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  • 1
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    Abstract 8955: Cardiopulmonary Phenotyping of Sex-Based Differences in a Feline Model of HFpEF
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. Suppl_1 ( 2021-11-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Abstract: Introduction: Approximately 50% of all heart failure (HF) diagnoses can be classified as HF with preserved ejection fraction (HFpEF), which has no FDA approved therapies. HFpEF is more prevalent in females compared to males, but the underlying mechanisms for the development as a sex-based disorder are unknown. We previously described how slow progressive pressure overload (PO) in male felines recapitulates the HFpEF phenotype but have not investigated the female phenotype. Hypothesis: Females will develop a less severe HFpEF phenotype compared to males under the same pathological stress. Methods & Results: Male (m) and female (f) domestic short felines (age 2mo) underwent aortic constriction (m: n=11; f: n=10) using a customized pre-shaped band or a sham procedure (m: n=7; f: n=7). Before surgery (baseline), there was no difference in body weight (BW) between groups and lung compliance was not different. Echocardiography revealed no significant difference in the ratio of left atrium to aortic root (LA/Ao), LA ejection fraction (LA EF), left ventricle (LV) ejection fraction, LV wall-thickness, and E/A ratio. By 4mo post-surgery, both males and females had developed cardiac dysfunction and decreased lung compliance. At this time, females had significantly smaller BWs than males. Despite the difference in BW, LV wall thickness and changes in E/A ratio were similar in both sexes in banded vs. shams. Importantly, LV EF did not change in any group. There was a decrease in LA EF and increased LA/Ao in all banded animals. Invasive hemodynamics at 4mo post-surgery showed no differences between sexes for the systolic pressure gradient generated by aortic banding. Banded males had higher LV end-diastolic pressure vs. banded females (m: 15.0±2.7mmHg; f: 8.1±1.9mmHg). However, there was a trend towards prolongation of tau and lower dp/dt min in banded females, suggestive of abnormal relaxation. There were no differences between banded males and females in heart weight/BW or cardiomyocyte cross-sectional area and both developed fibrosis. Conclusions: Exposure of male and female felines to PO resulted in similar cardiac hypertrophy, fibrosis, and decreased lung compliance. Females had lower LVEDP than males suggesting they may be protected from diastolic dysfunction.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.144.suppl_1.8955
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
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  • 2
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    Ca 2+ Influx–Induced Sarcoplasmic Reticulum Ca 2+ Overload Causes Mitochondrial-Dependent Apoptosis in Ventricular Myocytes
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Circulation Research Vol. 97, No. 10 ( 2005-11-11), p. 1009-1017
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 97, No. 10 ( 2005-11-11), p. 1009-1017
    Abstract: Increases in Ca 2+ influx through the L-type Ca 2+ channel (LTCC, Cav1.2) augment sarcoplasmic reticulum (SR) Ca 2+ loading and the amplitude of the cytosolic Ca 2+ transient to enhance cardiac myocyte contractility. Our hypothesis is that persistent increases in Ca 2+ influx through the LTCC cause apoptosis if the excessive influx results in SR Ca 2+ overload. Feline ventricular myocytes (VMs) in primary culture were infected with either an adenovirus (Ad) containing a rat Cav1.2 β 2a subunit-green fluorescent protein (GFP) fusion gene (Adβ 2a ) to increase Ca 2+ influx or with AdGFP as a control. Significantly fewer β 2a -VMs (21.4±5.6%) than GFP-VMs (99.6±1.7%) were viable at 96 hours. A fraction of β 2a -VMs (20.8±1.8%) contracted spontaneously (SC-β 2a -VMs), and viability was significantly correlated with the percentage of SC-β 2a -VMs. Higher percentages of apoptotic nuclei, DNA laddering, and cytochrome C release were detected in β 2a -VMs. This apoptosis was prevented with pancaspase or caspase-3 or caspase-9 inhibitors. L-type calcium current (I Ca-L ) density was greater in β 2a -VMs (23.4±2.8 pA/pF) than in GFP-VMs (7.6±1.6 pA/pF). SC-β 2a -VMs had higher diastolic intracellular Ca 2+ (Indo-1 ratio: 1.1±0.1 versus 0.7±0.03, P 〈 0.05) and systolic Ca 2+ transients (1.89±0.27 versus 0.80±0.08) than GFP-VMs. Inhibitors of Ca 2+ influx, SR Ca 2+ uptake and release, mitochondrial Ca 2+ uptake, mitochondrial permeation transition pore, calpain, and Bcl-2-associated X protein protected β 2a -VMs from apoptosis. These results show that persistent increases in Ca 2+ influx through the I Ca-L enhance contractility but lead to apoptosis through a mitochondrial death pathway if SR Ca 2+ overload is induced.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.0000189270.72915.D1
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 1467838-X
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  • 3
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    Alterations in Early Action Potential Repolarization Causes Localized Failure of Sarcoplasmic Reticulum Ca 2+ Release
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Circulation Research Vol. 96, No. 5 ( 2005-03-18), p. 543-550
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 96, No. 5 ( 2005-03-18), p. 543-550
    Abstract: Depressed contractility of failing myocytes involves a decreased rate of rise of the Ca 2+ transient. Synchronization of Ca 2+ release from the junctional sarcoplasmic reticulum (SR) is responsible for the rapid rise of the normal Ca 2+ transient. This study examined the idea that spatially and temporally dyssynchronous SR Ca 2+ release slows the rise of the cytosolic Ca 2+ transient in failing feline myocytes. Left ventricular hypertrophy (LVH) with and without heart failure (HF) was induced in felines by constricting the ascending aorta. Ca 2+ transients were measured in ventricular myocytes using confocal line scan imaging. Ca 2+ transients were induced by field stimulation, square wave voltage steps, or action potential (AP) voltage clamp. SR Ca 2+ release was significantly less well spatially and temporally synchronized in field-stimulated HF versus control or LVH myocytes. Surprisingly, depolarization of HF cells to potentials where Ca 2+ currents ( I Ca ) were maximal resynchronized SR Ca 2+ release. Correspondingly, decreases in the amplitude of I Ca desynchronized SR Ca 2+ release in control, LVH, and HF myocytes to the same extent. HF myocytes had significant loss of phase 1 AP repolarization and smaller I Ca density, which should both reduce Ca 2+ influx. When normal myocytes were voltage clamped with HF AP profiles SR Ca 2+ release was desynchronized. SR Ca 2+ release becomes dyssynchronized in failing feline ventricular myocytes because of reductions in Ca 2+ influx induced in part by alterations in early repolarization of the AP. Therefore, therapies that restore normal early repolarization should improve the contractility of the failing heart.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.0000158966.58380.37
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 1467838-X
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  • 4
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    Abstract P411: Sex-based Differences In A Feline Model Of Hfpef
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Research Vol. 129, No. Suppl_1 ( 2021-09-03)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 129, No. Suppl_1 ( 2021-09-03)
    Abstract: Rationale: Heart Failure with preserved Ejection Fraction (HFpEF) accounts for approximately 50% of all HF diagnoses with no FDA approved therapies. HFpEF is more prevalent in females versus males, but the mechanisms driving the development of HFpEF as a sex-based disorder are not well understood. We have recently shown that slow progressive pressure overload (PO) in male felines induces a HFpEF phenotype but have not investigated the differences in response to the same physiological stress in females. Hypothesis: Females will develop a phenotype that is distinct from males in response to PO. Methods and Results: Male (m) and female (f) domestic short felines (age 2mo) underwent either a sham procedure (m: n=7; f: n=7) or aortic constriction (m: n=11; f: n=10) using a customized pre-shaped band. At baseline (prior to surgery), there was no difference in body weight between groups and echocardiography revealed no significant difference in the ratio of left atrium to aortic root (LA/Ao), LA ejection fraction (LA EF), left ventricle (LV) ejection fraction, LV wall-thickness, and E/A ratio. At 4mo post-surgery, both males and females developed cardiac dysfunction. Females gained significantly less weight than males throughout the study. Despite the size difference, both sexes developed comparable LV wall thickness and changes in E/A ratio vs. sham groups. There was no change in LV EF. Furthermore, there was a decrease in LA EF and increased LA/Ao, indicating LA dysfunction and enlargement. Invasive hemodynamics at 4mo post-surgery showed no differences between sexes for the systolic pressure gradient generated by the aortic banding. Banded males had a significantly higher LV end-diastolic pressure vs. banded females, but there was a trend towards prolongation of tau and lower dp/dt min in banded females, reflective of worse active relaxation. Both sexes had comparable dP/dt max . There were no differences between banded males and females in heart weight to body weight or cardiomyocyte cross-sectional area. Conclusion: Despite similar pressure gradients as a result of PO and the development of similar cardiac hypertrophy between sexes and a higher LVEDP in males, females had a trend towards worse relaxation. Other causes of HFpEF may have sex-based differences.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.129.suppl_1.P411
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1467838-X
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  • 5
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    Abstract 311: Single-Dose Isoproterenol does not Depress Cardiac Function in Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation Research Vol. 117, No. suppl_1 ( 2015-07-17)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 117, No. suppl_1 ( 2015-07-17)
    Abstract: Rationale: Myocardial injury after repeated or continuous administration of isoproterenol (ISO) in preclinical models has been widely described in the literature by our lab and others. Recent controversial reports using a one-time dose of ISO, to mimic a Takotsubo-like cardiomyopathy, demonstrated pronounced and reversible depression of cardiac function at one-week post injection with widespread myocyte death followed by robust myocardial regeneration and recovery of cardiac function. Hypothesis: Single-dose ISO does not produce depression of cardiac function Methods and Results: C57Bl/6 mice were given a single subcutaneous injection of vehicle (saline) or 5, 200, or 300 mg/kg of ISO. Cardiac function was measured using transthoracic echocardiography with cardiac strain analysis at baseline prior to ISO injection and after 1, 7, 14, and 28 days post-injection. Animals were sacrificed after 1, 7, and 28 days post-injection for evaluation of gross heart weight (HW), HW/body weight (BW) and HW/tibia length (TL). Left ventricular (LV) functional measurements revealed no significant differences in global systolic function (ejection fraction and fractional shortening) between vehicle- or ISO-treated animals at any concentration. Additionally, no significant differences were detected between vehicle- or ISO-treated animals in any cardiac dimensions measured by echocardiography (LV cross-sectional area, internal diameter, end-diastolic or end-systolic volumes) or in gross HW, HW/BW or HW/TL. LV global cardiac strain was also not significantly different between vehicle and ISO-treated animals at any time point. When apical regions of the LV endocardium (the area most predominantly affected by Takotsubo cardiomyopathy) were specifically examined using strain analysis, no significant differences could be detected between vehicle and ISO-treated animals at any time point. Conclusion: Single-dose ISO injury in a mouse model does not produce any depression of cardiac function at 1 week post injection.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.117.suppl_1.311
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1467838-X
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  • 6
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    Abstract 227: Inhibition of Histone Deacetylase Catalytic Activity Improves Cardiac and Pulmonary Function in a Feline Model of Heart Failure with Preserved Ejection Fraction
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Circulation Research Vol. 123, No. Suppl_1 ( 2018-08-03)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 123, No. Suppl_1 ( 2018-08-03)
    Abstract: Rationale: Heart Failure with preserved Ejection Fraction (HFpEF) accounts for about 50% of all heart failure cases but has no effective therapies. Hypothesis: Inhibition of histone deacetylase (HDAC) catalytic activity exerts beneficial effects on the cardiopulmonary system in a feline model of HFpEF. Methods and Results: Male domestic short hair cats (n=21, aged 2mo), underwent either a sham procedure (n=5) or aortic constriction (n=16) using a customized pre-shaped band, resulting in slow progressive pressure overload during growth. 2 months post-banding, banded cats were treated daily with either 10mg/kg suberoylanilide hydroxamic acid ( b+SAHA ) (n=8), a pan-HDAC inhibitor, or vehicle ( b+veh ) (n=8) for 2 months. At 4 months post-banding, b+SAHA cats showed significantly reduced LV wall thickness and LA size (LA/Ao) compared to b+veh cats (Fig). Invasively measured left ventricular end-diastolic pressure (Fig. LVEDP) at 4 months was significantly elevated in b+veh cats compared to b+SAHA and sham cats (Fig). After dobutamine infusion, the increase in dp/dt max was significantly attenuated in b+veh , but not in b+SAHA cats (Fig). In vivo measurements of pulmonary function at 4 months post-banding demonstrated marked improvement in b+SAHA cats, reflected by an increase in lung compliance and a decrease in alveolar-arterial oxygen gradient (A-aDO 2 ) and intrapulmonary shunt (Fig). Efficacy of SAHA in vivo correlated with enhanced ex vivo myofibril relaxation. Conclusion: HDAC inhibition rescues the established HFpEF phenotype by reducing LV hypertrophy, LVEDP, LA size, and enhancing myofibril relaxation, which ultimately results in improved pulmonary function.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.123.suppl_1.227
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 1467838-X
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  • 7
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    Abstract 342: Cortical Bone Stem Cell Therapy Alters Macrophage Phenotype and Reduces Cardiac Cell Death After Myocardial Infarction
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Circulation Research Vol. 127, No. Suppl_1 ( 2020-07-31)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 127, No. Suppl_1 ( 2020-07-31)
    Abstract: Acute injuries to the heart, like myocardial infarction (MI), contribute to the development and pathology of heart failure (HF). Reperfusion of the ischemic heart greatly increases survival but results in reperfusion injury that can account for up to 50% of the final infarct size. The inflammatory response to MI-induced myocardial injury is thought to be responsible for the propagation of reperfusion injury into the infarct border zone, expanding myocardial damage. We have previously shown in a swine model of MI that intramyocardial injections of cortical bone-derived stem cells (CBSCs) into the infarct border zone has no acute cardioprotective effect but reduces scar size by half and prevents the decline of ejection fraction and LV dilation 3 months after MI. Our new preliminary data show that CBSCs have potent immunoregulatory capabilities. Therefore, we hypothesize that CBSC treatment has an effect on the immune response to MI that improves the wound healing response to myocardial injury and mitigates LV remodeling and infarct size 3 months later. To test this hypothesis, we characterized the effects of CBSC paracrine factors on macrophages in vitro and found that CBSC-treated macrophages express higher levels of CD206, produce more IL-1RA and IL-10, and phagocytose apoptotic myocytes more efficiently. In addition, macrophages were increased in CBSC-treated swine hearts 7 days after MI compared to controls with a corresponding increase in IL-1RA and TIMP-2. Apoptosis was decreased overall and in macrophages specifically in CBSC-treated animals. From these data we conclude CBSCs may exert an acute pro-reparative effect on the immune response after MI, reducing reperfusion injury and adverse remodeling resulting in improved functional outcomes at later time points.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.127.suppl_1.342
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 1467838-X
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  • 8
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    Abstract 2: Cortical Bone Stem Cells Derived Exosomes as Potent Modulator of Cardiac Immune Response and Repair After Injury
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation Research Vol. 119, No. suppl_1 ( 2016-07-22)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 119, No. suppl_1 ( 2016-07-22)
    Abstract: Rationale: Cortical bone derived stem cells (CBSCs) are known to have improved growth kinetics and myocardial repair properties that are superior to other known stem cell types used. Salutary effects of CBSCs in large are mediated by paracrine secretion. Since exosomes represent an active component of released factors we tested if CBSC derived exosomes (CBSCs-Exo) can recapitulate the beneficial reparative effects of CBSCs. Objective: Determine CBSCs derived exosomes and their contents for myocardial repair. Methods and Results: Exosomes were isolated from murine CBSCs by ultracentrifugation and had typical size (30-100nm), as validated by electron microscopy and dynamic light scattering. To determine cardiac therapeutic value, CBSCs- Exo (60μg) were injected into the border zone of the mouse heart after myocardial infarction (MI). Animals injected with CBSCs-Exo had reduced infarct size and increased myocyte survival after MI injury. Interestingly, serum levels of pro-inflammatory cytokines were significantly reduced along with decreased expression of CD68+ cells in animals receiving CBSCs-Exo versus control animals. Long term analysis of CBSC-Exo animals showed improved cardiac function and contractility compared to saline treated animals concurrent with enhanced angiogenesis 6 weeks after MI. Salutary effects of CBSC-Exo were confirmed in vitro. CBSCs-Exo increased cardiac protection in NRVMs after hypoxic challenge and enhanced tube formation in HUVECs. Simultaneously, treatment of bone marrow-derived macrophages stimulated with lipopolysaccharide (LPS) and treated with CBSCs-Exo showed increased polarization towards the M2 phenotype, demonstrating an immunomodulatory capacity of CBSCs-Exo. The underlying mechanism for beneficial effects was linked to increased packaging of cardioprotective miRs including miR125, miR20 and miR18a in CBSCs-Exo confirmed by MiRNA array analysis. Conclusion: Exosomes derived from CBSCs provide a cell free system that retains the reparative power of CBSC. CBSCs-Exo augment cardiac function after myocardial injury recapitulating earlier findings with CBSCs. The packaging of cardioprotective and immune-modulatory miRs in CBSCs-Exo appears to enhance their reparative effects after MI.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.119.suppl_1.2
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467838-X
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  • 9
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    Abstract 16434: Temporal Metabolomic and Transcriptomic Changes in a Large-Animal Model of Hfpef
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Circulation Vol. 142, No. Suppl_3 ( 2020-11-17)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 142, No. Suppl_3 ( 2020-11-17)
    Abstract: Heart failure with preserved ejection fraction (HFpEF) accounts for ~50% of HF cases, with no effective treatments. We previously reported that a feline aortic banding model recapitulates many of the multi-factorial features of HFpEF, including: LV hypertrophy, left atrial enlargement, elevated LV filling pressures, impaired pulmonary mechanics and fibrosis. Importantly, this model lacks obesity and hypertension enabling the discovery of cardiac centric targets independent of comorbidities. We examined early changes in metabolism and transcription to gain mechanistic insight into HFpEF development. Male short-hair kittens (2mo old) underwent aortic banding or sham operation. Cardiac function was assessed at baseline and 1mo post-banding prior to tissue collection and downstream analyses. Following banding, we observed significant cardiac hypertrophy and initiation of LV fibrosis in the absence of changes in cardiac function. We observed LV mitochondrial dysfunction, indicated by impaired complex-I and -II respiration prompting the examination of cardiac metabolism by unbiased metabolomics. 82 metabolites were significantly different (≥ 1.25 fold, p ≤ 0.1) between 1mo banded and sham hearts, with an overrepresentation of amino acid (aa) and lipid species. Pathway enrichment analysis highlighted an increase in aa metabolism (e.g. serine, proline) that is associated with ECM remodeling and tissue fibrosis. Additionally, an increase in lipid species (i.e. acyl-carnitines) suggests reduced fatty acid utilization and a shift towards glycolysis. Correlations of metabolomics data with mitochondrial function and cardiac phenotyping revealed strong associations between mitochondrial function and the cardiac energy state, as well as aa and LV fibrosis. RNA-seq and enrichment analyses revealed a significant inflammatory response early in disease progression and a decrease in protein/histone acetylation. Collectively, this systems-based approach provides new insights into the cellular biology underlying HFpEF-like disease progression. The metabolic and transcriptional signature that precede the clinical features of HFpEF, will provide new pre-clinical research directions and may yield novel therapeutic targets.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.142.suppl_3.16434
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 1466401-X
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  • 10
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    Abstract 157: Unique Features of Cortical Bone Stem Cells Associated With Enhanced Cardiac Repair
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation Research Vol. 117, No. suppl_1 ( 2015-07-17)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 117, No. suppl_1 ( 2015-07-17)
    Abstract: Rationale: Adoptive transfer of bone marrow and cardiac derived stem cells (CDCs) into failing human hearts has been shown to be safe, yet these cells have only induced modest improvements after myocardial infarction (MI). Recently we have shown in a mouse model that cortical bone derived stem cells (CBSCs) induced a greater enhancement of cardiac function after MI through enhanced paracrine signaling and transdifferentiation of CBSCs into new cardiac tissue. However, the reparative potential of CBSCs relative to other stem cell types including bone marrow derived mesenchymal stem cells (MSCs) and CDCs is not known. Objective: To characterize surface marker expression, proliferation, survival, migration and differentiation capacity of swine CBSCs relative to MSCs and CDCs. Methods and Results: CBSCs, MSCs and CDCs were isolated from Gottingen miniswine. CBSCs were morphologically distinct from MSCs and CDCs, with differences in length to width ratio and overall cell surface area. Cell surface marker profiling using RT-PCR analysis revealed that CBSCs express some of the classical MSC markers such as CD106, CD271, CD105, CD90 and CD29 and are negative for CD45 and CD11-b. CBSCs had an enhanced proliferation capacity versus CDCs and MSCs, measured by CyQuant assay. Concurrently CBSCs had significantly decreased population-doubling time (3.57 and 1.26 fold decrease) as compared to MSC and CDCs. CBSCs exhibit enhanced survival after exposure to apoptotic stimuli as compared to MSCs measured by Annexin-V staining. A significantly greater % of CBSCs expressed markers of cardiac lineage commitment when exposed to dexamethasone than did CDCs or MSCs. Markers of cardiac lineages including GATA-4, α SMA, Troponin T, sm22 were measured with RT-PCR and immunocytochemistry. Conclusion: CBSCs have enhanced proliferative, survival capacity and cardiac lineage commitment versus CDCs and MSCs that could account for their enhanced effects on cardiac regeneration after myocardial infarction.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.117.suppl_1.157
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1467838-X
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