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  • American Physiological Society  (25)
  • 1
    Online Resource
    Online Resource
    Genome-wide association study identifies loci and candidate genes for internal organ weights in Simmental beef cattle
    American Physiological Society ; 2018
    In:  Physiological Genomics Vol. 50, No. 7 ( 2018-07-01), p. 523-531
    Details
    In: Physiological Genomics, American Physiological Society, Vol. 50, No. 7 ( 2018-07-01), p. 523-531
    Abstract: Cattle internal organs as accessible raw materials have a long history of being widely used in beef processing, feed and pharmaceutical industry. These traits not only are of economic interest to breeders, but they are intrinsically linked to many valuable traits, such as growth, health, and productivity. Using the Illumina Bovine HD 770K SNP array, we performed a genome-wide association study for heart weight, liver weight, spleen weight, lung weight, and kidney weight in 1,217 Simmental cattle. In our research, 38 significant single nucleotide polymorphisms (SNPs) ( P 〈 1.49 × 10 −6 ) were identified for five internal organ weight traits. These SNPs are within or near 13 genes, and some of them have been reported previously, including NDUFAF4, LCORL, BT.94996, SLIT2, FAM184B, LAP3, BBS12, MECOM, CD300LF, HSD17B3, TLR4, MXI1, and MB21D2. In addition, we detected four haplotype blocks on BTA6 containing 18 significant SNPs associated with spleen weight. Our results offer worthy insights into understanding the genetic mechanisms of internal organs' development, with potential application in breeding programs of Simmental beef cattle.
    Type of Medium: Online Resource
    ISSN: 1094-8341 , 1531-2267
    URL: Article
    DOI: 10.1152/physiolgenomics.00022.2018
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
    detail.hit.zdb_id: 2031330-5
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  • 2
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    Genome-wide association study identifies the PLAG1-OXR1 region on BTA14 for carcass meat yield in cattle
    American Physiological Society ; 2019
    In:  Physiological Genomics Vol. 51, No. 5 ( 2019-05-01), p. 137-144
    Details
    In: Physiological Genomics, American Physiological Society, Vol. 51, No. 5 ( 2019-05-01), p. 137-144
    Abstract: Carcass meat yield is an important carcass trait that contributes to the production efficiency and economic benefits in beef cattle. It is therefore critical to identify quantitative trait loci associated with carcass traits to enable selection. Our previous studies have identified several causal variants within the pleomorphic adenoma gene 1 ( PLAG1) and coiled-coil-helix-coiled-coil-helix domain-containing 7 ( CHCHD7) genes on BTA14 for carcass traits in Chinese Simmental. In the current study, we carried out a genome-wide association study for carcass meat yield in 472 Wagyu cattle with Bovine HD SNP array. Our results showed that 27 single nucleotide polymorphisms (SNPs) were identified for tenderloin weight (TDW), striploin weight (SPW), chuck roll weight (CRW), bicep weight (BPW), knuckle weight (KCW), and flank steak weight (FSW) in Wagyu cattle. Of these SNPs, 10 distinct SNPs were detected within the oxidation resistance 1 ( OXR1), fatty acid binding protein 5 ( FABP5), TNF receptor superfamily member 11b ( TNFRSF11B), and zinc finger CCCH-type containing 3 ( ZC3H3) genes on BTA14. Notably, three significant SNPs, BovineHD1400016738, BovineHD1400016743, and BovineHD1400016665 within OXR1, were shown strong linkage disequilibrium (r 2 〉 0.8) and significantly associated with CRW ( P = 1.37 × 10 −8 ~ 1.94 × 10 −8 ). Moreover, Ingenuity Pathway Analysis showed that OXR1, FABP5, and CAP1A genes were involved in a single network and FABP5 may regulate the expression of OXR1 gene via node gene, peroxisome proliferator-activated receptor gamma ( PPARG). Overall, this study suggests that OXR1 and FABP5 are candidate genes affecting carcass traits in Wagyu and the PLAG1-OXR1 region on BTA14 as a putative susceptibility locus for carcass meat yield for both Chinese Simmental and Wagyu.
    Type of Medium: Online Resource
    ISSN: 1094-8341 , 1531-2267
    URL: Article
    DOI: 10.1152/physiolgenomics.00112.2018
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
    detail.hit.zdb_id: 2031330-5
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  • 3
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    Induced overexpression of Na + /Ca 2+ exchanger transgene: altered myocyte contractility, [Ca 2+ ] i transients, SR Ca 2+ contents, and action potential duration
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 297, No. 2 ( 2009-08), p. H590-H601
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 297, No. 2 ( 2009-08), p. H590-H601
    Abstract: We have produced mice in which expression of the rat cardiac Na + /Ca 2+ exchanger (NCX1) transgene was switched on when doxycycline was removed from the feed at 5 wk. At 8 to 10 wk, NCX1 expression in induced (Ind) mouse hearts was 2.5-fold higher but protein levels of sarco(endo)plasmic reticulum Ca 2+ -ATPase, α 1 - and α 2 -subunits of Na + -K + -ATPase, phospholamban, ryanodine receptor, calsequestrin, and unphosphorylated and phosphorylated phospholemman were unchanged compared with wild-type (WT) or noninduced (non-Ind) hearts. There was no cellular hypertrophy since WT, non-Ind, and Ind myocytes had similar whole cell membrane capacitance. In Ind myocytes, NCX1 current amplitude was ∼42% higher, L-type Ca 2+ current amplitude was unchanged, and action potential duration was prolonged compared with WT or non-Ind myocytes. Contraction and intracellular Ca 2+ concentration ([Ca 2+ ] i ) transient amplitudes in Ind myocytes were lower at 0.6, not different at 1.8, and higher at 5.0 mM extracellular Ca 2+ concentration ([Ca 2+ ] o ) compared with WT or non-Ind myocytes. Despite similar Ca 2+ current amplitude and sarcoplasmic reticulum (SR) Ca 2+ uptake, SR Ca 2+ content at 5.0 mM [Ca 2+ ] o was significantly higher in Ind compared with non-Ind myocytes, indicating that NCX1 directly contributed to SR Ca 2+ loading. Echocardiography demonstrated that heart rate, left ventricular mass, ejection fraction, stroke volume, and cardiac output were similar among the three groups of animals. In vivo close-chest catheterization demonstrated similar contractility and relaxation among the three groups of mice, both at baseline and after stimulation with isoproterenol. We conclude that induced expression of NCX1 transgene resulted in altered [Ca 2+ ] i homeostasis, myocyte contractility, and action potential morphology. In addition, heart failure did not occur 3 to 5 wk after NCX1 transgene was induced to be expressed at levels found in diseased hearts.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00190.2009
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477308-9
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  • 4
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    Role of MCP-1 in tumor necrosis factor-α-induced endothelial dysfunction in type 2 diabetic mice
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 297, No. 4 ( 2009-10), p. H1208-H1216
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 297, No. 4 ( 2009-10), p. H1208-H1216
    Abstract: Tumor necrosis factor-α (TNF-α) upregulates the expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in type 2 diabetes. We hypothesized that TNF-α and MCP-1 may interact to contribute to the evolution of vascular inflammation and endothelial dysfunction in coronary arterioles in type 2 diabetes. To test this hypothesis, we administered anti-MCP-1 to block MCP-1 signaling in genetically modified mice with type 2 diabetes (Lepr db ) and in heterozygote (m Lepr db ) lean control. Anti-MCP-1 partially restored vasodilation to the endothelium-dependent vasodilator acetylcholine in isolated, cannulated, and pressurized coronary arterioles in Lepr db mice but did not affect vasodilation in m Lepr db mice. Anti-MCP-1 attenuated superoxide production and the protein expression of nitrotyrosine, which is an indicator of peroxynitrite production, in isolated coronary arterioles of Lepr db mice. Immunostaining results showed that the expression of MCP-1 and vascular cellular adhesion molecule-1 is colocalized with endothelial cells and macrophages. Anti-TNF-α or anti-MCP-1 markedly reduced macrophage infiltration and the number of MCP-1-positive endothelium in Lepr db mice. The neutralization of TNF-α or anti-MCP-1 reduced the expression of adhesion molecules, suggesting that proinflammatory cytokines interact to amplify the signaling process that leads to vascular dysfunction. These findings demonstrate that the endothelial dysfunction occurring in type 2 diabetes is the result of the effects of the inflammatory cytokine TNF-α and TNF-α-related signaling, including the expression of MCP-1 and adhesion molecules, which further exacerbates vessel inflammation and oxidative stress.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00396.2009
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477308-9
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  • 5
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    Induced overexpression of phospholemman S68E mutant improves cardiac contractility and mortality after ischemia-reperfusion
    American Physiological Society ; 2014
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 306, No. 7 ( 2014-04-01), p. H1066-H1077
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 306, No. 7 ( 2014-04-01), p. H1066-H1077
    Abstract: Phospholemman (PLM), when phosphorylated at Ser 68 , inhibits cardiac Na + /Ca 2+ exchanger 1 (NCX1) and relieves its inhibition on Na + -K + -ATPase. We have engineered mice in which expression of the phosphomimetic PLM S68E mutant was induced when dietary doxycycline was removed at 5 wk. At 8–10 wk, compared with noninduced or wild-type hearts, S68E expression in induced hearts was ∼35–75% that of endogenous PLM, but protein levels of sarco(endo)plasmic reticulum Ca 2+ -ATPase, α 1 - and α 2 -subunits of Na + -K + -ATPase, α 1c -subunit of L-type Ca 2+ channel, and phosphorylated ryanodine receptor were unchanged. The NCX1 protein level was increased by ∼47% but the NCX1 current was depressed by ∼34% in induced hearts. Isoproterenol had no effect on NCX1 currents but stimulated Na + -K + -ATPase currents equally in induced and noninduced myocytes. At baseline, systolic intracellular Ca 2+ concentrations ([Ca 2+ ] i ), sarcoplasmic reticulum Ca 2+ contents, and [Ca 2+ ] i transient and contraction amplitudes were similar between induced and noninduced myocytes. Isoproterenol stimulation resulted in much higher systolic [Ca 2+ ] i , sarcoplasmic reticulum Ca 2+ content, and [Ca 2+ ] i transient and contraction amplitudes in induced myocytes. Echocardiography and in vivo close-chest catheterization demonstrated similar baseline myocardial function, but isoproterenol induced a significantly higher +dP/d t in induced compared with noninduced hearts. In contrast to the 50% mortality observed in mice constitutively overexpressing the S68E mutant, induced mice had similar survival as wild-type and noninduced mice. After ischemia-reperfusion, despite similar areas at risk and left ventricular infarct sizes, induced mice had significantly higher +dP/d t and −dP/d t and lower perioperative mortality compared with noninduced mice. We propose that phosphorylated PLM may be a novel therapeutic target in ischemic heart disease.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00861.2013
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
    detail.hit.zdb_id: 1477308-9
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  • 6
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    Role of EDHF in type 2 diabetes-induced endothelial dysfunction
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 295, No. 5 ( 2008-11), p. H1982-H1988
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 295, No. 5 ( 2008-11), p. H1982-H1988
    Abstract: Endothelium-derived hyperpolarizing factor (EDHF) plays a crucial role in modulating vasomotor tone, especially in microvessels when nitric oxide-dependent control is compromised such as in diabetes. Epoxyeicosatrienoic acids (EETs), potassium ions (K + ), and hydrogen peroxide (H 2 O 2 ) are proposed as EDHFs. However, the identity (or identities) of EDHF-dependent endothelial dilators has not been clearly elucidated in diabetes. We assessed the mechanisms of EDHF-induced vasodilation in wild-type (WT, normal), db/db (advanced type 2 diabetic) mice, and db/db mice null for TNF (db TNF− /db TNF− ). In db/db mice, EDHF-induced vasodilation [ACh-induced vasodilation in the presence of N G -nitro-l-arginine methyl ester (l-NAME, 10 μmol/l) and prostaglandin synthase inhibitor indomethacin (Indo, 10 μmol/l)] was diminished after the administration of catalase (an enzyme that selectively dismutates H 2 O 2 to water and oxygen, 1,000 U/ml); administration of the combination of charybdotoxin (a nonselective blocker of intermediate-conductance Ca 2+ -activated K + channels, 10 μmol/l) and apamin (a selective blocker of small-conductance Ca 2+ -activated K + channels, 50 μmol/l) also attenuated EDHF-induced vasodilation, but the inhibition of EETs synthesis [14,15-epoxyeicosa-5(Z)-enoic acid; 10 μmol/l] did not alter EDHF-induced vasodilation. In WT controls, EDHF-dependent vasodilation was significantly diminished after an inhibition of K + channel, EETs synthesis, or H 2 O 2 production. Our molecular results indicate that mRNA and protein expression of interleukin-6 (IL-6) were greater in db/db versus WT and db TNF− /db TNF− mice, but neutralizing antibody to IL-6 (anti-IL-6; 0.28 mg·ml −1 ·kg −1 ip for 3 days) attenuated IL-6 expression in db/db mice. The incubation of the microvessels with IL-6 (5 ng/ml) induced endothelial dysfunction in the presence of l-NAME and Indo in WT mice, but anti-IL-6 restored ACh-induced vasodilation in the presence of l-NAME and Indo in db/db mice. In db TNF− /db TNF− mice, EDHF-induced vasodilation was greater and comparable with controls, but IL-6 decreased EDHF-mediated vasodilation. Our results indicate that EDHF compensates for diminished NO-dependent dilation in IL-6-induced endothelial dysfunction by the activation of H 2 O 2 or a K + channel in type 2 diabetes.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01261.2007
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477308-9
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  • 7
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    Vitamin D/VDR signaling inhibits colitis by suppressing HIF-1α activation in colonic epithelial cells
    American Physiological Society ; 2021
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 320, No. 5 ( 2021-05-01), p. G837-G846
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 320, No. 5 ( 2021-05-01), p. G837-G846
    Abstract: Vitamin D/vitamin D receptor (VDR) signaling is reported to have a protective effect on the onset or progression of inflammatory bowel diseases (IBD), and hypoxia-inducible factor 1α (HIF-1α) activation is demonstrated to be closely associated with chemical-induced colitis. However, the association between vitamin D/VDR signaling and HIF-1α on IBD development remains a mystery. Here, we showed that HIF-1α expression was largely increased in the colonic epithelial cells of diseased tissues from patients with ulcerative colitis (UC). Consistently, HIF-1α activation was also improved in colonic epithelial cells upon TNFα treatment in a NF-κB pathway-dependent manner. HIF-1α inhibitors treatments ameliorated 2,4,6-trinitrobenzenesulfonic acid (TNBS)- or dextran sulfate sodium (DSS)-induced colitis in animal models. In cell or colitis animal models, vitamin D/VDR signaling suppressed HIF-1α overexpression in colonic epithelial cells via regulating NF-κB pathway, resulting in the inhibition of IFNγ and IL-1β overproductions in these cells. Collectively, these data suggest that vitamin D/VDR signaling relieves colitis development in animal models, at least in part, by suppressing HIF-1α expression in colonic epithelial cells. NEW & NOTEWORTHY This study demonstrates vitamin D/VDR signaling inhibits colitis by suppressing HIF-1α activation in colonic epithelial cells. Since the effect of vitamin D/VDR signaling is only apparent on patients who seem to be vitamin D deficient, the benefits of vitamin D supplementation in patients who are not vitamin D deficient need to be proven.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00061.2021
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2021
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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  • 8
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    Regulation of in vivo cardiac contractility by phospholemman: role of Na + /Ca 2+ exchange
    American Physiological Society ; 2011
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 300, No. 3 ( 2011-03), p. H859-H868
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 300, No. 3 ( 2011-03), p. H859-H868
    Abstract: Phospholemman (PLM), when phosphorylated at serine 68, relieves its inhibition on Na + -K + -ATPase but inhibits Na + /Ca 2+ exchanger 1 (NCX1) in cardiac myocytes. Under stress when catecholamine levels are high, enhanced Na + -K + -ATPase activity by phosphorylated PLM attenuates intracellular Na + concentration ([Na + ] i ) overload. To evaluate the effects of PLM on NCX1 on in vivo cardiac contractility, we injected recombinant adeno-associated virus (serotype 9) expressing either the phosphomimetic PLM S68E mutant or green fluorescent protein (GFP) directly into left ventricles (LVs) of PLM-knockout (KO) mice. Five weeks after virus injection, ∼40% of isolated LV myocytes exhibited GFP fluorescence. Expression of S68E mutant was confirmed with PLM antibody. There were no differences in protein levels of α 1 - and α 2 -subunits of Na + -K + -ATPase, NCX1, and sarco(endo)plasmic reticulum Ca 2+ -ATPase between KO-GFP and KO-S68E LV homogenates. Compared with KO-GFP myocytes, Na + /Ca 2+ exchange current was suppressed, but resting [Na + ] i , Na + -K + -ATPase current, and action potential amplitudes were similar in KO-S68E myocytes. Resting membrane potential was slightly lower and action potential duration at 90% repolarization (APD 90 ) was shortened in KO-S68E myocytes. Isoproterenol (Iso; 1 μM) increased APD 90 in both groups of myocytes. After Iso, [Na + ] i increased monotonically in paced (2 Hz) KO-GFP but reached a plateau in KO-S68E myocytes. Both systolic and diastolic [Ca 2+ ] i were higher in Iso-stimulated KO-S68E myocytes paced at 2 Hz. Echocardiography demonstrated similar resting heart rate, ejection fraction, and LV mass between KO-GFP and KO-S68E mice. In vivo closed-chest catheterization demonstrated enhanced contractility in KO-S68E compared with KO-GFP hearts stimulated with Iso. We conclude that under catecholamine stress when [Na + ] i is high, PLM minimizes [Na + ] i overload by relieving its inhibition of Na + -K + -ATPase and preserves inotropy by simultaneously inhibiting Na + /Ca 2+ exchanger.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00894.2010
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 9
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    Chronic continuous positive airway pressure (CPAP) reduces airway reactivity in vivo in an allergen-induced rabbit model of asthma
    American Physiological Society ; 2011
    In:  Journal of Applied Physiology Vol. 111, No. 2 ( 2011-08), p. 353-357
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 111, No. 2 ( 2011-08), p. 353-357
    Abstract: Previous studies have demonstrated that chronic mechanical strain produced by continuous positive airway pressure (CPAP) reduces in vivo airway reactivity in rabbits and ferrets. For CPAP to potentially have a therapeutic benefit for asthmatic subjects, the reduction in airway responsiveness would need to persist for 12–24 h after its discontinuation, require application for only part of the day, and be effective in the presence of atopic airway inflammation. In the present study, airway responsiveness to acetylcholine or methacholine was measured during mechanical ventilation following three different protocols in which active, nonanesthetized, tracheotomized rabbits were treated with High vs. Low CPAP (6 vs. 0 cmH 2 O). 1) High CPAP was applied continuously for 4 days followed by 1 day of Low CPAP; 2) High CPAP was applied at night and Low CPAP during the daytime for 4 days, and 3) High CPAP was applied for 4 days in animals following ovalbumin (Ova) sensitization and challenge. For all three protocols, treatment with High CPAP resulted in significantly reduced airway responsiveness compared with treatment with Low CPAP. Cumulatively, our in vivo results in rabbits suggest that high CPAP, even when applied only at night, produces a persistent reduction of airway responsiveness. In addition, CPAP reduces airway responsiveness even in the presence of atopic airway inflammation.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.01345.2010
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 10
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    Ca 2+ entry via Trpm2 is essential for cardiac myocyte bioenergetics maintenance
    American Physiological Society ; 2015
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 308, No. 6 ( 2015-03-15), p. H637-H650
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 308, No. 6 ( 2015-03-15), p. H637-H650
    Abstract: Ubiquitously expressed Trpm2 channel limits oxidative stress and preserves mitochondrial function. We first demonstrated that intracellular Ca 2+ concentration increase after Trpm2 activation was due to direct Ca 2+ influx and not indirectly via reverse Na + /Ca 2+ exchange. To elucidate whether Ca 2+ entry via Trpm2 is required to maintain cellular bioenergetics, we injected adenovirus expressing green fluorescent protein (GFP), wild-type (WT) Trpm2, and loss-of-function (E960D) Trpm2 mutant into left ventricles of global Trpm2 knockout (gKO) or WT hearts. Five days post-injection, gKO-GFP heart slices had higher reactive oxygen species (ROS) levels but lower oxygen consumption rate (OCR) than WT-GFP heart slices. Trpm2 but not E960D decreased ROS and restored OCR in gKO hearts back to normal levels. In gKO myocytes expressing Trpm2 or its mutants, Trpm2 but not E960D reduced the elevated mitochondrial superoxide (O 2 .− ) levels in gKO myocytes. After hypoxia-reoxygenation (H/R), Trpm2 but not E906D or P1018L (inactivates Trpm2 current) lowered O 2 .− levels in gKO myocytes and only in the presence of extracellular Ca 2+ , indicating sustained Ca 2+ entry is necessary for Trpm2-mediated preservation of mitochondrial function. After ischemic-reperfusion (I/R), cardiac-specific Trpm2 KO hearts exhibited lower maximal first time derivative of LV pressure rise (+dP/d t) than WT hearts in vivo. After doxorubicin treatment, Trpm2 KO mice had worse survival and lower +dP/d t. We conclude 1) cardiac Trpm2-mediated Ca 2+ influx is necessary to maintain mitochondrial function and protect against H/R injury; 2) Ca 2+ influx via cardiac Trpm2 confers protection against H/R and I/R injury by reducing mitochondrial oxidants; and 3) Trpm2 confers protection in doxorubicin cardiomyopathy.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00720.2014
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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