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  1. Article ; Online: Evaluation and Management of Noncardiac Comorbidities in Children With Congenital Heart Disease.

    Chowdhury, Devyani / Toms, Rune / Brumbaugh, Jane E / Bindom, Sharell / Ather, Mishaal / Jaquiss, Robert / Johnson, Jonathan N

    Pediatrics

    2022  Volume 150, Issue Suppl 2

    Abstract: Outcomes for patients with neonatal heart disease are affected by numerous noncardiac and genetic factors. These can include neonatal concerns, such as prematurity and low birth weight, and congenital anomalies, such as airway, pulmonary, ... ...

    Abstract Outcomes for patients with neonatal heart disease are affected by numerous noncardiac and genetic factors. These can include neonatal concerns, such as prematurity and low birth weight, and congenital anomalies, such as airway, pulmonary, gastrointestinal, and genitourinary anomalies, and genetic syndromes. This section will serve as a summary of these issues and how they may affect the evaluation and management of a neonate with heart disease. These noncardiac factors are heavily influenced by conditions common to neonatologists, making a strong argument for multidisciplinary care with neonatologists, cardiologists, surgeons, anesthesiologists, and cardiovascular intensivists. Through this section and this project, we aim to facilitate a comprehensive approach to the care of neonates with congenital heart disease.
    MeSH term(s) Infant, Newborn ; Child ; Humans ; Heart Defects, Congenital/surgery ; Infant, Premature, Diseases ; Comorbidity ; Lung
    Language English
    Publishing date 2022-11-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 207677-9
    ISSN 1098-4275 ; 0031-4005
    ISSN (online) 1098-4275
    ISSN 0031-4005
    DOI 10.1542/peds.2022-056415E
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The sweeter side of ACE2: physiological evidence for a role in diabetes.

    Bindom, Sharell M / Lazartigues, Eric

    Molecular and cellular endocrinology

    2008  Volume 302, Issue 2, Page(s) 193–202

    Abstract: Diabetes mellitus is a growing problem in all parts of the world. Both clinical trials and animal models of type I and type II diabetes have shown that hyperactivity of angiotensin-II (Ang-II) signaling pathways contribute to the development of diabetes ... ...

    Abstract Diabetes mellitus is a growing problem in all parts of the world. Both clinical trials and animal models of type I and type II diabetes have shown that hyperactivity of angiotensin-II (Ang-II) signaling pathways contribute to the development of diabetes and diabetic complications. Of clinical relevance, blockade of the renin-angiotensin system prevents new-onset diabetes and reduces the risk of diabetic complications. Angiotensin-converting enzyme (ACE) 2 is a recently discovered mono-carboxypeptidase and the first homolog of ACE. It is thought to inhibit Ang-II signaling cascades mostly by cleaving Ang-II to generate Ang-(1-7), which effects oppose Ang-II and are mediated by the Mas receptor. The enzyme is present in the kidney, liver, adipose tissue and pancreas. Its expression is elevated in the endocrine pancreas in diabetes and in the early phase during diabetic nephropathy. ACE2 is hypothesized to act in a compensatory manner in both diabetes and diabetic nephropathy. Recently, we have shown the presence of the Mas receptor in the mouse pancreas and observed a reduction in Mas receptor immuno-reactivity as well as higher fasting blood glucose levels in ACE2 knockout mice, indicating that these mice may be a new model to study the role of ACE2 in diabetes. In this review we will examine the role of the renin-angiotensin system in the physiopathology and treatment of diabetes and highlight the potential benefits of the ACE2/Ang-(1-7)/Mas receptor axis, focusing on recent data about ACE2.
    MeSH term(s) Angiotensin I/metabolism ; Animals ; Diabetes Mellitus/etiology ; Humans ; Insulin Resistance ; Peptide Fragments/metabolism ; Peptidyl-Dipeptidase A/physiology ; Proto-Oncogene Proteins/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Renin-Angiotensin System
    Chemical Substances Peptide Fragments ; Proto-Oncogene Proteins ; Receptors, G-Protein-Coupled ; proto-oncogene proteins c-mas-1 ; Angiotensin I (9041-90-1) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; angiotensin converting enzyme 2 (EC 3.4.17.-) ; angiotensin I (1-7) (IJ3FUK8MOF)
    Keywords covid19
    Language English
    Publishing date 2008-10-01
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2008.09.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Angiotensin I-converting enzyme type 2 (ACE2) gene therapy improves glycemic control in diabetic mice.

    Bindom, Sharell M / Hans, Chetan P / Xia, Huijing / Boulares, A Hamid / Lazartigues, Eric

    Diabetes

    2010  Volume 59, Issue 10, Page(s) 2540–2548

    Abstract: ... and methods: Both db/db and nondiabetic lean control (db/m) mice were infected with an adenovirus ... insulin sensitivity in both Ad-hACE2-eGFP- and Ad-eGFP-treated db/db mice. D-Ala(7)-Ang-(1-7) had no effect on db/m ...

    Abstract Objective: Several clinical studies have shown the benefits of renin-angiotensin system (RAS) blockade in the development of diabetes, and a local RAS has been identified in pancreatic islets. Angiotensin I-converting enzyme (ACE)2, a new component of the RAS, has been identified in the pancreas, but its role in β-cell function remains unknown. Using 8- and 16-week-old obese db/db mice, we examined the ability of ACE2 to alter pancreatic β-cell function and thereby modulate hyperglycemia.
    Research design and methods: Both db/db and nondiabetic lean control (db/m) mice were infected with an adenovirus expressing human ACE2 (Ad-hACE2-eGFP) or the control virus (Ad-eGFP) via injection into the pancreas. Glycemia and β-cell function were assessed 1 week later at the peak of viral expression.
    Results: In 8-week-old db/db mice, Ad-hACE2-eGFP significantly improved fasting glycemia, enhanced intraperitoneal glucose tolerance, increased islet insulin content and β-cell proliferation, and reduced β-cell apoptosis compared with Ad-eGFP. ACE2 overexpression had no effect on insulin sensitivity in comparison with Ad-eGFP treatment in diabetic mice. Angiotensin-(1-7) receptor blockade by D-Ala(7)-Ang-(1-7) prevented the ACE2-mediated improvements in intraperitoneal glucose tolerance, glycemia, and islet function and also impaired insulin sensitivity in both Ad-hACE2-eGFP- and Ad-eGFP-treated db/db mice. D-Ala(7)-Ang-(1-7) had no effect on db/m mice. In 16-week-old diabetic mice, Ad-hACE2-eGFP treatment improved fasting blood glucose but had no effect on any of the other parameters.
    Conclusions: These findings identify ACE2 as a novel target for the prevention of β-cell dysfunction and apoptosis occurring in type 2 diabetes.
    MeSH term(s) Angiotensin-Converting Enzyme 2 ; Animals ; Apoptosis ; Blood Glucose/metabolism ; Cell Division ; Diabetes Mellitus, Experimental/blood ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/therapy ; Gene Expression Regulation, Enzymologic ; Genes, Reporter ; Genetic Therapy/methods ; Glucose Tolerance Test ; Green Fluorescent Proteins/genetics ; Homeostasis ; Humans ; Insulin/metabolism ; Islets of Langerhans/metabolism ; Islets of Langerhans/pathology ; Islets of Langerhans/physiopathology ; Mice ; Mice, Transgenic ; Obesity/complications ; Pancreas/enzymology ; Pancreas/pathology ; Pancreas/physiopathology ; Peptidyl-Dipeptidase A/genetics ; Peptidyl-Dipeptidase A/metabolism
    Chemical Substances Blood Glucose ; Insulin ; Green Fluorescent Proteins (147336-22-9) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Ace2 protein, mouse (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Language English
    Publishing date 2010-07-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db09-0782
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: c-Myc is required for the CHREBP-dependent activation of glucose-responsive genes.

    Zhang, Pili / Metukuri, Mallikarjurna R / Bindom, Sharell M / Prochownik, Edward V / O'Doherty, Robert M / Scott, Donald K

    Molecular endocrinology (Baltimore, Md.)

    2010  Volume 24, Issue 6, Page(s) 1274–1286

    Abstract: Glucose regulates programs of gene expression that orchestrate changes in cellular phenotype in several metabolically active tissues. Carbohydrate response element-binding protein (ChREBP) and its binding partner, Mlx, mediate glucose-regulated gene ... ...

    Abstract Glucose regulates programs of gene expression that orchestrate changes in cellular phenotype in several metabolically active tissues. Carbohydrate response element-binding protein (ChREBP) and its binding partner, Mlx, mediate glucose-regulated gene expression by binding to carbohydrate response elements on target genes, such as the prototypical glucose-responsive gene, liver-type pyruvate kinase (Pklr). c-Myc is also required for the glucose response of the Pklr gene, although the relationship between c-Myc and ChREBP has not been defined. Here we describe the molecular events of the glucose-mediated activation of Pklr and determine the effects of decreasing the activity or abundance of c-Myc on this process. Time-course chromatin immunoprecipitation revealed a set of transcription factors [hepatocyte nuclear factor (HNF)1alpha, HNF4alpha, and RNA polymerase II (Pol II)] constitutively resident on the Pklr promoter, with a relative enrichment of acetylated histones 3 and 4 in the same region of the gene. Glucose did not affect HNF1alpha binding or the acetylation of histones H3 or H4. By contrast, glucose promoted the recruitment of ChREBP and c-Myc and increased the occupancy of HNF4alpha and RNA Pol II, which were coincident with the glucose-mediated increase in transcription as determined by a nuclear run-on assay. Depletion of c-Myc activity using a small molecule inhibitor (10058-F4/1RH) abolished the glucose-mediated recruitment of HNF4alpha, ChREBP, and RNA Pol II, without affecting basal gene expression, histone acetylation, and HNF1alpha or basal HNF4alpha occupancy. The activation and recruitment of ChREBP to several glucose-responsive genes were blocked by 1RH, indicating a general necessity for c-Myc in this process.
    MeSH term(s) Animals ; Base Sequence ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Binding Sites ; Cell Line, Tumor ; Glucose/pharmacology ; Humans ; Islets of Langerhans/drug effects ; Islets of Langerhans/metabolism ; Liver/drug effects ; Liver/enzymology ; Models, Genetic ; Molecular Sequence Data ; Organ Specificity/drug effects ; Promoter Regions, Genetic/genetics ; Protein Binding/drug effects ; Proto-Oncogene Proteins c-myc/metabolism ; Pyruvate Kinase/genetics ; Rats ; Thiazoles/pharmacology ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects ; Transcriptional Activation/drug effects
    Chemical Substances 5-(4-ethylbenzylidene)-2-thioxothiazolidin-4-one ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Max protein, rat ; Mlxipl protein, rat ; Proto-Oncogene Proteins c-myc ; Thiazoles ; Transcription Factors ; Pyruvate Kinase (EC 2.7.1.40) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2010-04-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 639167-9
    ISSN 1944-9917 ; 0888-8809
    ISSN (online) 1944-9917
    ISSN 0888-8809
    DOI 10.1210/me.2009-0437
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Angiotensin-converting enzyme 2 overexpression in the subfornical organ prevents the angiotensin II-mediated pressor and drinking responses and is associated with angiotensin II type 1 receptor downregulation.

    Feng, Yumei / Yue, Xinping / Xia, Huijing / Bindom, Sharell M / Hickman, Peter J / Filipeanu, Catalin M / Wu, Guangyu / Lazartigues, Eric

    Circulation research

    2008  Volume 102, Issue 6, Page(s) 729–736

    Abstract: We recently reported the presence of angiotensin-converting enzyme (ACE)2 in brain regions controlling cardiovascular function; however, the role of ACE2 in blood pressure regulation remains unclear because of the lack of specific tools to investigate ... ...

    Abstract We recently reported the presence of angiotensin-converting enzyme (ACE)2 in brain regions controlling cardiovascular function; however, the role of ACE2 in blood pressure regulation remains unclear because of the lack of specific tools to investigate its function. We hypothesized that ACE2 could play a pivotal role in the central regulation of cardiovascular function by regulating other renin-angiotensin system components. To test this hypothesis, we generated an adenovirus expressing the human ACE2 cDNA upstream of an enhanced green fluorescent protein (eGFP) reporter gene (Ad-hACE2-eGFP). In vitro characterization shows that neuronal cells infected with Ad-hACE2-eGFP (10 to 100 multiplicities of infection), but not Ad-eGFP (100 multiplicities of infection), exhibit dose-dependent ACE2 expression and activity. In addition, an active secreted form was detected in the conditioned medium. In vivo, Ad-hACE2-eGFP infection (2x10(6) plaque-forming units intracerebroventricularly) produced time-dependent expression and activity (with a peak at 7 days) in the mouse subfornical organ. More importantly, 7 days after virus infection, the pressor response to angiotensin (Ang) II (200 pmol intracerebroventricularly) was significantly reduced in Ad-hACE2-eGFP-treated mice compared with controls. Furthermore, subfornical organ-targeted ACE2 overexpression dramatically reduced the Ang II-mediated drinking response. Interestingly, ACE2 overexpression was associated with downregulation of the Ang II type 1 receptor expression both in vitro and in vivo. These data suggest that ACE2 overexpression in the subfornical organ impairs Ang II-mediated pressor and drinking responses at least by inhibiting the Ang II type 1 receptor expression. Taken together, our results show that ACE2 plays a pivotal role in the central regulation of blood pressure and volume homeostasis, offering a new target for the treatment of hypertension and other cardiovascular diseases.
    MeSH term(s) Adenoviridae/drug effects ; Angiotensin II/administration & dosage ; Angiotensin II/metabolism ; Angiotensin-Converting Enzyme 2 ; Animals ; Baroreflex/drug effects ; Blood Pressure ; Cell Line, Tumor ; Culture Media/metabolism ; Down-Regulation ; Drinking Behavior/drug effects ; Genes, Reporter ; Genetic Vectors ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Heart Rate ; Humans ; Injections, Intraventricular ; Mice ; Mice, Inbred C57BL ; Neurons/enzymology ; Neurons/metabolism ; Peptidyl-Dipeptidase A/genetics ; Peptidyl-Dipeptidase A/metabolism ; Receptor, Angiotensin, Type 1/agonists ; Receptor, Angiotensin, Type 1/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Subfornical Organ/drug effects ; Subfornical Organ/enzymology ; Subfornical Organ/metabolism ; Time Factors ; Transduction, Genetic ; Up-Regulation
    Chemical Substances Culture Media ; Receptor, Angiotensin, Type 1 ; Recombinant Fusion Proteins ; enhanced green fluorescent protein ; Angiotensin II (11128-99-7) ; Green Fluorescent Proteins (147336-22-9) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Ace2 protein, mouse (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Language English
    Publishing date 2008-02-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.107.169110
    Database MEDical Literature Analysis and Retrieval System OnLINE

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