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  1. Article ; Online: Differential effects of low-dose sacubitril and/or valsartan on renal disease in salt-sensitive hypertension.

    Polina, Iuliia / Domondon, Mark / Fox, Rebecca / Sudarikova, Anastasia V / Troncoso, Miguel / Vasileva, Valeriia Y / Kashyrina, Yuliia / Gooz, Monika Beck / Schibalski, Ryan S / DeLeon-Pennell, Kristine Y / Fitzgibbon, Wayne R / Ilatovskaya, Daria V

    American journal of physiology. Renal physiology

    2020  Volume 319, Issue 1, Page(s) F63–F75

    Abstract: Diuretics and renin-angiotensin system blockers are often insufficient to control the blood pressure (BP) in salt-sensitive (SS) subjects. Abundant data support the proposal that the level of atrial natriuretic peptide may correlate with the pathogenesis ...

    Abstract Diuretics and renin-angiotensin system blockers are often insufficient to control the blood pressure (BP) in salt-sensitive (SS) subjects. Abundant data support the proposal that the level of atrial natriuretic peptide may correlate with the pathogenesis of SS hypertension. We hypothesized here that increasing atrial natriuretic peptide levels with sacubitril, combined with renin-angiotensin system blockage by valsartan, can be beneficial for alleviation of renal damage in a model of SS hypertension, the Dahl SS rat. To induce a BP increase, rats were challenged with a high-salt 4% NaCl diet for 21 days, and chronic administration of vehicle or low-dose sacubitril and/or valsartan (75 μg/day each) was performed. Urine flow, Na
    MeSH term(s) Aminobutyrates/administration & dosage ; Aminobutyrates/therapeutic use ; Angiotensin Receptor Antagonists/administration & dosage ; Angiotensin Receptor Antagonists/therapeutic use ; Animals ; Blood Pressure/drug effects ; Drug Combinations ; Hypertension/drug therapy ; Hypertension/physiopathology ; Kidney Diseases/drug therapy ; Kidney Diseases/physiopathology ; Male ; Rats ; Rats, Inbred Dahl ; Sodium Chloride, Dietary ; Tetrazoles/administration & dosage ; Tetrazoles/therapeutic use ; Valsartan/administration & dosage ; Valsartan/therapeutic use
    Chemical Substances Aminobutyrates ; Angiotensin Receptor Antagonists ; Drug Combinations ; Sodium Chloride, Dietary ; Tetrazoles ; Valsartan (80M03YXJ7I) ; sacubitril and valsartan sodium hydrate drug combination (WB8FT61183)
    Language English
    Publishing date 2020-05-28
    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, Non-P.H.S.
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00125.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: ATP/ADP turnover and import of glycolytic ATP into mitochondria in cancer cells is independent of the adenine nucleotide translocator.

    Maldonado, Eduardo N / DeHart, David N / Patnaik, Jyoti / Klatt, Sandra C / Gooz, Monika Beck / Lemasters, John J

    The Journal of biological chemistry

    2017  Volume 292, Issue 41, Page(s) 16969

    Language English
    Publishing date 2017-07-31
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.A116.734814
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: ATP/ADP Turnover and Import of Glycolytic ATP into Mitochondria in Cancer Cells Is Independent of the Adenine Nucleotide Translocator.

    Maldonado, Eduardo N / DeHart, David N / Patnaik, Jyoti / Klatt, Sandra C / Gooz, Monika Beck / Lemasters, John J

    The Journal of biological chemistry

    2016  Volume 291, Issue 37, Page(s) 19642–19650

    Abstract: Non-proliferating cells oxidize respiratory substrates in mitochondria to generate a protonmotive force (Δp) that drives ATP synthesis. The mitochondrial membrane potential (ΔΨ), a component of Δp, drives release of mitochondrial ATP(4-) in exchange for ... ...

    Abstract Non-proliferating cells oxidize respiratory substrates in mitochondria to generate a protonmotive force (Δp) that drives ATP synthesis. The mitochondrial membrane potential (ΔΨ), a component of Δp, drives release of mitochondrial ATP(4-) in exchange for cytosolic ADP(3-) via the electrogenic adenine nucleotide translocator (ANT) located in the mitochondrial inner membrane, which leads to a high cytosolic ATP/ADP ratio up to >100-fold greater than matrix ATP/ADP. In rat hepatocytes, ANT inhibitors, bongkrekic acid (BA), and carboxyatractyloside (CAT), and the F1FO-ATP synthase inhibitor, oligomycin (OLIG), inhibited ureagenesis-induced respiration. However, in several cancer cell lines, OLIG but not BA and CAT inhibited respiration. In hepatocytes, respiratory inhibition did not collapse ΔΨ until OLIG, BA, or CAT was added. Similarly, in cancer cells OLIG and 2-deoxyglucose, a glycolytic inhibitor, depolarized mitochondria after respiratory inhibition, which showed that mitochondrial hydrolysis of glycolytic ATP maintained ΔΨ in the absence of respiration in all cell types studied. However in cancer cells, BA, CAT, and knockdown of the major ANT isoforms, ANT2 and ANT3, did not collapse ΔΨ after respiratory inhibition. These findings indicated that ANT was not mediating mitochondrial ATP/ADP exchange in cancer cells [corrected]. We propose that suppression of ANT contributes to low cytosolic ATP/ADP, activation of glycolysis, and a Warburg metabolic phenotype in proliferating cells.
    MeSH term(s) Adenine Nucleotide Translocator 2/metabolism ; Adenine Nucleotide Translocator 3/metabolism ; Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Cell Line, Tumor ; Enzyme Inhibitors/pharmacology ; Glycolysis/drug effects ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Male ; Mitochondria, Liver/metabolism ; Mitochondria, Liver/pathology ; Neoplasm Proteins/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Oxygen Consumption/drug effects ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Adenine Nucleotide Translocator 2 ; Adenine Nucleotide Translocator 3 ; Enzyme Inhibitors ; Neoplasm Proteins ; Adenosine Diphosphate (61D2G4IYVH) ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2016-07-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M116.734814
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Role of Adipose Tissue Endothelial ADAM17 in Age-Related Coronary Microvascular Dysfunction.

    Dou, Huijuan / Feher, Attila / Davila, Alec C / Romero, Maritza J / Patel, Vijay S / Kamath, Vinayak M / Gooz, Monika Beck / Rudic, R Daniel / Lucas, Rudolf / Fulton, David J / Weintraub, Neal L / Bagi, Zsolt

    Arteriosclerosis, thrombosis, and vascular biology

    2017  Volume 37, Issue 6, Page(s) 1180–1193

    Abstract: Objective: A disintegrin and metalloproteinase ADAM17 (tumor necrosis factor-α [TNF]-converting enzyme) regulates soluble TNF levels. We tested the hypothesis that aging-induced activation in adipose tissue (AT)-expressed ADAM17 contributes to the ... ...

    Abstract Objective: A disintegrin and metalloproteinase ADAM17 (tumor necrosis factor-α [TNF]-converting enzyme) regulates soluble TNF levels. We tested the hypothesis that aging-induced activation in adipose tissue (AT)-expressed ADAM17 contributes to the development of remote coronary microvascular dysfunction in obesity.
    Approach and results: Coronary arterioles (CAs, ≈90 µm) from right atrial appendages and mediastinal AT were examined in patients (aged: 69±11 years, BMI: 30.2±5.6 kg/m
    Conclusions: The present study indicates that aging and obesity cooperatively reduce caveolin-1 expression and increase vascular endothelial ADAM17 activity and soluble TNF release in AT, which may contribute to the development of remote coronary microvascular dysfunction in older obese patients.
    MeSH term(s) ADAM17 Protein/genetics ; ADAM17 Protein/metabolism ; Adipose Tissue/enzymology ; Adipose Tissue/transplantation ; Adult ; Age Factors ; Aged ; Aged, 80 and over ; Aging/genetics ; Aging/metabolism ; Animals ; Arterioles/enzymology ; Arterioles/physiopathology ; Caveolin 1/deficiency ; Caveolin 1/genetics ; Caveolin 1/metabolism ; Cells, Cultured ; Coronary Artery Disease/enzymology ; Coronary Artery Disease/genetics ; Coronary Artery Disease/physiopathology ; Coronary Vessels/enzymology ; Coronary Vessels/physiopathology ; Diet, High-Fat ; Disease Models, Animal ; Endothelial Cells/enzymology ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Obesity/enzymology ; Obesity/genetics ; Obesity/physiopathology ; RNA Interference ; Risk Factors ; Signal Transduction ; Transfection ; Tumor Necrosis Factor-alpha/metabolism ; Vasodilation
    Chemical Substances CAV1 protein, human ; Cav1 protein, mouse ; Caveolin 1 ; Tumor Necrosis Factor-alpha ; ADAM17 Protein (EC 3.4.24.86) ; ADAM17 protein, human (EC 3.4.24.86) ; Adam17 protein, mouse (EC 3.4.24.86)
    Language English
    Publishing date 2017-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.117.309430
    Database MEDical Literature Analysis and Retrieval System OnLINE

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