Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Abstract: Congestive heart failure is the common endpoint of various cardiac diseases representing a leading cause of cardiovascular mortality in Western countries. Characteristic functional alterations of the failing heart are explained by expressional changes of myocardial regulatory proteins; however, little is known about underlying mechanisms regulating cardiac gene expression in the failing heart. Here, we address the specific role of transcription factor CREM for cardiac function in CREM mutant mice with complete inactivation of the CREM gene. We show that CREM mutant mice display distinct alterations of cardiac function resembling characteristic functional defects of the failing heart. Left ventricular hemodynamic assessment of CREM mutant mice revealed impairment of both cardiac contraction and relaxation in basal state, as well as a decreased responsiveness to beta-adrenergic stimulation. The diminished cardiac contractile performance was associated with a selective down-regulation of beta1-adrenergic receptors and a decreased ventricular expression of SERCA, the Ca2+-ATPase of the sarcoplasmic reticulum. The cardiac phenotype of CREM mutant mice provides the first evidence that CREM represents an important key regulator of cardiac gene expression, which is essential for normal left ventricular contractile performance and response to beta-adrenoreceptor stimulation.
    Type of Publication: Journal article published
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: APOPTOSIS ; EXPRESSION ; CELL ; Germany ; IN-VIVO ; MODEL ; PATHWAY ; VIVO ; SYSTEM ; GENE ; GENE-EXPRESSION ; PROTEIN ; PROTEINS ; transcription ; HEART ; MICE ; ACTIVATION ; DNA ; TRANSCRIPTION FACTOR ; BIOLOGY ; ELEMENT-BINDING PROTEIN ; RESPONSE ELEMENT ; TARGETED MUTATION ; TRANSGENIC MICE ; gene expression ; fragmentation ; inactivation ; SIGNALING PATHWAY ; MORPHOLOGY ; FAILURE ; CYCLIC-AMP ; REGULATOR ; Bcl-2 ; CASPASE ; signaling ; GENE-TRANSCRIPTION ; CARDIAC MYOCYTES ; KNOCKOUT MICE ; USA ; function ; caspases ; in vivo ; Cre-loxP system ; NUCLEAR-PROTEIN ; VENTRICULAR FUNCTION ; cAMP responsive element binding protein ; CONGESTIVE-HEART-FAILURE ; SOMATOSTATIN GENE
    Abstract: The transcription factor cAMP response element (CRE)-binding protein (CREB, Creb1) plays a critical role in regulating gene expression in response to activation of the cAMP-dependent signaling pathway, which is implicated in the pathophysiology of heart failure. Using the Cre-loxP system, we generated mice with a cardiomyocyte- specific inactivation of CREB and studied in this model whether CREB is critical for cardiac function. CREB-deficient mice were viable and displayed neither changes in cardiac morphology nor alterations of basal or isoproterenol-stimulated left ventricular function in vivo or of important cardiac regulatory proteins. Since CREB was proposed as a negative regulator of cardiomyocyte apoptosis by enhancing the expression of the antiapoptotic protein Bcl-2, we analyzed the fragmentation of DNA, the activity of caspases 3/7 and the expression of Bcl-2 and did not observe any differences between CREB-deficient and CREB- normal hearts. Our results suggest that the presence of CREB is not critical for normal cardiac function in mice.-Matus M., Lewin G., Stumpel F., Buchwalow I. B., Schneider M. D., Schutz G., Schmitz W., and Muller F. U. Cardiomyocyte-specific inactivation of transcription factor CREB in mice
    Type of Publication: Journal article published
    PubMed ID: 17307839
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: NEW-YORK ; transcription ; TRANSCRIPTION FACTOR ; MICE ; CREB ; DELETION
    Type of Publication: Meeting abstract published
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: EXPRESSION ; CELL-PROLIFERATION ; MESSENGER-RNA ; BETA-CELLS ; BINDING-PROTEIN ; FEEDBACK LOOP ; CAMP EARLY REPRESSOR ; RESPONSE ELEMENT MODULATOR ; TRANSCRIPTION FACTORS CREB ; AMP EARLY REPRESSOR
    Abstract: The transcription factors cAMP-responsive element binding protein (CREB) and cAMP-responsive element modulator (CREM) regulate gene transcription in response to elevated cAMP levels. The Crem isoform inducible cAMP early repressor (Icer) is transcribed by the internal promoter P2 as a critical regulator of multiple cellular processes. Here, we describe a novel inducible Crem isoform, small Icer (smIcer), regulated by a newly identified promoter (P6). ChIP revealed binding of CREB to P6 in human and mouse myocardium. P6 activity was induced by constitutively active CREB or stimulation of adenylyl cyclase. In mice, smIcer mRNA was ubiquitously expressed and transiently induced by beta-adrenoceptor stimulation e.g., in heart and lung. SmICER repressed both basal and cAMP-induced activities of P6 and P2 promoters. Stimulation of adenylyl cyclase induced P2 and P6 in cell type-specific manner. Alternative translational start sites resulted in three different smICER proteins, linked to increased apoptosis sensitivity. In conclusion, the Crem gene provides two distinct and mutually controlled mechanisms of a cAMP-dependent induction of transcriptional repressors. Our results suggest not only that smICER is a novel regulator of cAMP-mediated gene regulation, but also emphasize that biological effects that have been ascribed solely to ICER, should be revised with regard to smICER.
    Type of Publication: Journal article published
    PubMed ID: 24022402
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    ISSN: 1618-2650
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 1435-1803
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 300 μM Vanadat (NH4VO3) steigerte an isolierten, elektrisch gereizten Katzenpapillarmuskeln die Kontraktionskraft um ca. 65%. Der positiv inotrope Effekt (PIE) ging einher mit einem nur geringen (ca. 20%), aber signifikanten Anstieg des c-AMP-Gehaltes. 0.3 μM Isoprenalin (ISO) verursachte einen sehr viel größeren Anstieg des myokardialen c-AMP-Gehaltes (ca. 80%), während der PIE von ISO gleich groß war wie der PIE von NH4VO3. In einer Adenylatcyclasepräparation von rechten Ventrikeln des Katzenherzens stimulierten NH4VO3 und ISO die Adenylatcyclaseaktivität in nahezu gleichem Ausmaß. Propranolol (1 μM und 5 μM) verhinderte die Aktivierung der Adenylatcyclase durch ISO, aber nicht die Aktivierung durch NH4VO3. Die Phosphodiesteraseaktivität wurde durch NH4VO3 (bis zu einer Konzentration von 1000 μM) nicht beeinflußt. Aus den Ergebnissen wird geschlossen, daß der geringe vanadatinduzierte c-AMP-Anstieg, der über eine Stimulation der Adenylatcyclase zustande kommt, zwar am Zustandekommen des PIE beteiligt sein mag, daß aber andere Mechanismen von mindestens ebenso großer physiologischer Bedeutung sind.
    Notes: Summary 300 μM vanadate (NH4VO3) caused an about 65% increase in force of contraction in isolated electrically driven cat papillary muscles. The positive inotropic effect (PIE) was accompanied by only a small (about 20%) but significant increase in c-AMP levels. 0.3 μM isoprenaline (ISO) produced a much greater increase in c-AMP levels (about 80%) while the PIE of ISO was as great as the PIE observed with 300 μM NH4VO3. In cat right ventricular adenylate cyclase preparations NH4VO3 and ISO stimulated adenylate cyclase activity by nearly the same extent. Propranolol (1 μM and 5 μM) prevented the ISO-induced adenylate cyclase stimulation but not the stimulation due to NH4VO3. Phosphodiesterase activity was not affected by NH4VO3 (up to 1000 μM). It is concluded that the small vanadate-induced increase in c-AMP levels, which is due to adenylate cyclase stimulation, inintact papillary muscles maycontribute to its PIE, but other mechanisms may be at least equally important.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Langenbeck's archives of surgery 313 (1965), S. 812-818 
    ISSN: 1435-2451
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    ISSN: 1435-2451
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zusammenfassung In Abhängigkeit von Sitz, Durchmesser und Zeitdauer des Kurzschlusses führen arterio-venöse Fisteln im Laufe von Monaten oder Jahren infolge zunehmender Volumen- und Druckbelastung zur kardialen und vasculären Dekompensation. Unter 200 an der Chirurg. Univ.-Klinik Heidelberg behandelten arterio-venösen Fisteln wird an Hand einer traumatisch entstandenen, 52 Jahre bestehenden Kurzschlußverbindung am Ellenbogen die Bedeutung des Zeitfaktors für die Entstehung pathologischer Herz- und Kreislaufveränderungen diskutiert. Die Entfernung der Fistel führte bei dem 75jährigen Patienten zu einer weitgehenden klinischen Besserung der bestehenden kardialen Dekompensation, zu einer Verkleinerung des Herzdurchmessers um 3,5 cm und zu einer altersentsprechenden Normalisierung der Lungenfunktionswerte. Das Herzminutenvolumen sank von 7,9 auf 4,1 l postoperativ.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    ISSN: 1435-2451
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    ISSN: 1435-2451
    Keywords: Resection of Aneurysm of the left Ventricle ; Blunt Chest Trauma ; Coronary Angiography ; Intermittent Obstruction of Coronary Artery ; Ventrikelaneurysmaresektion ; Stumpfes Thoraxtrauma ; Coronaro-graphie ; Intermittierender Coronarverachluß
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Ein Aneurysms des linken Ventrikels verursachte einen intermittierenden systolischen Verschluß eines Astes der linken Coronararterie bei einem 26jährigen Bauschlosser. Er wurde 6 1/2 Wochen nach stumpfem Thoraxtrauma wegen plötzlicher starker pektangionöser Beschwerden in die Klinik wieder aufgenommen. Das Aneurysms wurde mit Hilfe der Herz-Lungenmaschine erfolgreich reseziert. Postoperativ war der Coronararterienast systolisch and diastolisch frei durchgängig.
    Notes: Summary An aneurysm of the left ventricle that led to intermittent systolic obstruction of a branch of the left coronary artery was revealed by angiography studies in a 26-year-old locksmith. Because of severe Angina pectoris, which started suddenly 6 1/2 weeks after a blunt chest injury, he was readmitted to the hospital. The aneurysm was resected successfully with the aid of cardiopulmonary by-pass. Postoperative coronary angiography showed normal flow in the previously intermittently obstructed branch of the left coronary artery.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...