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  1. Article: The role of the adventitia in vascular inflammation.

    Maiellaro, Kathryn / Taylor, W Robert

    Cardiovascular research

    2007  Volume 75, Issue 4, Page(s) 640–648

    Abstract: Traditional concepts of vascular inflammation are considered "inside-out" responses centered on the monocyte adhesion and lipid oxidation hypotheses. These mechanisms likely operate in concert, holding the central tenet that the inflammatory response is ... ...

    Abstract Traditional concepts of vascular inflammation are considered "inside-out" responses centered on the monocyte adhesion and lipid oxidation hypotheses. These mechanisms likely operate in concert, holding the central tenet that the inflammatory response is initiated at the luminal surface. However, growing evidence supports a new paradigm of an "outside-in" hypothesis, in which vascular inflammation is initiated in the adventitia and progresses inward toward the intima. Hallmarks of the outside-in hypothesis include population of the adventitia with exogenous cell types, including monocytes, macrophages, and lymphocytes, the phenotypic switch of adventitial fibroblasts into migratory myofibroblasts, and increased vasa vasorum neovascularization. The resident and migrating cells deposit collagen and matrix components, respond to and upregulate inflammatory chemokines and/or antigens, and regulate the local redox state of the adventitia. B cells and T cells generate local humoral immune responses against local antigen presentation by foam cells and antigen presenting cells. These events result in increased local expression of cytokines and growth factors, evoking an inflammatory response that propagates inward toward the intima. Ultimately, it appears that the basic mechanisms of cellular activation and migration in vascular inflammation are highly conserved across a variety of cardiovascular disease states and that major inflammatory events begin in the adventitia.
    MeSH term(s) Animals ; Aortic Aneurysm, Abdominal/immunology ; Atherosclerosis/immunology ; Connective Tissue/immunology ; Fibroblasts/immunology ; Humans ; Hypertension/immunology ; Leukocytes, Mononuclear/immunology ; Macrophages/immunology ; Tunica Intima/immunology ; Vasculitis/immunology
    Language English
    Publishing date 2007-09-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1016/j.cardiores.2007.06.023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 565: Show issues Location:
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  2. Article ; Online: Catalase overexpression in aortic smooth muscle prevents pathological mechanical changes underlying abdominal aortic aneurysm formation.

    Maiellaro-Rafferty, Kathryn / Weiss, Daiana / Joseph, Giji / Wan, William / Gleason, Rudolph L / Taylor, W Robert

    American journal of physiology. Heart and circulatory physiology

    2011  Volume 301, Issue 2, Page(s) H355–62

    Abstract: The causality of the associations between cellular and mechanical mechanisms of abdominal aortic aneurysm (AAA) formation has not been completely defined. Because reactive oxygen species are established mediators of AAA growth and remodeling, our ... ...

    Abstract The causality of the associations between cellular and mechanical mechanisms of abdominal aortic aneurysm (AAA) formation has not been completely defined. Because reactive oxygen species are established mediators of AAA growth and remodeling, our objective was to investigate oxidative stress-induced alterations in aortic biomechanics and microstructure during subclinical AAA development. We investigated the mechanisms of AAA in an angiotensin II (ANG II) infusion model of AAA in apolipoprotein E-deficient (apoE(-/-)) mice that overexpress catalase in vascular smooth muscle cells (apoE(-/-)xTg(SMC-Cat)). At baseline, aortas from apoE(-/-)xTg(SMC-Cat) exhibited increased stiffness and the microstructure was characterized by 50% more collagen content and less elastin fragmentation. ANG II treatment for 7 days in apoE(-/-) mice altered the transmural distribution of suprarenal aortic circumferential strain (quantified by opening angle, which increased from 130 ± 1° at baseline to 198 ± 8° after 7 days of ANG II treatment) without obvious changes in the aortic microstructure. No differences in aortic mechanical behavior or suprarenal opening angle were observed in apoE(-/-)xTg(SMC-Cat) after 7 days of ANG II treatment. These data suggest that at the earliest stages of AAA development H(2)O(2) is functionally important and is involved in the control of local variations in remodeling across the vessel wall. They further suggest that reduced elastin integrity at baseline may predispose the abdominal aorta to aneurysmal mechanical remodeling.
    MeSH term(s) Analysis of Variance ; Angiotensin II ; Animals ; Aorta, Abdominal/enzymology ; Aorta, Abdominal/pathology ; Aorta, Abdominal/physiopathology ; Aortic Aneurysm, Abdominal/chemically induced ; Aortic Aneurysm, Abdominal/enzymology ; Aortic Aneurysm, Abdominal/genetics ; Aortic Aneurysm, Abdominal/pathology ; Aortic Aneurysm, Abdominal/physiopathology ; Aortic Aneurysm, Abdominal/prevention & control ; Apolipoproteins E/deficiency ; Apolipoproteins E/genetics ; Biomechanical Phenomena ; Blood Pressure ; Catalase/genetics ; Catalase/metabolism ; Collagen/metabolism ; Disease Models, Animal ; Elastin/metabolism ; Hydrogen Peroxide/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Stress, Mechanical ; Time Factors ; Up-Regulation
    Chemical Substances Apolipoproteins E ; Angiotensin II (11128-99-7) ; Collagen (9007-34-5) ; Elastin (9007-58-3) ; Hydrogen Peroxide (BBX060AN9V) ; Catalase (EC 1.11.1.6)
    Language English
    Publishing date 2011-05-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Webcast
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00040.2011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Acute preconditioning of cardiac progenitor cells with hydrogen peroxide enhances angiogenic pathways following ischemia-reperfusion injury.

    Pendergrass, Karl D / Boopathy, Archana V / Seshadri, Gokulakrishnan / Maiellaro-Rafferty, Kathryn / Che, Pao Lin / Brown, Milton E / Davis, Michael E

    Stem cells and development

    2013  Volume 22, Issue 17, Page(s) 2414–2424

    Abstract: There are a limited number of therapies available to prevent heart failure following myocardial infarction. One novel therapy that is currently being pursued is the implantation of cardiac progenitor cells (CPCs); however, their responses to oxidative ... ...

    Abstract There are a limited number of therapies available to prevent heart failure following myocardial infarction. One novel therapy that is currently being pursued is the implantation of cardiac progenitor cells (CPCs); however, their responses to oxidative stress during differentiation have yet to be elucidated. The objective of this study was to determine the effect of hydrogen peroxide (H2O2) treatment on CPC differentiation in vitro, as well as the effect of H2O2 preconditioning before implantation following ischemia-reperfusion (I/R) injury. CPCs were isolated and cloned from adult rat hearts, and then cultured in the absence or presence of H2O2 for 2 or 5 days. CPC survival was assessed with Annexin V, and cellular differentiation was evaluated through mRNA expression for cardiogenic genes. We found that 100 μM H2O2 decreased serum withdrawal-induced apoptosis by at least 45% following both 2 and 5 days of treatment. Moreover, 100 μM H2O2 treatment for 2 days significantly increased endothelial and smooth muscle markers compared to time-matched untreated CPCs. However, continued H2O2 treatment significantly decreased these markers. Left ventricular cardiac function was assessed 28 days after I/R and I/R with the implantation of Luciferase/GFP(+) CPCs, which were preconditioned with 100 μM H2O2 for 2 days. Hearts implanted with Luciferase/GFP(+) CPCs had significant improvement in both positive and negative dP/dT over I/R. Furthermore, cardiac fibrosis was significantly decreased in the preconditioned cells versus both I/R alone and I/R with control cells. We also observed a significant increase in endothelial cell density in the preconditioned CPC hearts compared to untreated CPC hearts, which also coincided with a higher density of Luciferase(+) vessels. These findings suggest that preconditioning of CPCs with H2O2 for 2 days stimulates neoangiogenesis in the peri-infarct area following I/R injury and could be a viable therapeutic option to prevent heart failure.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Cell Differentiation/drug effects ; Cells, Cultured ; Fibrosis/drug therapy ; Gene Expression ; Heart Failure/drug therapy ; Heart Failure/prevention & control ; Hydrogen Peroxide/metabolism ; Hydrogen Peroxide/pharmacology ; Ischemic Preconditioning, Myocardial/methods ; Male ; Myocardial Contraction/drug effects ; Myocardial Infarction/drug therapy ; Neovascularization, Physiologic/drug effects ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury/drug therapy ; Stem Cells/drug effects ; Stem Cells/metabolism ; Ventricular Function, Left/drug effects
    Chemical Substances Hydrogen Peroxide (BBX060AN9V)
    Language English
    Publishing date 2013-05-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2142214-X
    ISSN 1557-8534 ; 1547-3287
    ISSN (online) 1557-8534
    ISSN 1547-3287
    DOI 10.1089/scd.2012.0673
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    Zs.A 3616: Show issues Location:
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  4. Article ; Online: Temporal effects of catalase overexpression on healing after myocardial infarction.

    Pendergrass, Karl D / Varghese, Susan T / Maiellaro-Rafferty, Kathryn / Brown, Milton E / Taylor, W Robert / Davis, Michael E

    Circulation. Heart failure

    2010  Volume 4, Issue 1, Page(s) 98–106

    Abstract: Background: Reactive oxygen species, such as hydrogen peroxide (H(2)O(2)), contribute to progression of dysfunction after myocardial infarction (MI). However, chronic overexpression studies do not agree with acute protein delivery studies. The purpose ... ...

    Abstract Background: Reactive oxygen species, such as hydrogen peroxide (H(2)O(2)), contribute to progression of dysfunction after myocardial infarction (MI). However, chronic overexpression studies do not agree with acute protein delivery studies. The purpose of the present study was to assess the temporal role of cardiomyocyte-derived H(2)O(2) scavenging on cardiac function after infarction using an inducible system.
    Methods and results: We developed a tamoxifen-inducible, cardiomyocyte-specific, catalase-overexpressing mouse. Catalase overexpression was induced either 5 days before or after MI. Mice exhibited a 3-fold increase in cardiac catalase activity that was associated with a significant decrease in H(2)O(2) levels at both 7 and 21 days. However, cardiac function improved only at the later time point. Proinflammatory and fibrotic genes were acutely upregulated after MI, but catalase overexpression abolished the increase despite no acute change in function. This led to reduced overall scar formation, with lower levels of Collagen 1A and increased contractile Collagen 3A expression at 21 days.
    Conclusions: In contrast to prior studies, there were no acute functional improvements with physiological catalase overexpression before MI. Scavenging of H(2)O(2), however, reduced proinflammatory cytokines and altered cardiac collagen isoforms, associated with an improvement in cardiac function after 21 days. Our results suggest that sustained H(2)O(2) levels rather than acute levels immediately after MI may be critical in directing remodeling and cardiac function at later time points.
    MeSH term(s) Animals ; Catalase/drug effects ; Catalase/genetics ; Catalase/metabolism ; Collagen Type I/metabolism ; Collagen Type III/metabolism ; Gene Expression Regulation/drug effects ; Hydrogen Peroxide/metabolism ; Male ; Mice ; Mice, Transgenic ; Models, Animal ; Myocardial Infarction/metabolism ; Myocardial Infarction/physiopathology ; Myocardium/metabolism ; Recovery of Function/physiology ; Tamoxifen/pharmacology
    Chemical Substances Collagen Type I ; Collagen Type III ; Tamoxifen (094ZI81Y45) ; Hydrogen Peroxide (BBX060AN9V) ; Catalase (EC 1.11.1.6)
    Language English
    Publishing date 2010-10-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2429459-7
    ISSN 1941-3297 ; 1941-3289
    ISSN (online) 1941-3297
    ISSN 1941-3289
    DOI 10.1161/CIRCHEARTFAILURE.110.957712
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6745: Show issues Location:
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  5. Article ; Online: An in vivo murine model of low-magnitude oscillatory wall shear stress to address the molecular mechanisms of mechanotransduction--brief report.

    Willett, Nick J / Long, Robert C / Maiellaro-Rafferty, Kathryn / Sutliff, Roy L / Shafer, Richard / Oshinski, John N / Giddens, Don P / Guldberg, Robert E / Taylor, W Robert

    Arteriosclerosis, thrombosis, and vascular biology

    2010  Volume 30, Issue 11, Page(s) 2099–2102

    Abstract: Objective: Current understanding of shear-sensitive signaling pathways has primarily been studied in vitro largely because of a lack of adequate in vivo models. Our objective was to develop a simple and well-characterized murine aortic coarctation model ...

    Abstract Objective: Current understanding of shear-sensitive signaling pathways has primarily been studied in vitro largely because of a lack of adequate in vivo models. Our objective was to develop a simple and well-characterized murine aortic coarctation model to acutely alter the hemodynamic environment in vivo and test the hypothesis that endothelial inflammatory protein expression is acutely upregulated in vivo by low-magnitude oscillatory wall shear stress (WSS).
    Methods and results: Our model uses the shape memory response of nitinol clips to reproducibly induce an aortic coarctation and allow subsequent focal control over WSS in the aorta. We modeled the corresponding hemodynamic environment using computational fluid dynamics and showed that the coarctation produces low-magnitude oscillatory WSS distal to the clip. To assess the biological significance of this model, we correlated WSS to inflammatory protein expression and fatty streak formation. Vascular cell adhesion molecule-1 expression and fatty streak formation were both found to increase significantly in regions corresponding to acutely induced low-magnitude oscillatory WSS.
    Conclusions: We have developed a novel aortic coarctation model that will be a useful tool for analyzing the in vivo molecular mechanisms of mechanotransduction in various murine models.
    MeSH term(s) Animals ; Aorta/chemistry ; Aorta/metabolism ; Aortic Coarctation/metabolism ; Aortic Coarctation/physiopathology ; Biomechanical Phenomena ; Disease Models, Animal ; Immunohistochemistry ; Mice ; Shear Strength ; Signal Transduction ; Stress, Mechanical ; Vascular Cell Adhesion Molecule-1/analysis ; Vascular Cell Adhesion Molecule-1/metabolism
    Chemical Substances Vascular Cell Adhesion Molecule-1
    Language English
    Publishing date 2010-08-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.110.211532
    Database MEDical Literature Analysis and Retrieval System OnLINE

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