Increasing myocardial contraction and blood pressure  in C57BL/6 mice during early postnatal development

Tiemann, Klaus; Weyer, Dirk; Djoufack, Pierre Chryso; Ghanem, Alexander; Lewalter, Thorsten; Dreiner, Ulrike; Meyer, Rainer; Grohé, Christian; Fink, Klaus

doi:10.1152/ajpheart.00540.2002

Cited by 65 publications

(70 citation statements)

References 37 publications

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“…The postnatal arterial maturation of vSMC does not correlate with the temporal expression of the Notch ligands Jagged1 and Delta4 (data not shown). Instead, it parallels the increase in arterial blood pressure, which occurs during the first month after birth (Tiemann et al 2003). Thus, our current mechanistic hypothesis is that Notch3 may act as a sensor or transducer that affords vSMC the ability to rearrange the actin cytoskeleton in response to mechanical stretching of the vessel wall by the intraluminal blood pressure.…”

Section: Notch3mentioning

confidence: 89%

Notch3 is required for arterial identity and maturation of vascular smooth muscle cells

Domenga¹,

Fardoux²,

Lacombe³

et al. 2004

Genes Dev.

469

457

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Formation of a fully functional artery proceeds through a multistep process. Here we show that Notch3 is required to generate functional arteries in mice by regulating arterial differentiation and maturation of vascular smooth muscle cells (vSMC). In adult Notch3−/− mice distal arteries exhibit structural defects and arterial myogenic responses are defective. The postnatal maturation stage of vSMC is deficient in Notch3 −/− mice. We further show that Notch3 is required for arterial specification of vSMC but not of endothelial cells. Our data reveal Notch3 to be the first cell-autonomous regulator of arterial differentiation and maturation of vSMC.Supplemental material is available at http://www.genesdev.org.

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Section: Notch3mentioning

confidence: 89%

Notch3 is required for arterial identity and maturation of vascular smooth muscle cells

Domenga¹,

Fardoux²,

Lacombe³

et al. 2004

Genes Dev.

469

457

View full text Add to dashboard Cite

show abstract

“…The aortic sinus is not characteristically involved in human atherosclerosis. The very rapid heart rate (550 bpm in the mouse compared with 70 bpm in the average human) may account for this difference, 63 because flow in the murine aortic sinus is likely to be much more disrupted than in the human aortic sinus. Along these lines, Bassiouny and colleagues 64 have shown that heart rate is an important determinant of atherogenesis.…”

Section: Murine Atherosclerosis Mouse Modelsmentioning

confidence: 99%

Site Specificity of Atherosclerosis

VanderLaan

Reardon

Getz

2004

ATVB

499

213

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Abstract-Atherosclerosis is a complex disease process that affects very specific sites of the vasculature. It is recognized that hemodynamic forces are largely responsible for dictating which vascular sites are either susceptible or resistant to developing atherosclerosis. In addition, a number of systemic and local factors also modulate the pathogenesis of the disease. By studying the development of atherosclerosis in mice, investigators have gained insights into the molecular mechanisms of this disease, although studies have largely focused on a single vascular site. Here, we review those recent studies in which vascular site-specific effects on atherosclerosis were reported when more than 1 site was examined. We assess the hypothesis that regional differences in the hemodynamic profile prime the endothelial phenotype to respond distinctly to such systemic risk factors as hypercholesterolemia, genetics, immune status, gender, and oxidative stress. Because a given treatment may differentially affect the development of atherosclerotic lesions throughout the vasculature, the sites chosen for study are critically important. By accounting for the complex interplay of factors that may operate at these different sites, a more complete understanding of the overriding mechanisms that control the initiation and progression of the atherosclerotic lesion may be realized.

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“…Heart rate, P-wave duration, PR interval, QRS duration, QRS amplitude and QT interval were determined off-line as described recently ) on P5 using a commercially available ultrasound system (HDI 5000, Philips-Ultrasound, Bothell, WA) equipped with a 15 MHz linear array transducer. Volumetric analysis of left ventricular (LV) structures was performed to assess mass and function (Tiemann et al, 2003;Ghanem et al, 2005). Structures that are known to be prone to congenital defects in Cx43-deficient mice, in particular, the right-ventricular outflow tract, were investigated carefully by Bmode and pw-Doppler.…”

Section: Ecg Recording Of Neonatal Micementioning

confidence: 99%

Connexin31 cannot functionally replace connexin43 during cardiac morphogenesis in mice

Zheng-Fischhöfer

Ghanem

Kim

et al. 2006

Journal of Cell Science

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In the gastrulating mouse embryo, the gap junction protein connexin43 is expressed exclusively in cells derived from the inner cell mass, whereas connexin31 is expressed in cells of the trophoblast lineage. Since connexin43 and connexin31 do not form heterotypic gap junction channels in exogenous expression systems, such as HeLa cells and Xenopus oocytes, previous studies have suggested that the incompatibility of these two connexins could contribute to the separation of connexin43-expressing and connexin31-expressing compartments between embryo and extraembryonic tissues at gastrulation, respectively. Thus, we have generated connexin43 knock-in connexin31 mice, in which the coding region of the connexin43 gene was replaced by that of connexin31. Interbreeding of heterozygous connexin43 knock-in connexin31 mice resulted in homozygous connexin43 knock-in connexin31 mice, but none of them survived to adulthood. As these mice were born at the expected Mendelian frequency, we conclude that the reported incompatibility of connexin43 and connexin31 to form heterotypic gap junction channels does not interfere with normal embryonic development. Neonatal homozygous connexin43 knock-in connexin31 hearts showed malformation in the subpulmonary outlet of the right ventricle, similar to general connexin43-deficient mice. Electrocardiograms of neonatal hearts in homozygous connexin43 knock-in connexin31 mice revealed significantly low voltage of the QRS complex. This is in contrast to previous results from our laboratory which showed that replacement of connexin43 by connexin40 resulted in morphologically and functionally normal hearts. We conclude that connexin31 cannot functionally replace connexin43 during cardiac morphogenesis.

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Increasing myocardial contraction and blood pressure in C57BL/6 mice during early postnatal development

Cited by 65 publications

References 37 publications

Notch3 is required for arterial identity and maturation of vascular smooth muscle cells

Notch3 is required for arterial identity and maturation of vascular smooth muscle cells

Site Specificity of Atherosclerosis

Connexin31 cannot functionally replace connexin43 during cardiac morphogenesis in mice

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