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  • 1
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    Online Resource
    Abstract MP29: Skeletal Muscle Satellite Cells Enhance Vascular Growth Through Paracrine Signaling
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 41, No. Suppl_1 ( 2021-09)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 41, No. Suppl_1 ( 2021-09)
    Abstract: Peripheral arterial disease (PAD) is a major health problem that affects over 200 million people worldwide. Decreased blood flow to the limb muscles leads to ischemia that results in pain, decreased quality of life, and in severe cases amputation. Despite the prevalence and severity of the disease, effective treatment options are still limited. One factor correlated with improved prognosis is the generation of a more robust collateral vessel network. This study hypothesized that skeletal muscle satellite cells, which play a key role in skeletal muscle regeneration, also contribute to vascular regeneration in the setting of ischemia. Specifically, satellite cells are proposed to generate cytokine and growth factors which modulate vascular growth via paracrine signaling. Satellite cells were isolated and cultured for vasculogenic assays include migration co-cultures. Satellite cells encapsulated in alginate were delivered to a hindlimb ischemia model of vascular growth to assess their therapeutic potential in vivo. Gene expression of satellite cells from ischemic tissue was assessed using a microarray. The migration assays demonstrated that satellite cells produce chemokines which increased smooth muscle migration (3.5 fold) and endothelial cell migration (2.8 fold) over control conditions (n = 4, p 〈 0.05) In the hind limb ischemia model, alginate encapsulated satellite cells increased perfusion 17% closer to baseline (68% vs 51%, n = 11, p 〈 0.05) measured via Laser Doppler imaging. Capillary density as measured by Lectin staining increased 1.6 fold and smooth muscle positive vessels increase more than 2 fold (n=6, p 〈 0.05). Finally, Ingenuity pathway analysis of the gene array day suggested that vasculogenic and cell migration pathways were increased. Taken together, these findings demonstrate that satellite cells produce a number of factors that can serve as chemokines in vitro and increase vascular growth in vivo. Further work will explore the mechanisms by which satellite cells exhibit their effects and develop a therapeutic application of satellite cells as a novel treatment for patients with peripheral artery disease.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.41.suppl_1.MP29
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1494427-3
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  • 2
    Online Resource
    Online Resource
    Endothelial Poldip2 regulates sepsis-induced lung injury via Rho pathway activation
    Oxford University Press (OUP) ; 2022
    In:  Cardiovascular Research Vol. 118, No. 11 ( 2022-08-24), p. 2506-2518
    Details
    In: Cardiovascular Research, Oxford University Press (OUP), Vol. 118, No. 11 ( 2022-08-24), p. 2506-2518
    Abstract: Sepsis-induced lung injury is associated with significant morbidity and mortality. Previously, we showed that heterozygous deletion of polymerase δ-interacting protein 2 (Poldip2) was protective against sepsis-induced lung injury. Since endothelial barrier disruption is thought to be the main mechanism of sepsis-induced lung injury, we sought to determine if the observed protection was specifically due to the effect of reduced endothelial Poldip2. Methods and results Endothelial-specific Poldip2 knock-out mice (EC−/−) and their wild-type littermates (EC+/+) were injected with saline or lipopolysaccharide (18 mg/kg) to model sepsis-induced lung injury. At 18 h post-injection mice, were euthanized and bronchoalveolar lavage (BAL) fluid and lung tissue were collected to assess leucocyte infiltration. Poldip2 EC−/− mice showed reduced lung leucocyte infiltration in BAL (0.21 ± 0.9×106 vs. 1.29 ± 1.8×106 cells/mL) and lung tissue (12.7 ± 1.8 vs. 23 ± 3.7% neutrophils of total number of cells) compared to Poldip2 EC+/+ mice. qPCR analysis of the lung tissue revealed a significantly dampened induction of inflammatory gene expression (TNFα 2.23 ± 0.39 vs. 4.15 ± 0.5-fold, IκBα 4.32 ± 1.53 vs. 8.97 ± 1.59-fold), neutrophil chemoattractant gene expression (CXCL1 68.8 ± 29.6 vs. 147 ± 25.7-fold, CXCL2 65 ± 25.6 vs. 215 ± 27.3-fold) and a marker of endothelial activation (VCAM1 1.25 ± 0.25 vs. 3.8 ± 0.38-fold) in Poldip2 EC−/− compared to Poldip2 EC+/+ lungs. An in vitro model using human pulmonary microvascular endothelial cells was used to assess the effect of Poldip2 knock-down on endothelial activation and permeability. TNFα-induced endothelial permeability and VE-cadherin disruption were significantly reduced with siRNA-mediated knock-down of Poldip2 (5 ± 0.5 vs. 17.5 ± 3-fold for permeability, 1.5 ± 0.4 vs. 10.9 ± 1.3-fold for proportion of disrupted VE-cadherin). Poldip2 knock-down altered expression of Rho-GTPase-related genes, which correlated with reduced RhoA activation by TNFα (0.94 ± 0.05 vs. 1.29 ± 0.01 of relative RhoA activity) accompanied by redistribution of active-RhoA staining to the centre of the cell. Conclusion Poldip2 is a potent regulator of endothelial dysfunction during sepsis-induced lung injury, and its endothelium-specific inhibition may provide clinical benefit.
    Type of Medium: Online Resource
    ISSN: 0008-6363 , 1755-3245
    URL: Article
    DOI: 10.1093/cvr/cvab295
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1499917-1
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  • 3
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    Online Resource
    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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  • 4
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    Online Resource
    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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  • 5
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    Online Resource
    TRANSFORMING TRANSPORTATION
    Mallikarjuna Infosys ; 2023
    In:  international journal of engineering technology and management sciences Vol. 7, No. 4 ( 2023), p. 399-409
    Details
    In: international journal of engineering technology and management sciences, Mallikarjuna Infosys, Vol. 7, No. 4 ( 2023), p. 399-409
    Abstract: The world of transportation is changing. Due to increasing mobility demand, challenges like financing, dealing with emissions and volatile oil prices are going up. Decision-makers in the areas of policy and planning have to address these challenges and have try to develop a transportation system capable of meeting the future needs of society and the economy. This paper shows the results of future-oriented research. We first investigate a distributed dynamic computation offloading model for multi-access edge computing (MEC) enabled CITS under a heterogeneous road network, in which the multiple and heterogeneous computing power sources cooperatively provide computation offloading services for vehicles then to ensure smooth transmission of the overwhelming amounts of data, existing wireless transmission technologies have become increasingly insufficient. 5G, which succeeds 4G (LTE, WiMAX) and 3G (UMTS) and promises data rates of 20 Gbps, can help in this regard and Vehicular ad-hoc networks (VANETs) are the specific sort of ad-hoc networks that are utilized in intelligent transportation systems (ITS). VANETs have become one of the most reassuring, promising, and quickest developing subsets of the mobile ad-hoc networks (MANETs). They include smart vehicles, roadside units (RSUs), and on-board units (OBUs) which correspond through inconsistent wireless network. In this study we discuss and elaborate the challenges, along with the applications, and the future directions of transforming transportation using embracing the potential of 5G, Heterogeneous Networks, and Software Defined Networking in Intelligent Transportation Systems. At the end we provide the conclusion of the whole study.
    Type of Medium: Online Resource
    ISSN: 2581-4621
    URL: Issue
    URL: Journal
    URL: Article
    DOI: 10.46647/ijetms.2023.v07i04
    DOI: 10.46647/ijetms
    DOI: 10.46647/ijetms.2023.v07i04.054
    Language: English
    Publisher: Mallikarjuna Infosys
    Publication Date: 2023
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  • 6
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    Accelerated atherosclerosis in beta-thalassemia
    American Physiological Society ; 2023
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 325, No. 5 ( 2023-11-01), p. H1133-H1143
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 325, No. 5 ( 2023-11-01), p. H1133-H1143
    Abstract: Children with beta-thalassemia (BT) present with an increase in carotid intima-medial thickness, an early sign suggestive of premature atherosclerosis. However, it is unknown if there is a direct relationship between BT and atherosclerotic disease. To evaluate this, wild-type (WT, littermates) and BT (Hbb th3/+ ) mice, both male and female, were placed on a 3-mo high-fat diet with low-density lipoprotein receptor suppression via overexpression of proprotein convertase subtilisin/kexin type 9 (PCSK9) gain-of-function mutation (D377Y). Mechanistically, we hypothesize that heme-mediated oxidative stress creates a proatherogenic environment in BT because BT is a hemolytic anemia that has increased free heme and exhausted hemopexin, heme’s endogenous scavenger, in the vasculature. We evaluated the effect of hemopexin (HPX) therapy, mediated via an adeno-associated virus, to the progression of atherosclerosis in BT and a phenylhydrazine-induced model of intravascular hemolysis. In addition, we evaluated the effect of deferiprone (DFP)-mediated iron chelation in the progression of atherosclerosis in BT mice. Aortic en face and aortic root lesion area analysis revealed elevated plaque accumulation in both male and female BT mice compared with WT mice. Hemopexin therapy was able to decrease plaque accumulation in both BT mice and mice on our phenylhydrazine (PHZ)-induced model of hemolysis. DFP decreased atherosclerosis in BT mice but did not provide an additive benefit to HPX therapy. Our data demonstrate for the first time that the underlying pathophysiology of BT leads to accelerated atherosclerosis and shows that heme contributes to atherosclerotic plaque development in BT. NEW & NOTEWORTHY This work definitively shows for the first time that beta-thalassemia leads to accelerated atherosclerosis. We demonstrated that intravascular hemolysis is a prominent feature in beta-thalassemia and the resulting increases in free heme are mechanistically relevant. Adeno-associated virus (AAV)-hemopexin therapy led to decreased free heme and atherosclerotic plaque area in both beta-thalassemia and phenylhydrazine-treated mice. Deferiprone-mediated iron chelation led to deceased plaque accumulation in beta-thalassemia mice but provided no additive benefit to hemopexin therapy.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00306.2023
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 7
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    Online Resource
    Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis
    Wiley ; 2023
    In:  FASEB BioAdvances Vol. 5, No. 5 ( 2023-05), p. 199-210
    Details
    In: FASEB BioAdvances, Wiley, Vol. 5, No. 5 ( 2023-05), p. 199-210
    Abstract: The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice ( n  = 4, p   〈  0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression ( n  = 8–10, p   〈  0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n  = 5, p   〈  0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n  = 7–10, p   〈  0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression ( n  = 7–8, p   〈  0.05) concomitant to an increase in superoxide (2‐fold, n  = 4, p   〈  0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine.
    Type of Medium: Online Resource
    ISSN: 2573-9832 , 2573-9832
    URL: Article
    DOI: 10.1096/fba.2022-00121
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2969880-7
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