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  • 1
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    Online Resource
    Abstract 11: The Role of Human Osteopontin Isoforms in Post-Ischemic Neovascularization
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 36, No. suppl_1 ( 2016-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2016-05)
    Abstract: Coronary and peripheral artery diseases lead to ischemia, initiating processes that promote neovascularization to restore blood flow and preserve tissue function. We demonstrated previously that osteopontin (OPN), a matricellular cytokine, is critical to ischemia-induced neovascularization. Unlike rodents, humans express 3 OPN isoforms (a, b, and c); however, the roles of these isoforms in neovascularization and cell migration remain undefined. To assess how human OPN isoforms affect neovascularization, OPN -/- mice underwent hind limb ischemia surgery. At the time of surgery, 1.5x10 6 lentivirus particles expressing human OPNa, OPNb or OPNc were delivered by intramuscular injection. While OPNa improved limb perfusion 30.4%±0.8 in OPN -/- mice, OPNc improved perfusion by 70.9%±6.3 (d14; p 〈 0.001 vs. LVGFP), as measured by laser Doppler perfusion imaging. Importantly, both OPNa and OPNc isoforms significantly rescued neovascularization better than OPNb (n=6, p 〈 0.05). Isoform effects on vascular volume, density, connectivity and diameter were further assessed using Micro-CT angiograms. OPNa and OPNc rescued limb function compared to control and OPNb treated animals (61.1%±8.2; 76.2%±9.7; p 〈 0.05), as assessed by voluntary running wheel use. To verify the differences in neovascularization were due to divergent effects on receptor binding and/or signaling and not variations in isoform expression, we confirmed similar OPN isoform expression levels by ELISA (n=6, p=ns) and immunofluorescence. OPN isoforms a and c both increased macrophage infiltration 2.5 fold, as assessed by mRNA (d7; p 〈 0.05) and histology, leading to increases in vascular smooth muscle cell (VSMC) infiltration (d7; p 〈 0.05). Several pro-arteriogenic factors were also significantly increased at the mRNA level. Finally, we confirmed in vitro that OPNa and OPNc significantly increased VSMC migration compared to OPN b and control (49.8%±3.1; 75.2%±6.3; p 〈 0.05). In conclusion, human OPN isoforms may exhert divergent effects on neovascularization through varried effects on macrophage and VSMC recruitment. Human OPN isoforms may represent potential new therapeutic targets to promote neovascularization and preserve function in patients with peripheral artery disease.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.36.suppl_1.11
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1494427-3
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  • 2
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    Increasing nitric oxide bioavailability fails to improve collateral vessel formation in humanized sickle cell mice
    Elsevier BV ; 2022
    In:  Laboratory Investigation Vol. 102, No. 8 ( 2022-08), p. 805-813
    Details
    In: Laboratory Investigation, Elsevier BV, Vol. 102, No. 8 ( 2022-08), p. 805-813
    Type of Medium: Online Resource
    ISSN: 0023-6837
    URL: Article
    DOI: 10.1038/s41374-022-00780-0
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 2041329-4
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  • 3
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    Abstract 317: Paracrine Effects of Satellite Cells on Collateral Vessel Formation
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 36, No. suppl_1 ( 2016-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2016-05)
    Abstract: Peripheral artery disease is a major health problem in the United States that effects 8.5 million people and can lead to limb pain, decreased mobility, and in severe cases amputation. The ability to form a robust collateral network to restore blood flow and prevent ischemia leads to a better prognosis and restoration of function. The growth of collaterals is a complex process that involves recruitment of various cell types including smooth muscle cells, endothelial cells, and macrophages. Migration and proliferation of these cells are processes regulated by numerous cytokine and paracrine signals. We hypothesize that an important and novel source of these signals is satellite cells. Satellite cells are myogenic progenitor cells that lie below the basal lamina of muscle fibers. In healthy muscle, the cells are quiescent but in response to injury, such as ischemia, they become activated and proliferate. We hypothesized that activated satellite cells produce factors that will influence critical cells for vessel formation in addition to differentiating to repair muscle. To study the paracrine effects of satellite cells on vascular smooth muscle cells, we used a co-culture system with freshly isolated satellite cells from the ischemic leg as the stimulus. We found that satellite cells significantly increased smooth muscle migration 2.5 fold compared to media alone using a modified Boyden chamber assay. BrdU staining to assess proliferation showed modest increases in smooth muscle proliferation (1.3 fold change, p 〈 0.01). Finally, to investigate these paracrine effects in vivo, we delivered alginate encapsulated satellite cells to mice following the hind limb ischemia procedure, which is a model of collateral growth. We found that mice that received the encapsulated satellite cells had significantly improved perfusion as measured by Laser Doppler imaging at day 14 post surgery when compared to empty capsules (perfusion ratio of 0.87 ± 0.04 (cells) vs 0.68 ± 0.07 (empty capsules), p 〈 0.05). This result demonstrates that satellite cells can positively influence collateral growth in vivo. We believe that satellite cells play a critical role in collateral vessel formation and may potentially be a therapeutic strategy for the treatment of peripheral artery disease.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.36.suppl_1.317
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1494427-3
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  • 4
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    Overexpression of Catalase in Myeloid Cells Causes Impaired Postischemic Neovascularization
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 31, No. 10 ( 2011-10), p. 2203-2209
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 10 ( 2011-10), p. 2203-2209
    Abstract: Myeloid lineage cells (MLCs) such as macrophages are known to play a key role in postischemic neovascularization. However, the role of MLC-derived reactive oxygen species in this process and their specific chemical identity remain unknown. Methods and Results— Transgenic mice with MLC-specific overexpression of catalase (Tg Cat-MLC mice) were created on a C57BL/6 background. Macrophage catalase activity was increased 3.4-fold compared with wild-type mice. After femoral artery ligation, laser Doppler perfusion imaging revealed impaired perfusion recovery in Tg Cat-MLC mice. This was associated with fewer collateral vessels, as assessed by microcomputed tomography angiography, and decreased capillary density. Impaired functional recovery of the ischemic limb was also evidenced by a 50% reduction in spontaneous running activity. The deficient neovascularization was associated with a blunted inflammatory response, characterized by decreased macrophage infiltration of ischemic tissues, and lower mRNA levels of inflammatory markers, such as tumor necrosis factor-α, osteopontin, and matrix mettaloproteinase-9. In vitro macrophage migration was impaired in Tg Cat-MLC mice, suggesting a role for H 2 O 2 in regulating the ability of macrophages to infiltrate ischemic tissues. Conclusion— MLC-derived H 2 O 2 plays a key role in promoting neovascularization in response to ischemia and is a necessary factor for the development of ischemia-induced inflammation.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.111.233247
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
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  • 5
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    Overexpression of Catalase in Vascular Smooth Muscle Cells Prevents the Formation of Abdominal Aortic Aneurysms
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 33, No. 10 ( 2013-10), p. 2389-2396
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 10 ( 2013-10), p. 2389-2396
    Abstract: Elevated levels of oxidative stress have been reported in abdominal aortic aneurysms (AAA), but which reactive oxygen species promotes the development of AAA remains unclear. Here, we investigate the effect of hydrogen peroxide (H 2 O 2 )–degrading enzyme catalase on the formation of AAA. Approach and Results— AAA were induced with the application of calcium chloride (CaCl 2 ) on mouse infrarenal aortas. The administration of PEG-catalase, but not saline, attenuated the loss of tunica media and protected against AAA formation (0.91±0.1 versus 0.76±0.09 mm). Similarly, in a transgenic mouse model, catalase overexpression in the vascular smooth muscle cells preserved the thickness of tunica media and inhibited aortic dilatation by 50% (0.85±0.14 versus 0.57±0.08 mm). Further studies showed that injury with CaCl 2 decreased catalase expression and activity in the aortic wall. Pharmacological administration or genetic overexpression of catalase restored catalase activity and subsequently decreased matrix metalloproteinase activity. In addition, a profound reduction in inflammatory markers and vascular smooth muscle cell apoptosis was evident in aortas of catalase-overexpressing mice. Interestingly, as opposed to infusion of PEG-catalase, chronic overexpression of catalase in vascular smooth muscle cells did not alter the total aortic H 2 O 2 levels. Conclusions— The data suggest that a reduction in aortic wall catalase activity can predispose to AAA formation. Restoration of catalase activity in the vascular wall enhances aortic vascular smooth muscle cell survival and prevents AAA formation primarily through modulation of matrix metalloproteinase activity.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.113.302175
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 1494427-3
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  • 6
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    Abstract 649: Skeletal Muscle Satellite Cells Play a Role in Regulating Angiogenesis and Arteriogenesis
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 38, No. Suppl_1 ( 2018-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 38, No. Suppl_1 ( 2018-05)
    Abstract: Satellite cells are myogenic stem cells that play a critical role in skeletal muscle repair by proliferating and differentiating into myoblasts to repair muscle fibers. However, their role in reestablishing vascular supply following injury is not well defined. We hypothesized that satellite cells promote vascular growth through paracrine signaling induced following muscle injury or ischemic damage from diseases such as peripheral artery disease. We used a murine model of hind limb ischemia and found that satellite cells increased 3.4 fold (p 〈 0.01) in response to this ischemic insult. We used a co-culture system to determine that satellite cells led to a 3.5 fold and 2.8 fold increase in smooth muscle and endothelial cell migration (p 〈 0.0001). These results demonstrate the satellite cells produce paracrine factors which drive cell migration required for both angiogenesis and arteriogenesis. To test the potential therapeutic capability, alginate encapsulated satellite cells were delivered in the hind limb ischemic model. We found the encapsulated cells were viable for up to 2 weeks and mice that received satellite cells had significantly increased perfusion (28%, p 〈 0.05) at 2 weeks as measured by Laser Doppler imaging and a 1.9 fold (p 〈 0.5) increase in capillaries and small vessels measured by histological staining. To examine the role of satellite cells in a physiological setting and determine if they are critical to robust recovery in our model, we used a Cre-Lox system in which recombination results in the production of diphtheria toxin a (DTA) to deplete Pax7 specific cells. Mice which lacked satellite cells had decreased perfusion by Laser Doppler imaging (p 〈 0.05) and capillary density compared animals with intact satellite cells. A cytokine array and genomics analysis show that several factors related to angiogenesis and cell migration are upregulated in satellite cells in response to ischemia. In conclusion, we have found that satellite cells proliferate in response to ischemia, produce factors that drive cell migration, and their delivery or depletion affect vascular growth in vitro. We believe that our studies show that satellite cells play an important role vascular growth and are a novel potential therapy for peripheral artery disease.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.38.suppl_1.649
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
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  • 7
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    Abstract 398: Hydrogen Peroxide Mediates Calcium Chloride--Induced Aortic Wall Dilatation
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 32, No. suppl_1 ( 2012-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 32, No. suppl_1 ( 2012-05)
    Abstract: Rationale: Abdominal aneurysm formation is characterized by infiltration of the aortic wall with inflammatory cells, activation of proteolytic enzymes, loss of vascular smooth muscle cells (VSMC), and neovascularization. It is also known that hydrogen peroxide (H 2 O 2 ) plays an important role in these processes. Hypothesis: Since H 2 O 2 participates in the pathophysiologic processes that govern aneurysmal dilatation, we hypothesized that scavenging of H 2 O 2 with catalase protects against the formation of aortic aneurysms. Methods: To assess our hypothesis 3 groups of mice, all 8-10-week-old males on the C57BL6 background, were used. Aortic dilatation was induced with the application of CaCl 2 on the infrarenal aortas. We compared the aortic dilation in mice that specifically over-express catalase in the VSMC (group 1) or in the myeloid cell lineage (MCL) (group 2) with their wild type littermates. Chemical injury with CaCl 2 was also induced in wild type mice which were treated with continuous intravenous infusion of PEG-catalase or saline for 8 weeks (group 3). The aortic diameter was measured with a caliper and with videomicroscopy on the day of surgery and 8 weeks later. H 2 O 2 levels were quantified with the Amplex Red assay. Results: Application of CaCl 2 resulted in a significant increase in H 2 O 2 generation in the infrarenal aortas compared to saline controls, which peaked on post-operative day 10 (0.60±0.09 vs. 0.37±0.05 μM/aortic ring, n=3/grp, p=0.02). Compared to their wild type littermates, mice that over-express catalase in the VSMC had negligible dilation of the aorta (0.78±0.05 vs. 0.53±0.02 mm, n=7/grp, p=0.001). Similarly, over-expression of catalase in MCL protected against aortic dilation (0.76±0.02 vs. ±0.005 mm, n=7, p 〈 0.0001). Corroborating the above findings, continuous intravenous infusion of PEG-catalase, but not saline, protected from CaCl 2 induced aortic dilation (0.73±0.03 vs.0.56±0.02 mm, n=3-6/grp, p=0.007). Conclusions: Our data suggest that H 2 O 2 is essential in CaCl 2 induced aortic aneurysm formation.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.32.suppl_1.A398
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 8
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    Satellite Cell Expression of RAGE (Receptor for Advanced Glycation end Products) Is Important for Collateral Vessel Formation
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Journal of the American Heart Association Vol. 10, No. 21 ( 2021-11-02)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 10, No. 21 ( 2021-11-02)
    Abstract: The growth and remodeling of vascular networks is an important component of the prognosis for patients with peripheral artery disease. One protein that has been previously implicated to play a role in this process is RAGE (receptor for advanced glycation end products). This study sought to determine the cellular source of RAGE in the ischemic hind limb and the role of RAGE signaling in this cell type. Methods and Results Using a hind limb ischemia model of vascular growth, this study found skeletal muscle satellite cells to be a novel major cellular source of RAGE in ischemic tissue by both staining and cellular sorting. Although wild‐type satellite cells increased tumor necrosis factor‐α and monocyte chemoattractant protein‐1 production in response to ischemia in vivo and a RAGE ligand in vitro, satellite cells from RAGE knockout mice lacked the increase in cytokine production both in vivo in response to ischemia and in vitro after stimuli with the RAGE ligand high‐mobility group box 1. Furthermore, encapsulated wild‐type satellite cells improved perfusion after hind limb ischemia surgery by both perfusion staining and vessel quantification, but RAGE knockout satellite cells provided no improvement over empty capsules. Conclusions Thus, RAGE expression and signaling in satellite cells is crucial for their response to stimuli and angiogenic and arteriogenic functions.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.120.022127
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2653953-6
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  • 9
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    Mechanical Strain induced Osteopontin Expression in the Aorta (LB45)
    Wiley ; 2014
    In:  The FASEB Journal Vol. 28, No. S1 ( 2014-04)
    Details
    In: The FASEB Journal, Wiley, Vol. 28, No. S1 ( 2014-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v28.S1
    DOI: 10.1096/fasebj.28.1_supplement.lb45
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 10
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    Alginate microencapsulation of human mesenchymal stem cells as a strategy to enhance paracrine-mediated vascular recovery after hindlimb ischaemia : Encapsulated human MSCs enhance revascularization
    Hindawi Limited ; 2016
    In:  Journal of Tissue Engineering and Regenerative Medicine Vol. 10, No. 3 ( 2016-03), p. 222-232
    Details
    In: Journal of Tissue Engineering and Regenerative Medicine, Hindawi Limited, Vol. 10, No. 3 ( 2016-03), p. 222-232
    Type of Medium: Online Resource
    ISSN: 1932-6254
    URL: Issue
    URL: Article
    DOI: 10.1002/term.v10.3
    DOI: 10.1002/term.1680
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2016
    detail.hit.zdb_id: 2316155-3
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