Vascular effects of endothelin-1 in stage 21 chick embryos

Kajio, Fusae; Nakazawa, Makoto

doi:10.1007/bf02766807

Cited by 9 publications

(6 citation statements)

References 28 publications

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“…Our µPIV data do not show changes in veins smaller than 100 µm. Larger veins between 100 and 200 µm were reported [38] to show a response to ET-1 in the HH21 chicken embryo, although we have not been able to confirm this, as veins with a diameter larger than 100 µm are not optically accessible.…”

Section: Discussioncontrasting

confidence: 44%

The Endothelin-1 Pathway and the Development of Cardiovascular Defects in the Haemodynamically Challenged Chicken Embryo

Groenendijk

Vos²,

Vennemann³

et al. 2007

J Vasc Res

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Background/Aims: Ligating the right lateral vitelline vein of chicken embryos (venous clip) results in cardiovascular malformations. These abnormalities are similar to malformations observed in knockout mice studies of components of the endothelin-1 (ET-1)/endothelin-converting enzyme-1/endothelin-A receptor pathway. In previous studies we demonstrated that cardiac ET-1 expression is decreased 3 h after clipping, and ventricular diastolic filling is disturbed after 2 days. Therefore, we hypothesise that ET-1-related processes are involved in the development of functional and morphological cardiovascular defects after venous clip. Methods: In this study, ET-1 and endothelin receptor antagonists (BQ-123, BQ-788 and PD145065) were infused into the HH18 embryonic circulation. Immediate haemodynamic effects on the embryonic heart and extra-embryonic vitelline veins were examined by Doppler and micro-particle image velocimetry. Ventricular diastolic filling characteristics were studied at HH24, followed by cardiovascular morphologic investigation (HH35). Results: ET-1 and its receptor antagonists induced haemodynamic effects at HH18. At HH24, a reduced diastolic ventricular passive filling component was demonstrated, which was compensated by an increased active filling component. Thinner ventricular myocardium was shown in 42% of experimental embryos. Conclusion: We conclude that cardiovascular malformations after venous clipping arise from a combination of haemodynamic changes and altered gene expression patterns and levels, including those of the endothelin pathway.

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Section: Discussioncontrasting

confidence: 44%

The Endothelin-1 Pathway and the Development of Cardiovascular Defects in the Haemodynamically Challenged Chicken Embryo

Groenendijk

Vos²,

Vennemann³

et al. 2007

J Vasc Res

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“…The abnormal early melanocytic development resulting from these mutations in the neural-crest cells is mediated through endothelin, a G-protein– coupled receptor. 20 Since endothelin also has important roles in vasculogenesis, 21 dysregulation of this G-protein–coupled receptor as a result of the G α q p.Arg183Gln mutation in persons with the Sturge–Weber syndrome and those with nonsyndromic port-wine stains may also bring about vascular malformation.…”

Section: Discussionmentioning

confidence: 99%

“…We hypothesize that only the weaker effect of somatic G α q p.Arg183Gln would be compatible with the abnormal but nonlethal development of the cerebrovascular system seen in the Sturge–Weber syndrome. We also hypothesize that during vulnerable periods in embryonic development, moderately increased baseline signaling downstream of G α q , or dysregulated signaling through G-protein–coupled receptors such as that for endothelin, 21 may result in the malformed, progressively dilated, and abnormally innervated blood vessels underlying port-wine stains. There is some evidence in the literature to support this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Sturge–Weber Syndrome and Port-Wine Stains Caused by Somatic Mutation inGNAQ

et al. 2013

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BACKGROUND The Sturge–Weber syndrome is a sporadic congenital neurocutaneous disorder characterized by a port-wine stain affecting the skin in the distribution of the ophthalmic branch of the trigeminal nerve, abnormal capillary venous vessels in the leptomeninges of the brain and choroid, glaucoma, seizures, stroke, and intellectual disability. It has been hypothesized that somatic mosaic mutations disrupting vascular development cause both the Sturge–Weber syndrome and port-wine stains, and the severity and extent of presentation are determined by the developmental time point at which the mutations occurred. To date, no such mutation has been identified. METHODS We performed whole-genome sequencing of DNA from paired samples of visibly affected and normal tissue from 3 persons with the Sturge–Weber syndrome. We tested for the presence of a somatic mosaic mutation in 97 samples from 50 persons with the Sturge–Weber syndrome, a port-wine stain, or neither (controls), using amplicon sequencing and SNaPshot assays, and investigated the effects of the mutation on downstream signaling, using phosphorylation-specific antibodies for relevant effectors and a luciferase reporter assay. RESULTS We identified a nonsynonymous single-nucleotide variant (c.548G→A, p.Arg183Gln) in GNAQ in samples of affected tissue from 88% of the participants (23 of 26) with the Sturge–Weber syndrome and from 92% of the participants (12 of 13) with apparently nonsyndromic port-wine stains, but not in any of the samples of affected tissue from 4 participants with an unrelated cerebrovascular malformation or in any of the samples from the 6 controls. The prevalence of the mutant allele in affected tissues ranged from 1.0 to 18.1%. Extracellular signal-regulated kinase activity was modestly increased during transgenic expression of mutant Gαq. CONCLUSIONS The Sturge–Weber syndrome and port-wine stains are caused by a somatic activating mutation in GNAQ. This finding confirms a long-standing hypothesis. (Funded by the National Institutes of Health and Hunter’s Dream for a Cure Foundation.)

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“…Induction of gene expression by the binding of transcription factors to a SSRE would eventually give rise to changes in levels of, e.g., endothelin‐1 or NO, which are vasoactive substances in adults. Likewise, exogenous ET‐1 in embryos is involved in vasoconstriction (Kajio and Nakazawa, 1997). Shear related gene expression, therefore, is to be expected in embryos.…”

Section: Discussionmentioning

confidence: 99%

Development‐related changes in the expression of shear stress responsive genes KLF‐2, ET‐1, and NOS‐3 in the developing cardiovascular system of chicken embryos

Groenendijk¹,

Hierck²,

Groot³

et al. 2004

Developmental Dynamics

116

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Blood flow patterns play an important role in cardiovascular development, as changes can cause congenital heart malformations. Shear stress is positively correlated to blood flow. Therefore, it is likely that shear stress is also involved in cardiac development. In this study, we investigated the expression patterns of ET-1, NOS-3, and KLF-2 mRNA in a series of developmental stages of the chicken embryo. These genes are reported to be shear responsive. It has been demonstrated that KLF-2 is confined to areas of high shear stress in the adult human aorta. From in vitro studies, it is known that ET-1 is down-regulated by shear stress, whereas NOS-3 is up-regulated. Therefore, we expect ET-1 to be low or absent and NOS-3 to be high at sites where KLF-2 expression is high. Our study shows that, in the early stages, expression patterns are mostly not shear stress-related, whereas during development, this correlation becomes stronger. We demonstrate overlapping expression patterns of KLF-2 and NOS-3 in the narrow parts of the cardiovascular system, like the cardiac inflow tract, the atrioventricular canal, outflow tract, and in the early stages in the aortic sac and the pharyngeal arch arteries. In these regions, the expression patterns of KLF-2 and NOS-3 exclude that of ET-1. Our results suggest that, in the embryonic cardiovascular system, KLF-2 is expressed in regions of highest shear stress, and that ET-1 and NOS-3 expression, at least in the later stages, is related to shear stress. Developmental Dynamics 230:57-68, 2004.

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Vascular effects of endothelin-1 in stage 21 chick embryos

Cited by 9 publications

References 28 publications

The Endothelin-1 Pathway and the Development of Cardiovascular Defects in the Haemodynamically Challenged Chicken Embryo

The Endothelin-1 Pathway and the Development of Cardiovascular Defects in the Haemodynamically Challenged Chicken Embryo

Sturge–Weber Syndrome and Port-Wine Stains Caused by Somatic Mutation inGNAQ

Development‐related changes in the expression of shear stress responsive genes KLF‐2, ET‐1, and NOS‐3 in the developing cardiovascular system of chicken embryos

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