Database : MEDLINE
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[PMID]: 29361616
[Au] Autor:Shioyama W
[Ad] Address:Dept. of Cardiovascular Medicine, Onco-Cardiology Unit, Osaka International Cancer Institute, Osaka Prefectural Hospital Organization.
[Ti] Title:[Onco-Cardiology - From the Standpoint of Cardiology].
[So] Source:Gan To Kagaku Ryoho;44(13):2052-2057, 2017 Dec.
[Is] ISSN:0385-0684
[Cp] Country of publication:Japan
[La] Language:jpn
[Ab] Abstract:In Japan, cardiovascular diseases are frequent complications in cancer patients owing to the rapidly aging population and changes in the overall lifestyle. In addition, new anticancer therapies have substantially improved the prognosis of cancer patients. Cardiotoxicity, also referred to as cancer treatment-related cardiac dysfunction, has become an important cause of morbidity and mortality in cancer patients. Cardiotoxicity may consist of hypertension, arrhythmia, thromboembolism, coronary artery disease, valvular disease, and left ventricular dysfunction which may progress to heart failure. Close interactions between cardiologists and oncologists are required for the optimal care of many cancer patients. Although cardiologists are expected to assist and advise the oncologist by providing diagnostic and prognostic information regarding developing cardiotoxicity, little is known about the cardiovascular pathogenic mechanisms associated with cancer treatment. Onco-cardiology is a medical subspecialty that focuses on the diagnosis and treatment of cardiotoxicity in cancer patients. This review describes the concept of onco-cardiology, and focuses on the management of cardiotoxicity that may arise during or after cancer therapy from the standpoint of cardiology. We also discuss noninvasive diagnostic options to identify and characterize cardiotoxicity.
[Mh] MeSH terms primary: Antineoplastic Agents/adverse effects
Cardiotoxins/adverse effects
Cardiovascular Diseases/chemically induced
Neoplasms/drug therapy
[Mh] MeSH terms secundary: Antineoplastic Agents/therapeutic use
Biomarkers/blood
Cardiotoxins/therapeutic use
Cardiovascular Diseases/complications
Humans
Risk Factors
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Biomarkers); 0 (Cardiotoxins)
[Em] Entry month:1803
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[Js] Journal subset:IM
[Da] Date of entry for processing:180124
[St] Status:MEDLINE

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[PMID]: 29364903
[Au] Autor:Sala A; Cabassi CS; Santospirito D; Polverini E; Flisi S; Cavirani S; Taddei S
[Ad] Address:Department of Veterinary Science, University of Parma, Parma, Italy.
[Ti] Title:Novel Naja atra cardiotoxin 1 (CTX-1) derived antimicrobial peptides with broad spectrum activity.
[So] Source:PLoS One;13(1):e0190778, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Naja atra subsp. atra cardiotoxin 1 (CTX-1), produced by Chinese cobra snakes, belonging to Elapidae family, is included in the three-finger toxin family and exerts high cytotoxicity and antimicrobial activity too. Using as template mainly the tip and the subsequent ß-strand of the first "finger" of this toxin, different sequences of 20 amino acids linear peptides have been designed in order to avoid toxic effects but to maintain or even strengthen the partial antimicrobial activity already seen for the complete toxin. As a result, the sequence NCP-0 (Naja Cardiotoxin Peptide-0) was designed as ancestor and subsequently 4 other variant sequences of NCP-0 were developed. These synthesized variant sequences have shown microbicidal activity towards a panel of reference and field strains of Gram-positive and Gram-negative bacteria. The sequence named NCP-3, and its variants NCP-3a and NCP-3b, have shown the best antimicrobial activity, together with low cytotoxicity against eukaryotic cells and low hemolytic activity. Bactericidal activity has been demonstrated by minimum bactericidal concentration (MBC) assay at values below 10 µg/ml for most of the tested bacterial strains. This potent antimicrobial activity was confirmed even for unicellular fungi Candida albicans, Candida glabrata and Malassezia pachydermatis (MBC 50-6.3 µg/ml), and against the fast-growing mycobacteria Mycobacterium smegmatis and Mycobacterium fortuitum. Moreover, NCP-3 has shown virucidal activity on Bovine Herpesvirus 1 (BoHV1) belonging to Herpesviridae family. The bactericidal activity is maintained even in a high salt concentration medium (125 and 250 mM NaCl) and phosphate buffer with 20% Mueller Hinton (MH) medium against E. coli, methicillin resistant Staphylococcus aureus (MRSA) and Pseudomonas aeruginosa reference strains. Considering these in vitro obtained data, the search for active sequences within proteins presenting an intrinsic microbicidal activity could provide a new way for discovering a large number of novel and promising antimicrobial peptides families.
[Mh] MeSH terms primary: Anti-Infective Agents/pharmacology
Cobra Cardiotoxin Proteins/chemistry
Peptides/pharmacology
[Mh] MeSH terms secundary: Amino Acid Sequence
Animals
Anti-Infective Agents/chemistry
Candida/drug effects
Cattle
Circular Dichroism
Hemolysis/drug effects
Herpesvirus 1, Bovine/drug effects
Malassezia/drug effects
Microbial Sensitivity Tests
Mycobacterium/drug effects
Naja naja
Peptides/chemistry
Protein Conformation
Sheep
Staphylococcus aureus/drug effects
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Anti-Infective Agents); 0 (Cobra Cardiotoxin Proteins); 0 (Peptides)
[Em] Entry month:1802
[Cu] Class update date: 180221
[Lr] Last revision date:180221
[Js] Journal subset:IM
[Da] Date of entry for processing:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190778

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[PMID]: 29284479
[Au] Autor:Afsar T; Razak S; Batoo KM; Khan MR
[Ad] Address:Department of Biochemistry, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. tayyaba_sona@yahoo.com.
[Ti] Title:Acacia hydaspica R. Parker prevents doxorubicin-induced cardiac injury by attenuation of oxidative stress and structural Cardiomyocyte alterations in rats.
[So] Source:BMC Complement Altern Med;17(1):554, 2017 Dec 29.
[Is] ISSN:1472-6882
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The use of doxorubicin (DOX) an anthracycline antineoplastic agent is withdrawn due to its cardio-toxic side effects. Oxidative stress has been recognized as the primary cause of DOX induced cardiotoxicity. We have investigated whether polyphenol rich ethyl acetate extract of Acacia hydaspica (AHE) can attenuate doxorubicin-induced cardiotoxicity via inhibition of oxidative stress. METHODS: AHE was administered orally to rats once daily for 6 weeks at doses of 200 and 400 mg/kg b.w. DOX (3 mg/kg b.w. i.p., single dose/week) was administered for 6 weeks (chronic model). The parameters studied to evaluate cardioprotective potential were the serum cardiac function biomarkers (CK, CKMB, AST and LDH), hematological parameters, cardiac tissue antioxidant enzymatic status and oxidative stress markers, and histopathological analysis to validate biochemical findings. RESULTS: Chronic 6 week treatment of DOX significantly deteriorated cardiac function biomarkers and decreased the activities of antioxidant enzymes, whereas significant increase in oxidative stress biomarkers was noticed in comparison to control group. AHE dose dependently protected DOX-induced leakage of cardiac enzymes in serum and ameliorated DOX-induced oxidative stress; as evidenced by decreasing lipid peroxidation, H O and NO content with increase in phase I and phase II antioxidant enzymes. Doxorubicin treatment produced severe morphological lesions, leucopenia, decrease in red blood cell counts and hemoglobin concentrations. AHE co-treatment protected the heart and blood elements from the toxic effects of doxorubicin as indicated by the recovery of hematological parameters to normal values and prevention of myocardial injuries in a dose dependent way. The protective potency of AHE (400 mg/kg b.w) was equivalent to silymarin. CONCLUSION: Results revealed that AHE showed protective effects against DOX induce cardiotoxicity. The protective effect might attribute to its polyphenolic constituents and antioxidant properties. AHE might be helpful in combination therapies as safer and efficient.
[Mh] MeSH terms primary: Acacia/chemistry
Antioxidants/pharmacology
Cardiotoxins/toxicity
Doxorubicin/toxicity
Myocytes, Cardiac/drug effects
Oxidative Stress/drug effects
Plant Extracts/pharmacology
[Mh] MeSH terms secundary: Animals
Antioxidants/chemistry
Biomarkers/blood
Heart/drug effects
Male
Plant Extracts/chemistry
Polyphenols/chemistry
Polyphenols/pharmacology
Rats
Rats, Sprague-Dawley
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antioxidants); 0 (Biomarkers); 0 (Cardiotoxins); 0 (Plant Extracts); 0 (Polyphenols); 80168379AG (Doxorubicin)
[Em] Entry month:1801
[Cu] Class update date: 180122
[Lr] Last revision date:180122
[Js] Journal subset:IM
[Da] Date of entry for processing:171230
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-2061-0

  4 / 995 MEDLINE  
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[PMID]: 29189742
[Au] Autor:Urra FA; Araya-Maturana R
[Ad] Address:Anatomy and Developmental Biology Program, Institute of Biomedical Sciences, University of Chile, Independencia 1027, Casilla 7, Santiago 7800003, Chile. felix.urra@qf.uchile.cl.
[Ti] Title:Targeting Metastasis with Snake Toxins: Molecular Mechanisms.
[So] Source:Toxins (Basel);9(12), 2017 Nov 30.
[Is] ISSN:2072-6651
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Metastasis involves the migration of cancer cells from a primary tumor to invade and establish secondary tumors in distant organs, and it is the main cause for cancer-related deaths. Currently, the conventional cytostatic drugs target the proliferation of malignant cells, being ineffective in metastatic disease. This highlights the need to find new anti-metastatic drugs. Toxins isolated from snake venoms are a natural source of potentially useful molecular scaffolds to obtain agents with anti-migratory and anti-invasive effects in cancer cells. While there is greater evidence concerning the mechanisms of cell death induction of several snake toxin classes on cancer cells; only a reduced number of toxin classes have been reported on (i.e., disintegrins/disintegrin-like proteins, C-type lectin-like proteins, C-type lectins, serinproteases, cardiotoxins, snake venom cystatins) as inhibitors of adhesion, migration, and invasion of cancer cells. Here, we discuss the anti-metastatic mechanisms of snake toxins, distinguishing three targets, which involve (1) inhibition of extracellular matrix components-dependent adhesion and migration, (2) inhibition of epithelial-mesenchymal transition, and (3) inhibition of migration by alterations in the actin/cytoskeleton network.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1712
[Cu] Class update date: 180101
[Lr] Last revision date:180101
[St] Status:In-Process

  5 / 995 MEDLINE  
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[PMID]: 29183371
[Au] Autor:Attarde SS; Pandit SV
[Ad] Address:Department of Zoology, Savitribai Phule Pune University, Ganeshkhind, Pune, Maharashtra, 411007, India.
[Ti] Title:Cytotoxic activity of NN-32 toxin from Indian spectacled cobra venom on human breast cancer cell lines.
[So] Source:BMC Complement Altern Med;17(1):503, 2017 Nov 28.
[Is] ISSN:1472-6882
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Breast cancer is the most common cancer which causes significant morbidity and mortality among women worldwide. Lack of medical facilities for early detection, therapeutic strategies for treatment and side effects due to pharmacological compounds have encompassed the need for new therapies mostly from natural sources. A lot of components have been identified from different snake venoms as therapeutic agents. A group of polypeptides (60-70 amino acid residues) called cytotoxins or cardiotoxins present in an elapid family of snakes have a wide variety of pharmaceutical actions and have the tendency to damage a wide variety of cells including cancerous cells. The aim of the present study was to evaluate the cytotoxic effect of NN-32 protein toxin purified from Indian Spectacled Cobra venom against human breast cancer cell lines (MCF-7 and MDA-MB-231). METHODS: The NN-32 toxin was purified by ion exchange chromatography and further by RP-HPLC. The potential anticancer effects of the NN-32 toxin on MCF-7 and MDA-MB-231 cells were evaluated using MTT, anti-proliferation, neutral red (NR) uptake and Lactate Dehydrogenase (LDH) release assay. RESULTS: The ion exchange chromatography showed various peaks among fraction no. 35 showing cytotoxic activity and this fraction showed a single peak with retention time 3.6 mins by HPLC using C18 column. The NN-32 toxin induced cytotoxicity in MCF-7 and MDA-MB-231 cells with the IC value of 2.5 and 6.7 µg/ml respectively. The NN-32 showed significant cytotoxicity to both the cell lines along with low cytotoxicity to MCF-10A (normal breast epithelial) cells. The cytotoxic effect was further confirmed by the anti-proliferative, NR uptake and LDH release assays. CONCLUSION: The purified toxin NN-32 from Naja naja venom showed cytotoxic activity against MCF-7 (ER+) and MDA-MB-231(ER-) cells in both dose dependent and time dependent manner.
[Mh] MeSH terms primary: Antineoplastic Agents/pharmacology
Elapid Venoms/pharmacology
Naja naja
[Mh] MeSH terms secundary: Animals
Antineoplastic Agents/chemistry
Antineoplastic Agents/isolation & purification
Breast Neoplasms
Cell Line, Tumor
Cell Proliferation/drug effects
Elapid Venoms/chemistry
Humans
MCF-7 Cells
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Elapid Venoms)
[Em] Entry month:1712
[Cu] Class update date: 171219
[Lr] Last revision date:171219
[Js] Journal subset:IM
[Da] Date of entry for processing:171130
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-2018-3

  6 / 995 MEDLINE  
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[PMID]: 29073951
[Au] Autor:Lipshultz SE; Wilkinson JD; Thompson B; Cheng I; Briston DA; Shearer WT; Orav EJ; Westphal JA; Miller TL; Colan SD; CHAART-2 Investigator Group
[Ad] Address:Wayne State University School of Medicine, Detroit, Michigan; Children's Hospital of Michigan, Detroit, Michigan. Electronic address: slipshultz@med.wayne.edu.
[Ti] Title:Cardiac Effects of Highly Active Antiretroviral Therapy in Perinatally HIV-Infected Children: The CHAART-2 Study.
[So] Source:J Am Coll Cardiol;70(18):2240-2247, 2017 Oct 31.
[Is] ISSN:1558-3597
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Before the introduction of highly active antiretroviral therapy (HAART), cardiac mortality and morbidity were common in HIV-infected children. OBJECTIVES: This study sought to identify long-term cardiovascular effects of HAART in HIV-infected children. METHODS: The CHAART-2 (HAART-Associated Cardiotoxicity in HIV-Infected Children) study prospectively compared 148 echocardiograms from 74 HAART-exposed children to 860 echocardiograms from 140 HAART-unexposed but HIV-infected children from the Pulmonary and Cardiac Complications of Vertically Transmitted HIV Infection (P C HIV) study. Both studies used similar protocol, centralized echocardiographic interpretation, and measures expressed as z-scores referenced to healthy controls. Associations between HAART exposure and echocardiographic measures were evaluated using generalized estimating equations. RESULTS: Comparing the HAART-exposed and HAART-unexposed groups, any HAART exposure was positively associated with left ventricular (LV) fractional shortening (z-score for difference = 1.07; p = 0.02) and HAART exposure duration (z-score difference per year = 0.17; p = 0.003. LV mass was negatively associated with any HAART exposure (z-score difference = -0.64; p = 0.01) as was septal thickness (z-score difference = -0.93; p = 0.001). Duration of HAART exposure was negatively associated with LV end-systolic dimension and heart rate (z-score difference per year= -0.11; p = 0.05; and z-score difference per year = -0.10; p = 0.002, respectively). During 11 years of follow-up, in the HAART-exposed group, LV mass and LV end-diastolic septal thickness were lower whereas LV contractility and LV fractional shortening were higher when compared to the HAART-unexposed group. CONCLUSIONS: Cardiac structure and function were better in perinatally HIV-infected children exposed to HAART than in those of similar children from the pre-HAART era but did decline over time. Evidence-based strategies for cardiovascular monitoring are needed to inform treatment decisions to improve long-term cardiovascular health.
[Mh] MeSH terms primary: Antiretroviral Therapy, Highly Active/trends
Cardiotoxins/administration & dosage
HIV Infections/diagnostic imaging
HIV Infections/drug therapy
Perinatal Care/trends
[Mh] MeSH terms secundary: Adolescent
Adult
Antiretroviral Therapy, Highly Active/adverse effects
Cardiotoxins/adverse effects
Child
Child, Preschool
Cohort Studies
Cross-Sectional Studies
Female
Follow-Up Studies
Humans
Hypertrophy, Left Ventricular/chemically induced
Hypertrophy, Left Ventricular/diagnostic imaging
Hypertrophy, Left Ventricular/prevention & control
Longitudinal Studies
Male
Perinatal Care/methods
Pregnancy
Prospective Studies
Single-Blind Method
Ventricular Dysfunction, Left/chemically induced
Ventricular Dysfunction, Left/diagnostic imaging
Ventricular Dysfunction, Left/prevention & control
[Pt] Publication type:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Name of substance:0 (Cardiotoxins)
[Em] Entry month:1711
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:171028
[St] Status:MEDLINE

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[PMID]: 29053272
[Au] Autor:Konshina AG; Krylov NA; Efremov RG
[Ad] Address:Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences , 16/10 Miklukho-Maklaya str., 117997 GSP, Moscow V-437, Russia.
[Ti] Title:Cardiotoxins: Functional Role of Local Conformational Changes.
[So] Source:J Chem Inf Model;, 2017 Nov 03.
[Is] ISSN:1549-960X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cardiotoxins (CTs) from snake venoms are a family of homologous highly basic proteins that have extended hydrophobic patterns on their molecular surfaces. CTs are folded into three ß-structured loops stabilized by four disulfide bridges. Being well-structured in aqueous solution, most of these proteins are membrane-active, although the exact molecular mechanisms of CT-induced cell damage are still poorly understood. To elucidate the structure-function relationships in CTs, a detailed knowledge of their spatial organization and local conformational dynamics is required. Protein domain motions can be either derived from a set of experimental structures or generated via molecular dynamics (MD). At the same time, traditional clustering algorithms in the Cartesian coordinate space often fail to properly take into account the local large-scale dihedral angle transitions that occur in MD simulations. This is because such perturbations are usually offset by changes in the neighboring dihedrals, thus preserving the overall protein fold. States with a "locally perturbed" backbone were found in experimental 3D models of some globular proteins and have been shown to be functionally meaningful. In this work, the possibility of large-scale dihedral angle transitions in the course of long-term MD in explicit water was explored for three CTs with different membrane activities: CT 1, 2 (Naja oxiana) and CT A3 (Naja atra). Analysis of the MD-derived distributions of backbone torsion angles revealed several important common and specific features in the structural/dynamic behavior of these proteins. First, large-amplitude transitions were detected in some residues located in the functionally important loop I region. The K5/L6 pair of residues was found to induce a perturbation of the hydrophobic patterns on the molecular surface of CTs-reversible breaking of a large nonpolar zone ("bottom") into two smaller ones and their subsequent association. Second, the characteristic sizes of these patterns perfectly coincided with the dimensions of the nonpolar zones on the surfaces of model two-component (zwitterionic/anionic) membranes. Taken together with experimental data on the CT-induced leakage of fluorescent dye from such membranes, these results allowed us to formulate a two-stage mechanism of CT-membrane binding. The principal finding of this study is that even local conformational dynamics of CTs can seriously affect their functional activity via a tuning of the membrane binding site - specific "hot spots" (like the K5/L6 pair) in the protein structure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:Publisher
[do] DOI:10.1021/acs.jcim.7b00395

  8 / 995 MEDLINE  
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[PMID]: 28854256
[Au] Autor:Debaud C; Salga M; Begot L; Holy X; Chedik M; de l'Escalopier N; Torossian F; Levesque JP; Lataillade JJ; Le Bousse-Kerdilès MC; Genêt F
[Ad] Address:Spine Division Orthopaedic Surgery Department, Hôpital Européen Georges Pompidou, APHP, Paris, France.
[Ti] Title:Peripheral denervation participates in heterotopic ossification in a spinal cord injury model.
[So] Source:PLoS One;12(8):e0182454, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We previously reported the development of a new acquired neurogenic HO (NHO) mouse model, combining spinal cord transection (SCI) and chemical muscle injury. Pathological mechanisms responsible for ectopic osteogenesis after central neurological damage are still to be elucidated. In this study, we first hypothesized that peripheral nervous system (PNS) might convey pathological signals from injured spinal cord to muscles in NHO mouse model. Secondly, we sought to determine whether SCI could lead to intramuscular modifications of BMP2 signaling pathways. Twenty one C57Bl6 mice were included in this protocol. Bilateral cardiotoxin (CTX) injection in hamstring muscles was associated with a two-stage surgical procedure, combining thoracic SCI with unilateral peripheral denervation. Volumes of HO (Bone Volume, BV) were measured 28 days after surgery using micro-computed tomography imaging techniques and histological analyses were made to confirm intramuscular osteogenesis. Volume comparisons were conducted between right and left hind limb of each animal, using a Wilcoxon signed rank test. Quantitative polymerase chain reaction (qPCR) was performed to explore intra muscular expression of BMP2, Alk3 and Id1. Nineteen mice survive the complete SCI and peripheral denervation procedure. When CTX injections were done right after surgery (n = 7), bilateral HO were detected in all animals after 28 days. Micro-CT measurements showed significantly increased BV in denervated paws (1.47 mm3 +/- 0.5) compared to contralateral sides (0.56 mm3 +/-0.4), p = 0.03. When peripheral denervation and CTX injections were performed after sham SCI surgery (n = 6), bilateral HO were present in three mice at day 28. Quantitative PCR analyses showed no changes in intra muscular BMP2 expression after SCI as compared to control mice (shamSCI). Peripheral denervation can be reliably added to spinal cord transection in NHO mouse model. This new experimental design confirms that neuro inflammatory mechanisms induced by central or peripheral nervous system injury plays a key role in triggering ectopic osteogenesis.
[Mh] MeSH terms primary: Muscles/pathology
Ossification, Heterotopic/pathology
Spinal Cord Injuries/pathology
Spinal Cord/pathology
[Mh] MeSH terms secundary: Animals
Bone Morphogenetic Protein 2/analysis
Cobra Cardiotoxin Proteins
Denervation
Disease Models, Animal
Female
Mice, Inbred C57BL
Muscles/drug effects
Muscles/innervation
Ossification, Heterotopic/chemically induced
Ossification, Heterotopic/diagnostic imaging
Ossification, Heterotopic/etiology
Spinal Cord/diagnostic imaging
Spinal Cord/drug effects
Spinal Cord Injuries/chemically induced
Spinal Cord Injuries/diagnostic imaging
Spinal Cord Injuries/etiology
X-Ray Microtomography
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Bone Morphogenetic Protein 2); 0 (Cobra Cardiotoxin Proteins)
[Em] Entry month:1710
[Cu] Class update date: 171013
[Lr] Last revision date:171013
[Js] Journal subset:IM
[Da] Date of entry for processing:170831
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182454

  9 / 995 MEDLINE  
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[PMID]: 28362317
[Au] Autor:Tang Z; Liu N; Luo L; Kang K; Li L; Ni R; Qiu H; Gou D
[Ad] Address:Shenzhen Key Laboratory of Microbial Genetic Engineering, College of Life Sciences, Shenzhen University, Shenzhen 518060, China. zhizhi0719s@163.com.
[Ti] Title:MicroRNA-17-92 Regulates the Transcription Factor E2F3b during Myogenesis In Vitro and In Vivo.
[So] Source:Int J Mol Sci;18(4), 2017 Mar 31.
[Is] ISSN:1422-0067
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Myogenic differentiation, which occurs during muscle development, is a highly ordered process that can be regulated by E2F transcription factors. Available data show that E2F3b, but not E2F3a, is upregulated and required for myogenic differentiation. However, the regulation of E2F3b expression in myogenic differentiation is not well understood. To investigate whether E2Fb expression is controlled by miRNAs, we used bioinformatics to combine the database of microRNAs downregulated during myogenesis and those predicted to target E2F3. This identified miR-17 and miR-20a as miRNAs potentially involved in E2F3 regulation. We found that miR-17-92 controls the expression of E2F3b in C2C12 cells during myogenic differentiation. Moreover, we confirmed that miR-20a regulates the expression of E2F3b proteins in vivo using a muscle regeneration model.
[Mh] MeSH terms primary: E2F3 Transcription Factor/genetics
MicroRNAs/genetics
Muscle Development/genetics
Myoblasts/metabolism
[Mh] MeSH terms secundary: 3' Untranslated Regions/genetics
Animals
Cardiotoxins
Cell Differentiation/genetics
Cell Line
E2F3 Transcription Factor/metabolism
Gene Expression Regulation, Developmental
HEK293 Cells
Humans
Immunoblotting
Male
Mice, Inbred C57BL
Microscopy, Fluorescence
Muscle Development/physiology
Muscular Diseases/chemically induced
Muscular Diseases/physiopathology
Myoblasts/cytology
Regeneration/genetics
Reverse Transcriptase Polymerase Chain Reaction
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (3' Untranslated Regions); 0 (Cardiotoxins); 0 (E2F3 Transcription Factor); 0 (E2f3 protein, mouse); 0 (MIRN17-92 microRNA, mouse); 0 (MicroRNAs)
[Em] Entry month:1706
[Cu] Class update date: 170601
[Lr] Last revision date:170601
[Js] Journal subset:IM
[Da] Date of entry for processing:170401
[St] Status:MEDLINE

  10 / 995 MEDLINE  
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[PMID]: 28358805
[Au] Autor:Di Biase S; Shim HS; Kim KH; Vinciguerra M; Rappa F; Wei M; Brandhorst S; Cappello F; Mirzaei H; Lee C; Longo VD
[Ad] Address:Longevity Institute, Leonard Davis School of Gerontology and Department of Biological Sciences, University of Southern California, Los Angeles, California, United States of America.
[Ti] Title:Fasting regulates EGR1 and protects from glucose- and dexamethasone-dependent sensitization to chemotherapy.
[So] Source:PLoS Biol;15(3):e2001951, 2017 Mar.
[Is] ISSN:1545-7885
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Fasting reduces glucose levels and protects mice against chemotoxicity, yet drugs that promote hyperglycemia are widely used in cancer treatment. Here, we show that dexamethasone (Dexa) and rapamycin (Rapa), commonly administered to cancer patients, elevate glucose and sensitize cardiomyocytes and mice to the cancer drug doxorubicin (DXR). Such toxicity can be reversed by reducing circulating glucose levels by fasting or insulin. Furthermore, glucose injections alone reversed the fasting-dependent protection against DXR in mice, indicating that elevated glucose mediates, at least in part, the sensitizing effects of rapamycin and dexamethasone. In yeast, glucose activates protein kinase A (PKA) to accelerate aging by inhibiting transcription factors Msn2/4. Here, we show that fasting or glucose restriction (GR) regulate PKA and AMP-activated protein kinase (AMPK) to protect against DXR in part by activating the mammalian Msn2/4 ortholog early growth response protein 1 (EGR1). Increased expression of the EGR1-regulated cardioprotective peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in heart tissue may also contribute to DXR resistance. Our findings suggest the existence of a glucose-PKA pathway that inactivates conserved zinc finger stress-resistance transcription factors to sensitize cells to toxins conserved from yeast to mammals. Our findings also describe a toxic role for drugs widely used in cancer treatment that promote hyperglycemia and identify dietary interventions that reverse these effects.
[Mh] MeSH terms primary: Antineoplastic Agents/pharmacology
Dexamethasone/pharmacology
Early Growth Response Protein 1/metabolism
Fasting/metabolism
Glucose/pharmacology
[Mh] MeSH terms secundary: AMP-Activated Protein Kinases/metabolism
Animals
Atrial Natriuretic Factor/metabolism
Cardiotoxins/toxicity
Cyclic AMP-Dependent Protein Kinases/metabolism
Cytoprotection/drug effects
Diet
Female
Hyperglycemia/pathology
Metformin/pharmacology
Mice
Mice, Inbred C57BL
Natriuretic Peptide, Brain/metabolism
Stress, Physiological/drug effects
Time Factors
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Cardiotoxins); 0 (Early Growth Response Protein 1); 114471-18-0 (Natriuretic Peptide, Brain); 7S5I7G3JQL (Dexamethasone); 85637-73-6 (Atrial Natriuretic Factor); 9100L32L2N (Metformin); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.31 (AMP-Activated Protein Kinases); IY9XDZ35W2 (Glucose)
[Em] Entry month:1706
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:IM
[Da] Date of entry for processing:170331
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2001951


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