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  1. Article ; Online: Loss of ADAM15 in female mice does not worsen pressure overload cardiomyopathy, independent of ovarian hormones.

    Krishnan, Vidhya / Atanasova, Nikki / Aujla, Preetinder K / Hupka, Devon / Owen, Caroline A / Kassiri, Zamaneh

    American journal of physiology. Heart and circulatory physiology

    2024  

    Abstract: Cardiac hypertrophy is a common feature in several cardiomyopathies. We previously reported that loss of ADAM15 (disintegrin and metalloproteinase 15) worsened cardiac hypertrophy and dilated cardiomyopathy following cardiac pressure overload. Here, we ... ...

    Abstract Cardiac hypertrophy is a common feature in several cardiomyopathies. We previously reported that loss of ADAM15 (disintegrin and metalloproteinase 15) worsened cardiac hypertrophy and dilated cardiomyopathy following cardiac pressure overload. Here, we investigated the impact of ADAM15 loss in female mice following cardiac pressure overload induced by transverse aortic constriction (TAC). Female
    Language English
    Publishing date 2024-04-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00116.2024
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Diverse origins and activation of fibroblasts in cardiac fibrosis.

    Aujla, Preetinder K / Kassiri, Zamaneh

    Cellular signalling

    2020  Volume 78, Page(s) 109869

    Abstract: Cardiac fibroblasts (cFBs) have emerged as a heterogenous cell population. Fibroblasts are considered the main cell source for synthesis of the extracellular matrix (ECM) and as such a dysregulation in cFB function, activity, or viability can lead to ... ...

    Abstract Cardiac fibroblasts (cFBs) have emerged as a heterogenous cell population. Fibroblasts are considered the main cell source for synthesis of the extracellular matrix (ECM) and as such a dysregulation in cFB function, activity, or viability can lead to disrupted ECM structure or fibrosis. Fibrosis can be initiated in response to different injuries and stimuli, and can be reparative (beneficial) or reactive (damaging). FBs need to be activated to myofibroblasts (MyoFBs) which have augmented capacity in synthesizing ECM proteins, causing fibrosis. In addition to the resident FBs in the myocardium, a number of other cells (pericytes, fibrocytes, mesenchymal, and hematopoietic cells) can transform into MyoFBs, further driving the fibrotic response. Multiple molecules including hormones, cytokines, and growth factors stimulate this process leading to generation of activated MyoFBs. Contribution of different cell types to cFBs and MyoFBs can result in an exponential increase in the number of MyoFBs and an accelerated pro-fibrotic response. Given the diversity of the cell sources, and the array of interconnected signalling pathways that lead to formation of MyoFBs and subsequently fibrosis, identifying a single target to limit the fibrotic response in the myocardium has been challenging. This review article will delineate the importance and relevance of fibroblast heterogeneity in mediating fibrosis in different models of heart failure and will highlight important signalling pathways implicated in myofibroblast activation.
    MeSH term(s) Animals ; Extracellular Matrix/metabolism ; Fibrosis ; Heart Failure/metabolism ; Humans ; Myocardium/metabolism ; Myofibroblasts/metabolism ; Signal Transduction
    Language English
    Publishing date 2020-12-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1002702-6
    ISSN 1873-3913 ; 0898-6568
    ISSN (online) 1873-3913
    ISSN 0898-6568
    DOI 10.1016/j.cellsig.2020.109869
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2579: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Sex- and age-specific regulation of ACE2: Insights into severe COVID-19 susceptibility.

    Viveiros, Anissa / Gheblawi, Mahmoud / Aujla, Preetinder K / Sosnowski, Deanna K / Seubert, John M / Kassiri, Zamaneh / Oudit, Gavin Y

    Journal of molecular and cellular cardiology

    2021  Volume 164, Page(s) 13–16

    Abstract: Aged males disproportionately succumb to increased COVID-19 severity, hospitalization, and mortality compared to females. Angiotensin-converting enzyme 2 (ACE2) and transmembrane protease, serine 2 (TMPRSS2) facilitate SARS-CoV-2 viral entry and may have ...

    Abstract Aged males disproportionately succumb to increased COVID-19 severity, hospitalization, and mortality compared to females. Angiotensin-converting enzyme 2 (ACE2) and transmembrane protease, serine 2 (TMPRSS2) facilitate SARS-CoV-2 viral entry and may have sexually dimorphic regulation. As viral load dictates disease severity, we investigated the expression, protein levels, and activity of ACE2 and TMPRSS2. Our data reveal that aged males have elevated ACE2 in both mice and humans across organs. We report the first comparative study comprehensively investigating the impact of sex and age in murine and human levels of ACE2 and TMPRSS2, to begin to elucidate the sex bias in COVID-19 severity.
    MeSH term(s) Aging/genetics ; Aging/metabolism ; Angiotensin-Converting Enzyme 2/biosynthesis ; Angiotensin-Converting Enzyme 2/genetics ; Animals ; COVID-19/epidemiology ; Disease Susceptibility ; Female ; Gene Expression Regulation, Enzymologic ; Heart/virology ; Humans ; Intestine, Small/enzymology ; Intestine, Small/virology ; Kidney/enzymology ; Kidney/virology ; Lung/enzymology ; Lung/virology ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Myocardium/enzymology ; Organ Specificity ; Receptors, Virus/biosynthesis ; Receptors, Virus/genetics ; SARS-CoV-2/physiology ; Serine Endopeptidases/biosynthesis ; Serine Endopeptidases/genetics ; Sex Characteristics ; Young Adult
    Chemical Substances Receptors, Virus ; ACE2 protein, human (EC 3.4.17.23) ; Ace2 protein, mouse (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Serine Endopeptidases (EC 3.4.21.-) ; TMPRSS2 protein, human (EC 3.4.21.-) ; TMPRSS2 protein, mouse (EC 3.4.21.-)
    Language English
    Publishing date 2021-11-11
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2021.11.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 426: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Loss of ADAM15 Exacerbates Transition to Decompensated Myocardial Hypertrophy and Dilation Through Activation of the Calcineurin Pathway.

    Aujla, Preetinder K / Hu, Mei / Hartley, Bridgette / Kranrod, Joshua W / Viveiros, Anissa / Kilic, Tolga / Owen, Caroline A / Oudit, Gavin Y / Seubert, John M / Julien, Olivier / Kassiri, Zamaneh

    Hypertension (Dallas, Tex. : 1979)

    2022  Volume 80, Issue 1, Page(s) 97–110

    Abstract: Background: Myocardial hypertrophy and dilation are key features of cardiomyopathies and involve several cellular and molecular events. ADAMs (a disintegrin and metalloproteinases) are membrane-bound proteinases with diverse functions whose role in ... ...

    Abstract Background: Myocardial hypertrophy and dilation are key features of cardiomyopathies and involve several cellular and molecular events. ADAMs (a disintegrin and metalloproteinases) are membrane-bound proteinases with diverse functions whose role in heart disease remains underexplored. ADAM15 is expressed in the heart and is downregulated in the failing human heart. We investigated the role ADAM15 in pressure overload cardiomyopathy.
    Methods: We assessed ADAM15 levels in myocardial specimens from patients. Its direct role in pressure overload was investigated by subjecting wildtype and
    Results: ADAM15 levels did not change in patients with concentric hypertrophy, but markedly decreased in eccentric hypertrophy and heart failure. Loss of ADAM15 alone did not cause cardiomyopathy in mice (1 year old). After TAC,
    Conclusion: This is the first report demonstrating that ADAM15 can suppress hypertrophy through regulating the integrin-laminin interaction and the calcineurin pathway.
    MeSH term(s) Humans ; Mice ; Animals ; Infant ; Laminin ; Cardiomyopathies ; Membrane Proteins/genetics ; ADAM Proteins/genetics
    Chemical Substances Laminin ; ADAM15 protein, human (EC 3.4.24.-) ; Membrane Proteins ; ADAM Proteins (EC 3.4.24.-) ; Adam15 protein, mouse (EC 3.4.24.-)
    Language English
    Publishing date 2022-11-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.122.19411
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1488: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: ADAM15 is required for optimal collagen cross-linking and scar formation following myocardial infarction.

    Chute, Michael / Aujla, Preetinder K / Li, Yingxi / Jana, Sayantan / Zhabyeyev, Pavel / Rasmuson, Jaslyn / Owen, Caroline A / Abraham, Thomas / Oudit, Gavin Y / Kassiri, Zamaneh

    Matrix biology : journal of the International Society for Matrix Biology

    2022  Volume 105, Page(s) 127–143

    Abstract: Collagen cross-linking is an important step in optimal scar formation. Myocardial infarction (MI) results in loss of cardiomyocytes that are replaced with a scar (infarct) tissue. Disintegrin and metalloproteinases (ADAMs) are membrane-bound proteases ... ...

    Abstract Collagen cross-linking is an important step in optimal scar formation. Myocardial infarction (MI) results in loss of cardiomyocytes that are replaced with a scar (infarct) tissue. Disintegrin and metalloproteinases (ADAMs) are membrane-bound proteases that can interact with molecules intra- and extra-cellularly to mediate various cellular functions. ADAM15 is expressed in the myocardium, however its function in heart disease has been poorly explored. We utilized mice lacking ADAM15 (Adam15
    MeSH term(s) ADAM Proteins/metabolism ; Animals ; Cicatrix/genetics ; Cicatrix/pathology ; Collagen/metabolism ; Female ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardial Infarction/genetics ; Myocardial Infarction/metabolism ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Ventricular Remodeling/genetics
    Chemical Substances Membrane Proteins ; Collagen (9007-34-5) ; ADAM Proteins (EC 3.4.24.-) ; Adam15 protein, mouse (EC 3.4.24.-)
    Language English
    Publishing date 2022-01-05
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1183793-7
    ISSN 1569-1802 ; 0945-053X
    ISSN (online) 1569-1802
    ISSN 0945-053X
    DOI 10.1016/j.matbio.2021.12.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1694: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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