USA .

                Tel.: (718) 678 1151; fax: (718) 430 8878; e‐mail: silvia.gravina0@ 123456gmail.com

                Jan Vijg, PhD, Department of Genetics, Albert Einstein College of Medicine, Michael F. Price Center, 1301 Morris Park Avenue, Bronx, NY 10461, USA.

                Tel.: (718) 678 1151; fax: (718) 430 8878; e‐mail: jan.vijg@ 123456einstein.yu.edu

                Article
                Publisher ID: ACEL12454
                DOI: 10.1111/acel.12454
                PMC ID: 4854914
                PubMed ID: 26910468
                SO-VID: ebbfadd3-144b-4936-b291-af5fcc7fd614
                Copyright © © 2016 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date accepted : 15 January 2016
                Page count
                Pages: 2
                Categories
                Subject: Review
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                component-id acel12454
                cover-date June 2016
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.1 mode:remove_FC converted:10.06.2016

                ScienceOpen disciplines: Cell biology
                Keywords: aging,cell‐free dna,dna damage,mutagenesis
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: aging, cell‐free dna, dna damage, mutagenesis

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