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  • Nature Publishing Group (NPG)  (11)
  • The American Physiological Society (APS)  (10)
  • American Society of Hematology (ASH)  (3)
  • 1
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    Plasma choline metabolites associate with metabolic stress among young overweight men in a genotype-specific manner (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-09
    Description: Plasma choline metabolites associate with metabolic stress among young overweight men in a genotype-specific manner Nutrition and Diabetes 2, e49 (October 2012). doi:10.1038/nutd.2012.23 Authors: J Yan, L B Winter, B Burns-Whitmore, F Vermeylen & M A Caudill
    Keywords: cholinebetainebody mass indexmetabolic stressphosphatidylethanolamine N-methyltransferase 5465GA (rs7946)methylenetetrahydrofolate dehydrogenase 1 1958GA (rs2236225)
    Electronic ISSN: 2044-4052
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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  • 2
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    Adenylyl cyclase type 5 in cardiac disease, metabolism, and aging (2013)
    The American Physiological Society (APS)
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    Publication Date: 2013-07-02
    Description: G protein-coupled receptor/adenylyl cyclase (AC)/cAMP signaling is crucial for all cellular responses to physiological and pathophysiological stimuli. There are nine isoforms of membrane-bound AC, with type 5 being one of the two major isoforms in the heart. Since the role of AC in the heart in regulating cAMP and acute changes in inotropic and chronotropic state are well known, this review will address our current understanding of the distinct regulatory role of the AC5 isoform in response to chronic stress. Transgenic overexpression of AC5 in cardiomyocytes of the heart (AC5-Tg) improves baseline cardiac function but impairs the ability of the heart to withstand stress. For example, chronic catecholamine stimulation induces cardiomyopathy, which is more severe in AC5-Tg mice, mediated through the AC5/sirtuin 1/forkhead box O3a pathway. Conversely, disrupting AC5, i.e., AC5 knockout, protects the heart from chronic catecholamine cardiomyopathy as well as the cardiomyopathies resulting from chronic pressure overload or aging. Moreover, AC5 knockout results in a 30% increase in a healthy life span, resembling the most widely studied model of longevity, i.e., calorie restriction. These two models of longevity share similar gene regulation in the heart, muscle, liver, and brain in that they are both protected against diabetes, obesity, and diabetic and aging cardiomyopathy. A pharmacological inhibitor of AC5 also provides protection against cardiac stress, diabetes, and obesity. Thus AC5 inhibition has novel, potential therapeutic applicability to several diseases not only in the heart but also in aging, diabetes, and obesity.
    Print ISSN: 0363-6135
    Electronic ISSN: 1522-1539
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 3
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    Replication of associations between genetic polymorphisms and chronic graft-versus-host disease (2016)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2016-11-18
    Description: Previous studies have identified single-nucleotide polymorphisms (SNPs) associated with the risk of chronic graft-versus-host disease (GVHD) after allogeneic hematopoietic cell transplantation. The current study determined whether these associations could be replicated in large cohorts of donors and recipients. Each SNP was tested with cohorts of patients having the same donor type (HLA-matched related, unrelated, or both) reported in the original publication, and testing was limited to the same genome (recipient or donor) and genetic model (dominant, recessive, or allelic) reported in the original study. The 21 SNPs reported in this study represent 19 genes, and the analysis encompassed 22 SNP association tests. The hazard ratio (HR) point estimates and risk ratio point estimates corresponding to odds ratios in previous studies consistently fall outside the 95% confidence intervals of HR estimates in the current study. Despite the large size of the cohorts available for the current study, the 95% confidence intervals for most HRs did not exclude 1.0. Three SNPs representing CTLA4 , HPSE , and IL1R1 showed evidence of association with the risk of chronic GVHD in unrelated donor-recipient pairs from 1 cohort, but none of these associations was replicated when tested in unrelated donor-recipient pairs from an independent cohort. Two SNPs representing CCR6 and FGFR1OP showed possible associations with the risk of chronic GVHD in related donor-recipient pairs but not in unrelated donor-recipient pairs. These results remain to be tested for replication in other cohorts of related donor-recipient pairs.
    Keywords: Transplantation, Clinical Trials and Observations
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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  • 4
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    Catalpol restores LPS-elicited rat microcirculation disorder by regulation of a network of signaling involving inhibition of TLR-4 and SRC (2016)
    The American Physiological Society (APS)
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    Publication Date: 2016-12-15
    Description: LPS-induced microvascular hyperpermeability and hemorrhage play a key role in the development of sepsis, the attenuation of which might be an important strategy to prevent sepsis. However, the current clinical therapies have proven to be inefficient in improving the prognosis for patients with sepsis. Catalpol, an iridoid glycoside extracted from the roots of Rehmannia , has been reported to protect against LPS-induced acute lung injury through a Toll-like receptor-4 (TLR-4)-mediated NF-B signaling pathway. However, it is still unknown whether catalpol can be an effective treatment to ameliorate the LPS-induced microvascular disorder. The present study aimed to investigate the impact of catalpol on LPS-induced mesenteric microvascular disorder and its underlying mechanism. Male Wistar rats were challenged by infusion of LPS (10 mg·kg –1 ·h –1 ) through the left femoral vein for 120 min. Post-treatment with catalpol (10 mg/kg) alleviated the LPS-induced microvascular hyperpermeability and hemorrhage; reduced mortality; ameliorated the alteration in the distribution of claudin-5 and the junctional adhesion molecule-1, as well as the degradation of collagen IV and laminin; and attenuated the increase of TLR-4 level, phosphorylations of Src tyrosine kinase, phosphatidyl inositol 3-kinase, focal adhesion kinase, and cathepsin B activation. In vitro study in human umbilical vein endothelial cells verified these results and further revealed that inhibition of TLR-4 and Src each simulated some, but not all, of the effects that catalpol exerted. Besides, surface plasmon resonance showed that catalpol could directly bind to TLR-4 and Src. These results demonstrated that catalpol was able to ameliorate the LPS-induced microvascular barrier damage and hemorrhage by targeting both TLR-4 and Src, thus attenuating the phosphorylation of Src kinase, phosphatidyl inositol 3-kinase, and focal adhesion kinase, as well as cathepsin B activation.
    Print ISSN: 0193-1857
    Electronic ISSN: 1522-1547
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 5
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    Replication and validation of genetic polymorphisms associated with survival after allogeneic blood or marrow transplant (2017)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2017-09-30
    Description: Multiple candidate gene-association studies of non-HLA single-nucleotide polymorphisms (SNPs) and outcomes after blood or marrow transplant (BMT) have been conducted. We identified 70 publications reporting 45 SNPs in 36 genes significantly associated with disease-related mortality, progression-free survival, transplant-related mortality, and/or overall survival after BMT. Replication and validation of these SNP associations were performed using DISCOVeRY-BMT (Determining the Influence of Susceptibility COnveying Variants Related to one-Year mortality after BMT), a well-powered genome-wide association study consisting of 2 cohorts, totaling 2888 BMT recipients with acute myeloid leukemia, acute lymphoblastic leukemia, or myelodysplastic syndrome, and their HLA-matched unrelated donors, reported to the Center for International Blood and Marrow Transplant Research. Gene-based tests were used to assess the aggregate effect of SNPs on outcome. None of the previously reported significant SNPs replicated at P 〈 .05 in DISCOVeRY-BMT. Validation analyses showed association with one previously reported donor SNP at P 〈 .05 and survival; more associations would be anticipated by chance alone. No gene-based tests were significant at P 〈 .05. Functional annotation with publicly available data shows these candidate SNPs most likely do not have biochemical function; only 13% of candidate SNPs correlate with gene expression or are predicted to impact transcription factor binding. Of these, half do not impact the candidate gene of interest; the other half correlate with expression of multiple genes. These findings emphasize the peril of pursing candidate approaches and the importance of adequately powered tests of unbiased genome-wide associations with BMT clinical outcomes given the ultimate goal of improving patient outcomes.
    Keywords: Transplantation
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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  • 6
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    Exosomal Wnt-induced dedifferentiation of colorectal cancer cells contributes to chemotherapy resistance (2018)
    Nature Publishing Group (NPG)
    In: Oncogene
    Details
    Publication Date: 2018-11-03
    Description: Exosomal Wnt-induced dedifferentiation of colorectal cancer cells contributes to chemotherapy resistance Exosomal Wnt-induced dedifferentiation of colorectal cancer cells contributes to chemotherapy resistance, Published online: 02 November 2018; doi:10.1038/s41388-018-0557-9 Exosomal Wnt-induced dedifferentiation of colorectal cancer cells contributes to chemotherapy resistance
    Print ISSN: 0950-9232
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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  • 7
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    Cardiomyocyte overexpression of the {alpha}1A-adrenergic receptor in the rat phenocopies second but not first window preconditioning (2012)
    The American Physiological Society (APS)
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    Publication Date: 2012-04-16
    Description: We examined α 1A -adrenergic receptor (AR) mediation of preconditioning in a novel α 1A -AR cardiac transgenic (TG) rat model (α 1A -TG). Compared with nontransgenic littermates (NTLs), in conscious α 1A -TG rats, heart rate was reduced, contractility [left ventricle (LV) +dP/d t , ejection fraction, end-systolic elastance] was significantly enhanced, and triple product (LV systolic wall stress x LV +dP/d t x heart rate) was unchanged. However, infarct size (IS)/area at risk (AAR) in response to ischemia-reperfusion (30 min coronary occlusion/3 h reperfusion) was reduced to 35 ± 4.6% in α 1A -TGs vs. 52 ± 2.2% in NTLs ( P 〈 0.05). Second window preconditioning reduced IS/AAR in NTLs to 29 ± 2.7% but did not afford further protection in α 1A -TGs. In contrast, with first window preconditioning, IS/AAR was reduced to similar levels in both α 1A -TGs (12 ± 1.4%) and NTLs (10 ± 1.1%). In untreated α 1A -TGs, cardioprotection was associated with enhanced myocardial phosphorylated (p)-mitogen/extracellular signal-regulated kinase (MEK), p-extracellular signal-regulated kinase (ERK), and inducible nitric oxide synthase (iNOS) at the protein level, along with a 1.3-fold increase in total nitric oxide synthase activity like in second window preconditioning. Affymetrix microarrays revealed that few genes (4.6% of 3,172 upregulated; 8.8% of 3,498 downregulated) showed directionally similar changes in α 1A -TGs vs. NTLs subjected to second window preconditioning. Thus, second, but not first, window cardioprotection is evident in α 1A -TGs in the absence of ischemic preconditioning and is mediated by iNOS activation associated with MEK/ERK phosphorylation. Transcriptionally, however, second window preconditioning is considerably more complex than α 1A -TG preconditioning, with the alteration of thousands of additional genes affording no further protection than that already available in α 1A -TG rats.
    Print ISSN: 0363-6135
    Electronic ISSN: 1522-1539
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 8
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    Prevention of heart failure in mice by an antiviral agent that inhibits type 5 cardiac adenylyl cyclase (2012)
    The American Physiological Society (APS)
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    Publication Date: 2012-06-16
    Description: Despite numerous discoveries from genetically engineered mice, relatively few have been translated to the bedside, mainly because it is difficult to translate from genes to drugs. This investigation examines an antiviral drug, which also has an action to selectively inhibit type 5 adenylyl cyclase (AC5), a pharmaceutical correlate of the AC5 knockout (KO) model, which exhibits longevity and stress resistance. Our objective was to examine the extent to which pretreatment with this drug, adenine 9-β- d -arabinofuranoside (Ara-A), favorably ameliorates the development of heart failure (HF). Ara-A exhibited selective inhibition for AC5 compared with the other major cardiac AC isoform, AC6, i.e., it reduced AC activity significantly in AC5 transgenic (Tg) mice, but not in AC5KO mice and had little effect in either wild-type or AC6Tg mice. Permanent coronary artery occlusion for 3 wk in C57Bl/6 mice increased mortality and induced HF in survivors, as reflected by reduced cardiac function, while increasing cardiac fibrosis. The AC5 inhibitor Ara-A significantly improved all of these end points and also ameliorated chronic isoproterenol-induced cardiomyopathy. As with the AC5KO mice, Ara-A increased mitogen/extracellular signal-regulated kinase (MEK)/extracellular signal-regulated kinase (ERK) phosphorylation. A MEK inhibitor abolished the beneficial effects of the AC5 inhibitor in the HF model, indicating the involvement of the downstream MEK-ERK pathway of AC5. Our data suggest that pharmacological AC5 inhibition may serve as a new therapeutic approach for HF.
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    Electronic ISSN: 1522-1539
    Topics: Medicine
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  • 9
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    Overexpression of adenylyl cyclase type 5 (AC5) confers a proarrhythmic substrate to the heart (2015)
    The American Physiological Society (APS)
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    Publication Date: 2015-02-02
    Description: Inhibition of β-adrenergic receptor (β-AR) signaling is one of the most common therapeutic approaches for patients with arrhythmias. Adenylyl cyclase (AC) is the key enzyme responsible for transducing β-AR stimulation to increases in cAMP. The two major AC isoforms in the heart are types 5 and 6. Therefore, it is surprising that prior studies on overexpression of AC5 and AC6 in transgenic (Tg) mice have not examined mediation of arrhythmogenesis. Our goal was to examine the proarrhythmic substrate in AC5Tg hearts. Intracellular calcium ion (Ca 2+ i ) was imaged in fluo-4 AM-loaded ventricular myocytes. The sarcoplasmic reticulum (SR) Ca 2+ content, fractional Ca 2+ release, and twitch Ca 2+ transient were significantly higher in the AC5Tg vs. wild-type (WT) myocytes, indicating Ca 2+ overload in AC5Tg myocytes. Action potential (AP) duration was significantly longer in AC5Tg than in WT myocytes. Additionally, AC5Tg myocytes developed spontaneous Ca 2+ waves in a larger fraction compared with WT myocytes, particularly when cells were exposed to isoproterenol. The Ca 2+ waves further induced afterdepolarizations and triggered APs. AC5Tg hearts had increased level of SERCA2a, oxidized Ca 2+ /calmodulin-dependent protein kinase II (CaMKII), and phosphorylation of ryanodine receptors (RyR) at the CaMKII site, especially after isoproterenol treatment. This was consistent with higher reactive oxygen species production in AC5Tg myocytes after isoproterenol treatment. Isoproterenol induced more severe arrhythmias in AC5Tg than in WT mice. We conclude that AC5 overexpression promotes arrhythmogenesis, by inducing SR Ca 2+ overload and hyperactivation of RyR (phosphorylation by CaMKII), which in turn induces spontaneous Ca 2+ waves and afterdepolarizations.
    Print ISSN: 0363-6135
    Electronic ISSN: 1522-1539
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 10
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    The impact of plasma epstein–barr virus DNA and fibrinogen on nasopharyngeal carcinoma prognosis: an observational study (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-09-11
    Description: The impact of plasma epstein–barr virus DNA and fibrinogen on nasopharyngeal carcinoma prognosis: an observational study British Journal of Cancer 111, 1102 (09 September 2014). doi:10.1038/bjc.2014.393 Authors: L-Q Tang, Q-Y Chen, S-S Guo, W-H Chen, C-F Li, L Zhang, X-P Lai, Y He, Y-X-X Xu, D-P Hu, S-H Wen, Y-T Peng, H Liu, L-T Liu, S-M Yan, L Guo, C Zhao, K-J Cao, Q Liu, C-N Qian, J Ma, X Guo, M-S Zeng & H-Q Mai
    Keywords: nasopharyngeal carcinomaEBV DNAfibrinogensurvival
    Print ISSN: 0007-0920
    Electronic ISSN: 1532-1827
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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