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  1. Article: A Reappraisal of the Utility of L-012 to Measure Superoxide from Biologically Relevant Sources.

    Haigh, Stephen / Brown, Zach L / Shivers, Mitch A / Sellers, Hunter G / West, Madison A / Barman, Scott A / Stepp, David W / Csanyi, Gabor / Fulton, David J R

    Antioxidants (Basel, Switzerland)

    2023  Volume 12, Issue 9

    Abstract: The detection of superoxide anion ( ... ...

    Abstract The detection of superoxide anion (O
    Language English
    Publishing date 2023-08-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox12091689
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Galectin-3 Mediates Vascular Dysfunction in Obesity by Regulating NADPH Oxidase 1.

    Padgett, Caleb A / Bátori, Róbert K / Speese, Andrew C / Rosewater, Cody L / Bush, Weston B / Derella, Cassandra C / Haigh, Stephen B / Sellers, Hunter G / Corley, Zachary L / West, Madison A / Mintz, James D / Ange, Brittany B / Harris, Ryan A / Brands, Michael W / Fulton, David J R / Stepp, David W

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Rationale: Obesity increases the risk of cardiovascular disease (CVD) through mechanisms that remain incompletely defined. Metabolic dysfunction, especially hyperglycemia, is thought to be a major contributor but how glucose impacts vascular function is ...

    Abstract Rationale: Obesity increases the risk of cardiovascular disease (CVD) through mechanisms that remain incompletely defined. Metabolic dysfunction, especially hyperglycemia, is thought to be a major contributor but how glucose impacts vascular function is unclear. Galectin-3 (GAL3) is a sugar binding lectin upregulated by hyperglycemia but its role as a causative mechanism of CVD remains poorly understood.
    Objective: To determine the role of GAL3 in regulating microvascular endothelial vasodilation in obesity.
    Methods and results: GAL3 was markedly increased in the plasma of overweight and obese patients, as well as in the microvascular endothelium of diabetic patients. To investigate a role for GAL3 in CVD, mice deficient in GAL3 were bred with obese
    Conclusions: Deletion of GAL3 normalizes microvascular endothelial function in obese
    Language English
    Publishing date 2023-04-21
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.04.19.537592
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Galectin-3 Mediates Vascular Dysfunction in Obesity by Regulating NADPH Oxidase 1.

    Padgett, Caleb A / Bátori, Róbert K / Speese, Andrew C / Rosewater, Cody L / Bush, Weston B / Derella, Cassandra C / Haigh, Stephen B / Sellers, Hunter G / Corley, Zachary L / West, Madison A / Mintz, James D / Ange, Brittany B / Harris, Ryan A / Brands, Michael W / Fulton, David J R / Stepp, David W

    Arteriosclerosis, thrombosis, and vascular biology

    2023  Volume 43, Issue 10, Page(s) e381–e395

    Abstract: Background: Obesity is associated with increased risk of cardiovascular disease, but underlying mechanisms remain elusive. Metabolic dysfunction, especially hyperglycemia, is thought to be a major contributor, but how glucose impacts vascular function ... ...

    Abstract Background: Obesity is associated with increased risk of cardiovascular disease, but underlying mechanisms remain elusive. Metabolic dysfunction, especially hyperglycemia, is thought to be a major contributor, but how glucose impacts vascular function is unclear. GAL3 (galectin-3) is a sugar-binding lectin upregulated by hyperglycemia, but its role as a causative mechanism of cardiovascular disease remains poorly understood. Therefore, the objective of this study was to determine the role of GAL3 in regulating microvascular endothelial vasodilation in obesity.
    Methods: GAL3 was measured and found to be markedly increased in the plasma of overweight and obese patients, as well as in the microvascular endothelium of diabetic patients. To investigate causative mechanisms in cardiovascular disease, mice deficient in GAL3 were bred with obese
    Results: Deletion of GAL3 did not alter body mass, adiposity, or plasma indices of glycemia and lipidemia, but levels of plasma reactive oxygen species as assessed by plasma thiobarbituric acid reactive substances were normalized in obese GAL3 knockout mice. Obese mice exhibited profound endothelial dysfunction and hypertension, both of which were rescued by GAL3 deletion. Isolated microvascular endothelial cells from obese mice had increased expression of NOX1 (nicotinamide adenine dinucleotide phosphate oxidase 1), which we have previously shown to contribute to increased oxidative stress and endothelial dysfunction, which was normalized in microvascular endothelium from mice lacking GAL3. Cell-specific deletion confirmed that endothelial GAL3 regulates obesity-induced NOX1 overexpression and subsequent microvascular function. Furthermore, improvement of metabolic syndrome by increasing muscle mass, improving insulin signaling, or treating with metformin decreased microvascular GAL3, and thereby NOX1, expression levels.
    Conclusions: Deletion of GAL3 normalizes microvascular endothelial function in obese
    MeSH term(s) Animals ; Humans ; Mice ; Cardiovascular Diseases ; Endothelial Cells/metabolism ; Endothelium, Vascular/metabolism ; Galectin 3/genetics ; Galectin 3/metabolism ; Hyperglycemia/metabolism ; Hypertension ; Mice, Knockout ; Mice, Obese ; NADPH Oxidase 1/metabolism ; NADPH Oxidases/metabolism ; Obesity/complications ; Obesity/genetics ; Obesity/metabolism ; Oxidative Stress
    Chemical Substances Galectin 3 ; NADPH Oxidase 1 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; NOX1 protein, mouse (EC 1.6.3.-)
    Language English
    Publishing date 2023-08-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.123.319476
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1705: 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: Early Endothelial Dysfunction in a Novel Model of Sustained Hyperphagia and Obesity in Mice Using a Brain Targeting Adeno-Associated Virus.

    Sellers, Hunter G / Padgett, Caleb A / Mintz, James D / Speese, Andrew C / Brown, Zachary L / Haigh, Stephen / Sword, Jeremy / Rosewater, Cody L / Shivers, Mitchell A / Barris, Candee T / Kirov, Sergei A / Weintraub, Neal L / Belin de Chantemele, Eric J / Stepp, David W / Fulton, David J R

    Arteriosclerosis, thrombosis, and vascular biology

    2023  Volume 43, Issue 8, Page(s) 1592–1594

    MeSH term(s) Mice ; Animals ; Dependovirus/genetics ; Obesity/genetics ; Hyperphagia/genetics ; Brain ; Vascular Diseases
    Language English
    Publishing date 2023-05-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.122.318658
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1705: 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: Obesity Induces Disruption of Microvascular Endothelial Circadian Rhythm.

    Padgett, Caleb A / Butcher, Joshua T / Haigh, Steven B / Speese, Andrew C / Corley, Zachary L / Rosewater, Cody L / Sellers, Hunter G / Larion, Sebastian / Mintz, James D / Fulton, David J R / Stepp, David W

    Frontiers in physiology

    2022  Volume 13, Page(s) 887559

    Abstract: Obese individuals are at significantly elevated risk of developing cardiovascular disease (CVD). Additionally, obesity has been associated with disrupted circadian rhythm, manifesting in abnormal sleeping and feeding patterns. To date, the mechanisms ... ...

    Abstract Obese individuals are at significantly elevated risk of developing cardiovascular disease (CVD). Additionally, obesity has been associated with disrupted circadian rhythm, manifesting in abnormal sleeping and feeding patterns. To date, the mechanisms linking obesity, circadian disruption, and CVD are incompletely understood, and insight into novel mechanistic pathways is desperately needed to improve therapeutic potential and decrease morbidity and mortality. The objective of this study was to investigate the roles of metabolic and circadian disruptions in obesity and assess their contributions in promoting vascular disease. Lean (
    Language English
    Publishing date 2022-05-05
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2022.887559
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  6. Article ; Online: Purine synthesis suppression reduces the development and progression of pulmonary hypertension in rodent models.

    Ma, Qian / Yang, Qiuhua / Xu, Jiean / Sellers, Hunter G / Brown, Zach L / Liu, Zhiping / Bordan, Zsuzsanna / Shi, Xiaofan / Zhao, Dingwei / Cai, Yongfeng / Pareek, Vidhi / Zhang, Chunxiang / Wu, Guangyu / Dong, Zheng / Verin, Alexander D / Gan, Lin / Du, Quansheng / Benkovic, Stephen J / Xu, Suowen /
    Asara, John M / Ben-Sahra, Issam / Barman, Scott / Su, Yunchao / Fulton, David J R / Huo, Yuqing

    European heart journal

    2023  Volume 44, Issue 14, Page(s) 1265–1279

    Abstract: Aims: Proliferation of vascular smooth muscle cells (VSMCs) is a hallmark of pulmonary hypertension (PH). Proliferative cells utilize purine bases from the de novo purine synthesis (DNPS) pathways for nucleotide synthesis; however, it is unclear whether ...

    Abstract Aims: Proliferation of vascular smooth muscle cells (VSMCs) is a hallmark of pulmonary hypertension (PH). Proliferative cells utilize purine bases from the de novo purine synthesis (DNPS) pathways for nucleotide synthesis; however, it is unclear whether DNPS plays a critical role in VSMC proliferation during development of PH. The last two steps of DNPS are catalysed by the enzyme 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/inosine monophosphate cyclohydrolase (ATIC). This study investigated whether ATIC-driven DNPS affects the proliferation of pulmonary artery smooth muscle cells (PASMCs) and the development of PH.
    Methods and results: Metabolites of DNPS in proliferative PASMCs were measured by liquid chromatography-tandem mass spectrometry. ATIC expression was assessed in platelet-derived growth factor-treated PASMCs and in the lungs of PH rodents and patients with pulmonary arterial hypertension. Mice with global and VSMC-specific knockout of Atic were utilized to investigate the role of ATIC in both hypoxia- and lung interleukin-6/hypoxia-induced murine PH. ATIC-mediated DNPS at the mRNA, protein, and enzymatic activity levels were increased in platelet-derived growth factor-treated PASMCs or PASMCs from PH rodents and patients with pulmonary arterial hypertension. In cultured PASMCs, ATIC knockdown decreased DNPS and nucleic acid DNA/RNA synthesis, and reduced cell proliferation. Global or VSMC-specific knockout of Atic attenuated vascular remodelling and inhibited the development and progression of both hypoxia- and lung IL-6/hypoxia-induced PH in mice.
    Conclusion: Targeting ATIC-mediated DNPS compromises the availability of purine nucleotides for incorporation into DNA/RNA, reducing PASMC proliferation and pulmonary vascular remodelling and ameliorating the development and progression of PH.
    MeSH term(s) Mice ; Animals ; Hypertension, Pulmonary ; Pulmonary Arterial Hypertension ; Rodentia/metabolism ; Vascular Remodeling/physiology ; Pulmonary Artery ; Purines/metabolism ; Cells, Cultured ; Hypoxia/metabolism ; RNA, Messenger/metabolism ; Platelet-Derived Growth Factor/metabolism ; Cell Proliferation ; Myocytes, Smooth Muscle/metabolism
    Chemical Substances Purines ; RNA, Messenger ; Platelet-Derived Growth Factor
    Language English
    Publishing date 2023-01-27
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 603098-1
    ISSN 1522-9645 ; 0195-668X
    ISSN (online) 1522-9645
    ISSN 0195-668X
    DOI 10.1093/eurheartj/ehad044
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1563: 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)
    Zs.MO 640: Show issues

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