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  1. Article ; Online: Strengthening ancient mtDNA equid sequences from Pompeii.

    Cipollaro, Marilena

    Journal of cellular biochemistry

    2011  Volume 112, Issue 2, Page(s) 363–364

    MeSH term(s) Animals ; Base Sequence ; DNA, Mitochondrial/genetics ; Equidae/genetics ; Italy
    Chemical Substances DNA, Mitochondrial
    Language English
    Publishing date 2011-02
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 392402-6
    ISSN 1097-4644 ; 0730-2312
    ISSN (online) 1097-4644
    ISSN 0730-2312
    DOI 10.1002/jcb.22965
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Is there a role for autophagy in ascending aortopathy associated with tricuspid or bicuspid aortic valve?

    Forte, Amalia / Cipollaro, Marilena / De Feo, Marisa / Della Corte, Alessandro

    Clinical science (London, England : 1979)

    2019  Volume 133, Issue 7, Page(s) 805–819

    Abstract: Autophagy is a conserved process by which cytoplasmatic elements are sequestered in vesicles and degraded after their fusion with lysosomes, thus recycling the precursor molecules. The autophagy-mediated removal of redundant/harmful/damaged organelles ... ...

    Abstract Autophagy is a conserved process by which cytoplasmatic elements are sequestered in vesicles and degraded after their fusion with lysosomes, thus recycling the precursor molecules. The autophagy-mediated removal of redundant/harmful/damaged organelles and biomolecules plays not only a replenishing function, but protects against stressful conditions through an adaptive mechanism. Autophagy, known to play a role in several pathological conditions, is now gaining increasing attention also in the perspective of the identification of the pathogenetic mechanisms at the basis of ascending thoracic aortic aneurysm (TAA), a localized or diffused dilatation of the aorta with an abnormal widening greater than 50 percent of the vessel's normal diameter. TAA is less frequent than abdominal aortic aneurysm (AAA), but is encountered with a higher percentage in patients with congenital heart disease or known genetic syndromes. Several biological aspects of TAA pathophysiology remain to be elucitated and therapeutic needs are still widely unmet. One of the most controversial and epidemiologically important forms of TAA is that associated with the congenital bicuspid malformation of the aortic valve (BAV). Dysregulated autophagy in response, for example, to wall shear stress alterations, has been demonstrated to affect the phenotype of vascular cells relevant to aortopathy, with potential consequences on signaling, remodeling, and angiogenesis. The most recent findings and hypotheses concerning the multiple aspects of autophagy and of its dysregulation are summarized, both in general and in the context of the different vascular cell types and of TAA progression, with particular reference to BAV-related aortopathy.
    MeSH term(s) Animals ; Aorta, Thoracic/metabolism ; Aorta, Thoracic/pathology ; Aortic Aneurysm, Thoracic/etiology ; Aortic Aneurysm, Thoracic/metabolism ; Aortic Aneurysm, Thoracic/pathology ; Aortic Valve/abnormalities ; Aortic Valve/metabolism ; Aortic Valve/pathology ; Autophagy ; Autophagy-Related Proteins/metabolism ; Bicuspid Aortic Valve Disease ; Dilatation, Pathologic ; Heart Valve Diseases/complications ; Heart Valve Diseases/metabolism ; Heart Valve Diseases/pathology ; Humans ; Prognosis ; Risk Factors ; Signal Transduction
    Chemical Substances Autophagy-Related Proteins
    Language English
    Publishing date 2019-04-02
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20181092
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  3. Article ; Online: Ascending aortas from heart donors and CABG patients are not equivalent as control in aortopathy studies.

    Forte, Amalia / Bancone, Ciro / Cipollaro, Marilena / De Feo, Marisa / Della Corte, Alessandro

    Scandinavian cardiovascular journal : SCJ

    2018  Volume 52, Issue 5, Page(s) 281–286

    Abstract: Objectives: A careful selection of reference samples in studies on the pathogenesis of thoracic ascending aorta (TAA) dilation is crucial for reliability, consistency and reproducibility of experimental results. Several studies include control TAA ... ...

    Abstract Objectives: A careful selection of reference samples in studies on the pathogenesis of thoracic ascending aorta (TAA) dilation is crucial for reliability, consistency and reproducibility of experimental results. Several studies include control TAA samples from heart donors. Others include samples harvested during coronary artery bypass graft (CABG) procedures or a mix of samples from heart donors and CABG patients. We verified the equivalence/homogeneity of TAA samples from heart donors and CABG patients in terms of basal gene expression and thus their reliability as reference groups in aortopathy studies.
    Design: We analysed by RT-PCR and Western blot the differential expression of smoothelin, α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1), selected as major players in smooth muscle cell and myofibroblast phenotype and remodelling. The mean age and comorbidities of subjects were consistent with data routinely seen in clinical practice.
    Results: Data revealed the loss of smoothelin in samples from CABG patients, together with a significant increase of α-SMA, while TGF-β1 dimer showed a marked increase in CABG patients versus heart donors, accompanied by a decrease of the corresponding mRNA. Differences in gene expression were maintained after adjustment for age. However, TGF-β1 mRNA and CABG patients' age showed a positive correlation (ρ = 0.89, p < .05), while α-SMA mRNA and age showed a negative correlation (ρ = -0.85, p < .05).
    Conclusions: We revealed the non-equivalence of samples from heart donors and CABG patients, presumably for the presence of microscopic atherosclerotic lesions in CABG patients, suggesting the necessity of a careful selection of control groups in aortopathy studies.
    MeSH term(s) Actins/analysis ; Actins/genetics ; Adult ; Aged ; Aorta, Thoracic/chemistry ; Aorta, Thoracic/pathology ; Aorta, Thoracic/surgery ; Aortic Diseases/metabolism ; Aortic Diseases/pathology ; Biomarkers/analysis ; Case-Control Studies ; Coronary Artery Bypass ; Cytoskeletal Proteins/analysis ; Cytoskeletal Proteins/genetics ; Female ; Heart Transplantation ; Humans ; Male ; Middle Aged ; Muscle Proteins/analysis ; Muscle Proteins/genetics ; Tissue Donors ; Tissue and Organ Harvesting/methods ; Transforming Growth Factor beta1/analysis ; Transforming Growth Factor beta1/genetics
    Chemical Substances ACTA2 protein, human ; Actins ; Biomarkers ; Cytoskeletal Proteins ; Muscle Proteins ; SMTN protein, human ; TGFB1 protein, human ; Transforming Growth Factor beta1
    Language English
    Publishing date 2018-07-25
    Publishing country England
    Document type Comparative Study ; Journal Article
    ZDB-ID 1379906-x
    ISSN 1651-2006 ; 1401-7431
    ISSN (online) 1651-2006
    ISSN 1401-7431
    DOI 10.1080/14017431.2018.1494303
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  4. Article ; Online: Genetic, epigenetic and stem cell alterations in endometriosis: new insights and potential therapeutic perspectives.

    Forte, Amalia / Cipollaro, Marilena / Galderisi, Umberto

    Clinical science (London, England : 1979)

    2014  Volume 126, Issue 2, Page(s) 123–138

    Abstract: Human endometrium is a highly dynamic tissue, undergoing periodic growth and regression at each menstrual cycle. Endometriosis is a frequent chronic pathological status characterized by endometrial tissue with an ectopic localization, causing pelvic pain ...

    Abstract Human endometrium is a highly dynamic tissue, undergoing periodic growth and regression at each menstrual cycle. Endometriosis is a frequent chronic pathological status characterized by endometrial tissue with an ectopic localization, causing pelvic pain and infertility and a variable clinical presentation. In addition, there is well-established evidence that, although endometriosis is considered benign, it is associated with an increased risk of malignant transformation in approximately 1.0% of affected women, with the involvement of multiple pathways of development. Increasing evidence supports a key contribution of different stem/progenitor cell populations not only in the cyclic regeneration of eutopic endometrium, but also in the pathogenesis of at least some types of endometriosis. Evidence has arisen from experiments in animal models of disease through different kinds of assays (including clonogenicity, the label-retaining cell approach, the analysis of undifferentiation markers), as well as from descriptive studies on ectopic and eutopic tissue samples harvested from affected women. Changes in stem cell populations in endometriotic lesions are associated with genetic and epigenetic alterations, including imbalance of miRNA expression, histone and DNA modifications and chromosomal aberrations. The present short review mainly summarizes the latest observations contributing to the current knowledge regarding the presence and the potential contribution of stem/progenitor cells in eutopic endometrium and the aetiology of endometriosis, together with a report of the most recently identified genetic and epigenetic alterations in endometriosis. We also describe the potential advantages of single cell molecular profiling in endometrium and in endometriotic lesions. All these data can have clinical implications and provide a basis for new potential therapeutic applications.
    MeSH term(s) Animals ; DNA/metabolism ; Down-Regulation ; Endometriosis/complications ; Endometriosis/genetics ; Endometriosis/pathology ; Endometrium/cytology ; Endometrium/metabolism ; Endometrium/pathology ; Epigenesis, Genetic/physiology ; Female ; Histones/metabolism ; Humans ; Menstruation/blood ; MicroRNAs/metabolism ; Ovarian Neoplasms/etiology ; RNA, Messenger/metabolism ; Stem Cells/metabolism ; Stem Cells/pathology ; Up-Regulation
    Chemical Substances Histones ; MicroRNAs ; RNA, Messenger ; DNA (9007-49-2)
    Language English
    Publishing date 2014-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20130099
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Locally different proteome in aortas from patients with stenotic tricuspid and bicuspid aortic valves†.

    Forte, Amalia / Yin, Xiaoke / Fava, Marika / Bancone, Ciro / Cipollaro, Marilena / De Feo, Marisa / Mayr, Manuel / Jahangiri, Marjan / Della Corte, Alessandro

    European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery

    2019  Volume 56, Issue 3, Page(s) 458–469

    Abstract: Objectives: We aimed to compare the intracellular proteome of ascending aortas from patients with stenotic bicuspid (BAV) and tricuspid aortic valves (TAV) to identify BAV-specific pathogenetic mechanisms of aortopathy and to verify the previously ... ...

    Abstract Objectives: We aimed to compare the intracellular proteome of ascending aortas from patients with stenotic bicuspid (BAV) and tricuspid aortic valves (TAV) to identify BAV-specific pathogenetic mechanisms of aortopathy and to verify the previously reported asymmetric expression of BAV aortopathy [concentrated at the convexity (CVX)] in its 'ascending phenotype' form.
    Methods: Samples were collected from the CVX and concavity sides of non-aneurysmal ascending aortas in 26 TAV and 26 BAV patients undergoing stenotic aortic valve replacement. Aortic lysates were subjected to cellular protein enrichment by subfractionation, and to proteome comparison by 2-dimensional fluorescence difference in-gel electrophoresis. Differentially regulated protein spots were identified by liquid chromatography-tandem mass spectrometry and analysed in silico. Selected results were verified by immunofluorescence and reverse transcription-polymerase chain reaction.
    Results: In BAV samples, 52 protein spots were differentially regulated versus TAV samples at the CVX and 10 spots at the concavity: liquid chromatography-tandem mass spectrometry identified 35 and 10 differentially regulated proteins, respectively. Charge trains of individual proteins (e.g. annexins) suggested the presence of post-translational modifications possibly modulating their activity. At the CVX, 37 of the 52 different protein spots showed decreased expression in BAV versus TAV. The affected biological pathways included those involved in smooth muscle cell contractile phenotype, metabolism and cell stress.
    Conclusions: The observed differential proteomics profiles may have a significant impact on the pathogenesis of the aortopathy, pointing the way for further studies. At a preaneurysmal stage, an aorta with BAV shows more protein expression changes and potentially more post-translational modifications at the CVX of the ascending aorta than at the concavity, compared to that of TAV.
    MeSH term(s) Aged ; Aorta/metabolism ; Aortic Valve/abnormalities ; Aortic Valve/metabolism ; Aortic Valve Stenosis/metabolism ; Bicuspid Aortic Valve Disease ; Electrophoresis, Gel, Two-Dimensional ; Female ; Heart Valve Diseases/metabolism ; Humans ; Male ; Microscopy, Fluorescence ; Phenotype ; Proteome/metabolism ; RNA/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Specimen Handling ; Tricuspid Valve/metabolism
    Chemical Substances Proteome ; RNA (63231-63-0)
    Language English
    Publishing date 2019-02-22
    Publishing country Germany
    Document type Comparative Study ; Journal Article
    ZDB-ID 639293-3
    ISSN 1873-734X ; 1010-7940 ; 1567-4258
    ISSN (online) 1873-734X
    ISSN 1010-7940 ; 1567-4258
    DOI 10.1093/ejcts/ezz032
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  6. Article ; Online: Epigenetic regulation of TGF-β1 signalling in dilative aortopathy of the thoracic ascending aorta.

    Forte, Amalia / Galderisi, Umberto / Cipollaro, Marilena / De Feo, Marisa / Della Corte, Alessandro

    Clinical science (London, England : 1979)

    2016  Volume 130, Issue 16, Page(s) 1389–1405

    Abstract: The term 'epigenetics' refers to heritable, reversible DNA or histone modifications that affect gene expression without modifying the DNA sequence. Epigenetic modulation of gene expression also includes the RNA interference mechanism. Epigenetic ... ...

    Abstract The term 'epigenetics' refers to heritable, reversible DNA or histone modifications that affect gene expression without modifying the DNA sequence. Epigenetic modulation of gene expression also includes the RNA interference mechanism. Epigenetic regulation of gene expression is fundamental during development and throughout life, also playing a central role in disease progression. The transforming growth factor β1 (TGF-β1) and its downstream effectors are key players in tissue repair and fibrosis, extracellular matrix remodelling, inflammation, cell proliferation and migration. TGF-β1 can also induce cell switch in epithelial-to-mesenchymal transition, leading to myofibroblast transdifferentiation. Cellular pathways triggered by TGF-β1 in thoracic ascending aorta dilatation have relevant roles to play in remodelling of the vascular wall by virtue of their association with monogenic syndromes that implicate an aortic aneurysm, including Loeys-Dietz and Marfan's syndromes. Several studies and reviews have focused on the progression of aneurysms in the abdominal aorta, but research efforts are now increasingly being focused on pathogenic mechanisms of thoracic ascending aorta dilatation. The present review summarizes the most recent findings concerning the epigenetic regulation of effectors of TGF-β1 pathways, triggered by sporadic dilative aortopathy of the thoracic ascending aorta in the presence of a tricuspid or bicuspid aortic valve, a congenital malformation occurring in 0.5-2% of the general population. A more in-depth comprehension of the epigenetic alterations associated with TGF-β1 canonical and non-canonical pathways in dilatation of the ascending aorta could be helpful to clarify its pathogenesis, identify early potential biomarkers of disease, and, possibly, develop preventive and therapeutic strategies.
    MeSH term(s) Animals ; Aorta, Thoracic/metabolism ; Aortic Diseases/genetics ; Aortic Diseases/metabolism ; Epigenesis, Genetic ; Humans ; Signal Transduction ; Transforming Growth Factor beta1/genetics ; Transforming Growth Factor beta1/metabolism
    Chemical Substances Transforming Growth Factor beta1
    Language English
    Publishing date 2016-07-07
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20160222
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  7. Article ; Online: Author Correction: Pro-inflammatory cytokines activate hypoxia-inducible factor 3α via epigenetic changes in mesenchymal stromal/stem cells.

    Cuomo, Francesca / Coppola, Antonietta / Botti, Chiara / Maione, Ciro / Forte, Amalia / Scisciola, Lucia / Liguori, Giuseppina / Caiafa, Ilaria / Ursini, Matilde Valeria / Galderisi, Umberto / Cipollaro, Marilena / Altucci, Lucia / Cobellis, Gilda

    Scientific reports

    2020  Volume 10, Issue 1, Page(s) 6776

    Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

    Abstract An amendment to this paper has been published and can be accessed via a link at the top of the paper.
    Language English
    Publishing date 2020-04-17
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-62861-8
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  8. Article ; Online: Chromatin modification and senescence.

    Di Bernardo, Giovanni / Cipollaro, Marilena / Galderisi, Umberto

    Current pharmaceutical design

    2011  Volume 18, Issue 13, Page(s) 1686–1693

    Abstract: Cells are the fundamental structure composing our bodies and hence cellular decline (called senescence) contributes to ageing. Endogenous and exogenous stresses may induce cellular senescence. Stressors are mainly macromolecule damage events, which ... ...

    Abstract Cells are the fundamental structure composing our bodies and hence cellular decline (called senescence) contributes to ageing. Endogenous and exogenous stresses may induce cellular senescence. Stressors are mainly macromolecule damage events, which include: shortening of chromosome telomeres; non-telomeric DNA damage; excessive mitogenic signals, which may cause DNA damage; and non-genotoxic stress, such as perturbations to chromatin organization. For many years the analysis of chromatin perturbation as a leading event in triggering senescence has been overlooked. Now, it is well recognized that chromatin DNA packaging is not immune to the ravages of time. All eukaryotes experience changes in chromatin organization and gene-expression patterns as they age. This can be due to perturbation in the function of chromatin modifiers. In this review we will discuss the role in the senescence process of the different types of chromatin modifiers, such as the ATP-dependent chromatin remodelling complexes, the enzymes that covalently modify histone tails and proteins involved in DNA methylation.
    MeSH term(s) Animals ; Cellular Senescence ; Chromatin Assembly and Disassembly ; Humans
    Language English
    Publishing date 2011-08-04
    Publishing country United Arab Emirates
    Document type Journal Article ; Review
    ZDB-ID 1304236-1
    ISSN 1873-4286 ; 1381-6128
    ISSN (online) 1873-4286
    ISSN 1381-6128
    DOI 10.2174/138161212799859693
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  9. Article ; Online: Impact of lysosomal storage disorders on biology of mesenchymal stem cells: Evidences from in vitro silencing of glucocerebrosidase (GBA) and alpha-galactosidase A (GLA) enzymes.

    Squillaro, Tiziana / Antonucci, Ivana / Alessio, Nicola / Esposito, Anna / Cipollaro, Marilena / Melone, Mariarosa Anna Beatrice / Peluso, Gianfranco / Stuppia, Liborio / Galderisi, Umberto

    Journal of cellular physiology

    2017  Volume 232, Issue 12, Page(s) 3454–3467

    Abstract: Lysosomal storage disorders (LDS) comprise a group of rare multisystemic diseases resulting from inherited gene mutations that impair lysosomal homeostasis. The most common LSDs, Gaucher disease (GD), and Fabry disease (FD) are caused by deficiencies in ... ...

    Abstract Lysosomal storage disorders (LDS) comprise a group of rare multisystemic diseases resulting from inherited gene mutations that impair lysosomal homeostasis. The most common LSDs, Gaucher disease (GD), and Fabry disease (FD) are caused by deficiencies in the lysosomal glucocerebrosidase (GBA) and alpha-galactosidase A (GLA) enzymes, respectively. Given the systemic nature of enzyme deficiency, we hypothesized that the stem cell compartment of GD and FD patients might be also affected. Among stem cells, mesenchymal stem cells (MSCs) are a commonly investigated population given their role in hematopoiesis and the homeostatic maintenance of many organs and tissues. Since the impairment of MSC functions could pose profound consequences on body physiology, we evaluated whether GBA and GLA silencing could affect the biology of MSCs isolated from bone marrow and amniotic fluid. Those cell populations were chosen given the former's key role in organ physiology and the latter's intriguing potential as an alternative stem cell model for human genetic disease. Our results revealed that GBA and GLA deficiencies prompted cell cycle arrest along with the impairment of autophagic flux and an increase of apoptotic and senescent cell percentages. Moreover, an increase in ataxia-telangiectasia-mutated staining 1 hr after oxidative stress induction and a return to basal level at 48 hr, along with persistent gamma-H2AX staining, indicated that MSCs properly activated DNA repair signaling, though some damages remained unrepaired. Our data therefore suggest that MSCs with reduced GBA or GLA activity are prone to apoptosis and senescence due to impaired autophagy and DNA repair capacity.
    MeSH term(s) Amniotic Fluid/cytology ; Apoptosis ; Autophagy ; Bone Marrow Cells/enzymology ; Bone Marrow Cells/pathology ; Cell Separation ; Cells, Cultured ; Cellular Senescence ; Child ; DNA Repair ; Fabry Disease/enzymology ; Fabry Disease/genetics ; Fabry Disease/pathology ; Female ; Gaucher Disease/enzymology ; Gaucher Disease/genetics ; Gaucher Disease/pathology ; Glucosylceramidase/deficiency ; Glucosylceramidase/genetics ; Humans ; Mesenchymal Stem Cells/enzymology ; Mesenchymal Stem Cells/pathology ; RNA Interference ; Retinoblastoma Protein/genetics ; Retinoblastoma Protein/metabolism ; S Phase Cell Cycle Checkpoints ; Signal Transduction ; Stem Cell Niche ; Transfection ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; alpha-Galactosidase/genetics ; alpha-Galactosidase/metabolism
    Chemical Substances Retinoblastoma Protein ; TP53 protein, human ; Tumor Suppressor Protein p53 ; GLA protein, human (EC 3.2.1.22) ; alpha-Galactosidase (EC 3.2.1.22) ; Glucosylceramidase (EC 3.2.1.45)
    Language English
    Publishing date 2017-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.25807
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  10. Article ; Online: Misidentified Human Gene Functions with Mouse Models: The Case of the Retinoblastoma Gene Family in Senescence.

    Alessio, Nicola / Capasso, Stefania / Ferone, Angela / Di Bernardo, Giovanni / Cipollaro, Marilena / Casale, Fiorina / Peluso, Gianfranco / Giordano, Antonio / Galderisi, Umberto

    Neoplasia (New York, N.Y.)

    2017  Volume 19, Issue 10, Page(s) 781–790

    Abstract: Although mice models rank among the most widely used tools for understanding human genetics, biology, and diseases, differences between orthologous genes among species as close as mammals are possible, particularly in orthologous gene pairs in which one ... ...

    Abstract Although mice models rank among the most widely used tools for understanding human genetics, biology, and diseases, differences between orthologous genes among species as close as mammals are possible, particularly in orthologous gene pairs in which one or more paralogous (i.e., duplicated) genes appear in the genomes of the species. Duplicated genes can possess overlapping functions and compensate for each other. The retinoblastoma gene family demonstrates typical composite functionality in its three member genes (i.e., RB1, RB2/P130, and P107), all of which participate in controlling the cell cycle and associated phenomena, including proliferation, quiescence, apoptosis, senescence, and cell differentiation. We analyzed the role of the retinoblastoma gene family in regulating senescence in mice and humans. Silencing experiments with each member of the gene family in mesenchymal stromal cells (MSCs) and fibroblasts from mouse and human tissues demonstrated that RB1 may be indispensable for senescence in mouse cells, but not in human ones, as an example of species specificity. Furthermore, although RB2/P130 seems to be implicated in maintaining human cell senescence, the function of RB1 within any given species might differ by cell type, as an example of cell specificity. For instance, silencing RB1 in mouse fibroblasts induced a reduced senescence not observed in mouse MSCs. Our findings could be useful as a general paradigm of cautions to take when inferring the role of human genes analyzed in animal studies and when examining the role of the retinoblastoma gene family in detail.
    Language English
    Publishing date 2017-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1483840-0
    ISSN 1476-5586 ; 1522-8002
    ISSN (online) 1476-5586
    ISSN 1522-8002
    DOI 10.1016/j.neo.2017.06.005
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