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  • 1
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    Abstract P207: High Salt Intake desynchronizes the Molecular Clock in Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Hypertension Vol. 68, No. suppl_1 ( 2016-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 68, No. suppl_1 ( 2016-09)
    Abstract: Circadian rhythms in physiologic functions are driven, at the molecular level, by a group of transcription factors that oscillate over a 24 hour period, collectively termed the molecular clock. Within the kidney, it has been shown that the molecular clock directly influences transcription of Na + transporters and channels, including ENaC. ENaC is regulated by endothelin-1 (ET-1), via ET B receptor activation, in response to high salt intake. Thus, we hypothesized that increases in dietary sodium regulate the renal molecular clock (which in turn would facilitate Na+ homeostasis) through an ET B dependent mechanism. To address this question, we examined the effect of high salt (HS) intake on renal clock gene ( Bmal1, Cry1, Per1, Per2 ) expression. Control and ET B receptor deficient (ET B def) rats (a model of elevated renal ENaC) were placed on either HS or normal salt (NS) for two weeks and euthanized every 4 hours beginning at Zeitgeber Time 0 (Lights on). In the inner medulla, HS causes a phase delay in Bmal1 (Fig 1A) expression in control but not ET B def rats (Fig 1B). In addition, HS suppressed the expression of Cry1 , and Per2 during the respective acrophase in both control and ET B def rats (Fig 1C-1F) with no significant effect on Per1 . In contrast, no significant difference in the expression of Bmal1, Cry1, Per2, or Per1 (Fig 1I-1P) was found in response to HS in the renal cortex of either control or ET B def. These data indicate that HS feeding desynchronizes the molecular clock within the kidney and provides evidence that peripheral clocks are regulated in a cell type specific manner, even within the same organ.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.68.suppl_1.p207
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2094210-2
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  • 2
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    Renal Collecting Duct NOS1 Maintains Fluid–Electrolyte Homeostasis and Blood Pressure
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Hypertension Vol. 62, No. 1 ( 2013-07), p. 91-98
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 62, No. 1 ( 2013-07), p. 91-98
    Abstract: Nitric oxide is a pronatriuretic and prodiuretic factor. The highest renal NO synthase (NOS) activity is found in the inner medullary collecting duct. The collecting duct (CD) is the site of daily fine-tune regulation of sodium balance, and led us to hypothesize that a CD-specific deletion of NOS1 would result in an impaired ability to excrete a sodium load leading to a salt-sensitive blood pressure phenotype. We bred AQP2-CRE mice with NOS1 floxed mice to produce flox control and CD-specific NOS1 knockout (CDNOS1KO) littermates. CDs from CDNOS1KO mice produced 75% less nitrite, and urinary nitrite+nitrate (NOx) excretion was significantly blunted in the knockout genotype. When challenged with high dietary sodium, CDNOS1KO mice showed significantly reduced urine output, sodium, chloride, and NOx excretion, and increased mean arterial pressure relative to flox control mice. In humans, urinary NOx is a newly identified biomarker for the progression of hypertension. These findings reveal that NOS1 in the CD is critical in the regulation of fluid–electrolyte balance, and this new genetic model of CD NOS1 gene deletion will be a valuable tool to study salt-dependent blood pressure mechanisms.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.113.01291
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 2094210-2
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  • 3
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    Collecting Duct Nitric Oxide Synthase 1ß Activation Maintains Sodium Homeostasis During High Sodium Intake Through Suppression of Aldosterone and Renal Angiotensin II Pathways
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of the American Heart Association Vol. 6, No. 10 ( 2017-10-11)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 10 ( 2017-10-11)
    Abstract: During high sodium intake, the renin‐angiotensin‐aldosterone system is downregulated and nitric oxide signaling is upregulated in order to remain in sodium balance. Recently, we showed that collecting duct nitric oxide synthase 1β is critical for fluid‐electrolyte balance and subsequently blood pressure regulation during high sodium feeding. The current study tested the hypothesis that high sodium activation of the collecting duct nitric oxide synthase 1β pathway is critical for maintaining sodium homeostasis and for the downregulation of the renin‐angiotensin‐aldosterone system–epithelial sodium channel axis. Methods and Results Male control and collecting duct nitric oxide synthase 1β knockout ( CDNOS 1 KO ) mice were placed on low, normal, and high sodium diets for 1 week. In response to the high sodium diet, plasma sodium was significantly increased in control mice and to a significantly greater level in CDNOS 1 KO mice. CDNOS 1 KO mice did not suppress plasma aldosterone in response to the high sodium diet, which may be partially explained by increased adrenal AT 1R expression. Plasma renin concentration was appropriately suppressed in both genotypes. Furthermore, CDNOS 1 KO mice had significantly higher intrarenal angiotensin II with high sodium diet, although intrarenal angiotensinogen levels and angiotensin‐converting enzyme activity were similar between knockout mice and controls. In agreement with inappropriate renin‐angiotensin‐aldosterone system activation in the CDNOS 1 KO mice on a high sodium diet, epithelial sodium channel activity and sodium transporter abundance were significantly higher compared with controls. Conclusions These data demonstrate that high sodium activation of collecting duct nitric oxide synthase 1β signaling induces suppression of systemic and intrarenal renin‐angiotensin‐aldosterone system, thereby modulating epithelial sodium channel and other sodium transporter abundance and activity to maintain sodium homeostasis.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.117.006896
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2653953-6
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  • 4
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    Dynamic regulation of lysine acetylation: the balance between acetyltransferase and deacetylase activities
    American Physiological Society ; 2017
    In:  American Journal of Physiology-Renal Physiology Vol. 313, No. 4 ( 2017-10-01), p. F842-F846
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 313, No. 4 ( 2017-10-01), p. F842-F846
    Abstract: Reversible posttranslational modification of proteins is a critically important process in physiological regulation in all tissues, including the kidney. Lysine acetylation occurs in all organisms, including prokaryotes, and is regulated by a balance between the lysine acetyltransferases (adding an acetyl group to the ε-amino group of a lysine) and deacetylases (removing it). The kidney is an organ rich with acetylated lysines, which map to 〉 2,000 unique histone and nonhistone proteins. However, the functional significance of these modifications remains to be discovered. Here, we have compiled gene lists of the acetyltransferases and deacetylases in the mammalian genomes and mapped their mRNA expression along the renal tubule. These lists will be useful for generating targeted approaches to test the physiological or pathophysiological significance of lysine acetylation changes in the kidney.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00313.2017
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1477287-5
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  • 5
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    Functional morphology of the gills of the shortfin mako, Isurus oxyrinchus , a lamnid shark
    Wiley ; 2010
    In:  Journal of Morphology Vol. 271, No. 8 ( 2010-08), p. 937-948
    Details
    In: Journal of Morphology, Wiley, Vol. 271, No. 8 ( 2010-08), p. 937-948
    Abstract: This study examines the functional gill morphology of the shortfin mako, Isurus oxyrinchus , to determine the extent to which its gill structure is convergent with that of tunas for specializations required to increase gas exchange and withstand the forceful branchial flow induced by ram ventilation. Mako gill structure is also compared to that of the blue shark, Prionace glauca , an epipelagic species with lower metabolic requirements and a reduced dependence on fast, continuous swimming to ventilate the gills. The gill surface area of the mako is about one‐half that of a comparably sized tuna, but more than twice that of the blue shark and other nonlamnid shark species. Mako gills are also distinguished from those of other sharks by shorter diffusion distances and a more fully developed diagonal blood‐flow pattern through the gill lamellae, which is similar to that found in tunas. Although the mako lacks the filament and lamellar fusions of tunas and other ram‐ventilating teleosts, its gill filaments are stiffened by the elasmobranch interbranchial septum, and the lamellae appear to be stabilized by one to two vascular sacs that protrude from the lamellar surface and abut sacs of adjacent lamellae. Vasoactive agents and changes in vascular pressure potentially influence sac size, consequently effecting lamellar rigidity and both the volume and speed of water through the interlamellar channels. However, vascular sacs also occur in the blue shark, and no other structural elements of the mako gill appear specialized for ram ventilation. Rather, the basic elasmobranch gill design and pattern of branchial circulation are both conserved. Despite specializations that increase mako gill area and efficacy relative to other sharks, the basic features of the elasmobranch gill design appear to have limited selection for a larger gill surface area, and this may ultimately constrain mako aerobic performance in comparison to tunas. J. Morphol. 271:937–948, 2010. © 2010 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0362-2525 , 1097-4687
    URL: Issue
    URL: Article
    DOI: 10.1002/jmor.v271:8
    DOI: 10.1002/jmor.10845
    Language: English
    Publisher: Wiley
    Publication Date: 2010
    detail.hit.zdb_id: 1479991-1
    SSG: 12
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  • 6
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    Proteomic determination of the lysine acetylome and phosphoproteome in the rat native inner medullary collecting duct
    American Physiological Society ; 2018
    In:  Physiological Genomics Vol. 50, No. 9 ( 2018-09-01), p. 669-679
    Details
    In: Physiological Genomics, American Physiological Society, Vol. 50, No. 9 ( 2018-09-01), p. 669-679
    Abstract: Phosphorylation and lysine (K)-acetylation are dynamic posttranslational modifications of proteins. Previous proteomic studies have identified over 170,000 phosphorylation sites and 15,000 K-acetylation sites in mammals. We recently reported that the inner medullary collecting duct (IMCD), which functions in the regulation of water-reabsorption, via the actions of vasopressin, expresses many of the enzymes that can modulated K-acetylation. The purpose of this study was to determine the K-acetylated or phosphorylated proteins expressed in IMCD cells. Second we questioned whether vasopressin V2 receptor activation significantly affects the IMCD acetylome or phosphoproteome? K-acetylated or serine-, threonine-, or tyrosine-phosphorylated peptides were identified from native rat IMCDs by proteomic analysis with four different enzymes (trypsin, chymotrypsin, ASP-N, or Glu-C) to generate a high-resolution proteome. K-acetylation was identified in 431 unique proteins, and 64% of the K-acetylated sites were novel. The acetylated proteins were expressed in all compartments of the cell and were enriched in pathways including glycolysis and vasopressin-regulated water reabsorption. In the vasopressin-regulated water reabsorption pathway, eight proteins were acetylated, including the novel identification of the basolateral water channel, AQP3, acetylated at K282; 215 proteins were phosphorylated in this IMCD cohort, including AQP2 peptides that were phosphorylated at four serines: 256, 261, 264, and 269. Acute dDAVP did not significantly affect the IMCD acetylome; however, it did significantly affect previously known vasopressin-regulated phosphorylation sites. In conclusion, presence of K-acetylated proteins involved in metabolism, ion, and water transport in the IMCD points to multiple roles of K-acetylation beyond its canonical role in transcriptional regulation.
    Type of Medium: Online Resource
    ISSN: 1094-8341 , 1531-2267
    URL: Article
    DOI: 10.1152/physiolgenomics.00029.2018
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
    detail.hit.zdb_id: 2031330-5
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  • 7
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    Evidence for extrarenal vascular endothelin-1 in the maintenance of sodium homeostasis
    Elsevier BV ; 2013
    In:  Life Sciences Vol. 93, No. 25-26 ( 2013-12), p. e15-e16
    Details
    In: Life Sciences, Elsevier BV, Vol. 93, No. 25-26 ( 2013-12), p. e15-e16
    Type of Medium: Online Resource
    ISSN: 0024-3205
    URL: Article
    DOI: 10.1016/j.lfs.2013.12.073
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
    detail.hit.zdb_id: 2013911-1
    SSG: 12
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  • 8
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    Collecting duct NOS1 knockout mice lack ET-1 mediated inhibition of collecting duct ENaC
    Elsevier BV ; 2013
    In:  Life Sciences Vol. 93, No. 25-26 ( 2013-12), p. e16-e17
    Details
    In: Life Sciences, Elsevier BV, Vol. 93, No. 25-26 ( 2013-12), p. e16-e17
    Type of Medium: Online Resource
    ISSN: 0024-3205
    URL: Article
    DOI: 10.1016/j.lfs.2013.12.076
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
    detail.hit.zdb_id: 2013911-1
    SSG: 12
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  • 9
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    Abstract 141: Histone Deacetylase 1 Regulates Nitric Oxide Production and Nitric Oxide Synthase-3 Acetylation in Endothelial Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Hypertension Vol. 60, No. suppl_1 ( 2012-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 60, No. suppl_1 ( 2012-09)
    Abstract: Previous reports showed that NOS3 is regulated by acetylation through transcriptional mechanisms via histone acetylation or through direct lysine acetylation. Histone deacetylase (HDAC) enzymes and histone acetyltransferases (HATs) modulate acetylation processes. Recent work by our lab, demonstrated increased expression of aortic HDAC1 and HDAC6 while HATs were unchanged in a mouse model of early life stress with endothelial dysfunction. These data suggest a negative correlation between endothelial dysfunction and HDAC expression. The purpose of this study was to test the hypothesis that HDAC1 and 6 regulate endothelial NO production and/or NOS3 acetylation. Initial immunoprecipitation studies with anti-acetyl lysine and anti-NOS3 antibodies demonstrated that NOS3 is basally acetylated in primary bovine aortic endothelial cells (BAECs). Treatment with the HDAC inhibitor, trichostatin A (500 nM) for 1 hr, significantly increased NOS3 acetylation. BAECs were transfected with HDAC1, HDAC6, vector expression plasmids, or untransfected, with nitrite production determined by HPLC and NOS3 acetylation and expression probed by immunoprecipitation and Western blotting. Untransfected and vector transfected control BAECs had similar NO production (357 ± 10 and 344 ± 30 pmol/mg pr/h, respectively, N=6) as well as NOS3 acetylation (7.8 ± 1.6 and 6.8 ±0.3 AU, N=3). HDAC6 transfected BAECs had similar NO production to the control BAECs (272 ± 93 pmol/mg pr/h, N=3) with an increase in NOS3 acetylation (17.4 ± 1.7 AU, N=3). In contrast, HDAC1 overexpression significantly decreased NO production (89 ± 50 pmol/mg pr/h, P 〈 0.05, N=3) and reduced NOS3 acetylation (3.8 ± 0.5 A.U, N=3), P 〈 0.05). Control transfections, HDAC6, and HDAC1 transfected BAECS all had similar NOS3 expression (10.14 ± 1.8; 9.8 ±1.6; 8.9 ± 1.5; 10.6 ± 1.0 AU, respectively, N=3). Thus, we conclude that HDAC1 regulates NO production via direct lysine deacetylation of NOS3.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.60.suppl_1.A141
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2094210-2
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  • 10
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    Relationship between oxidizable fatty acid content and level of antioxidant glutathione peroxidases in marine fish
    The Company of Biologists ; 2011
    In:  Journal of Experimental Biology Vol. 214, No. 22 ( 2011-11-15), p. 3751-3759
    Details
    In: Journal of Experimental Biology, The Company of Biologists, Vol. 214, No. 22 ( 2011-11-15), p. 3751-3759
    Abstract: Biological membranes can be protected from lipid peroxidation by antioxidant enzymes including catalase (CAT) and selenium-dependent glutathione peroxidases 1 and 4 (GPx1 and GPx4). Unlike GPx1, GPx4 can directly detoxify lipid hydroperoxides in membranes without prior action of phospholipase A2. We hypothesized that (1) GPx4 is enhanced in species that contain elevated levels of highly oxidizable polyunsaturated fatty acids (PUFA) and (2) activities of antioxidant enzymes are prioritized to meet species-specific oxidative stresses. In this study we examined (i) activities of the oxidative enzyme citrate synthase (CS) and antioxidant (CAT, GPx1 and GPx4) enzymes, (ii) GPx4 protein expression, and (iii) phospholipid composition in livers of five species of marine fish (Myxine glutinosa, Petromyzon marinus, Squalus acanthias, Fundulus heteroclitus and Myoxocephalus octodecemspinosus) that contain a range of PUFA. GPx4 activity was, on average, 5.8 times higher in F. heteroclitus and S. acanthias than in the other three marine fish species sampled. Similarly, activities of CAT and GPx1 were highest in S. acanthias and F. heteroclitus, respectively. GPx4 activity for all species correlates with membrane unsaturation, as well as oxidative activity as indicated by CS. These data support our hypothesis that GPx4 level in marine fish is a function, at least in part, of high PUFA content in these animals. GPx1 activity was also correlated with membrane unsaturation, indicating that marine species partition resources among glutathione-dependent defenses for protection from the initial oxidative insult (e.g. H2O2) and to repair damaged lipids within biological membranes.
    Type of Medium: Online Resource
    ISSN: 1477-9145 , 0022-0949
    URL: Article
    DOI: 10.1242/jeb.058214
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2011
    detail.hit.zdb_id: 1482461-9
    SSG: 12
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