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Heparan sulfate expression in the neural crest is essential for mouse cardiogenesis

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Heparan sulfate expression in the neural crest is essential for mouse cardiogenesis. / Pan, Yi; Carbe, Christian; Kupich, Sabine; Pickhinke, Ute; Ohlig, Stefanie; Frye, Maike; Seelige, Ruth; Pallerla, Srinivas R; Moon, Anne M; Lawrence, Roger; Esko, Jeffrey D; Zhang, Xin; Grobe, Kay.

in: MATRIX BIOL, Jahrgang 35, 04.2014, S. 253-65.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Pan, Y, Carbe, C, Kupich, S, Pickhinke, U, Ohlig, S, Frye, M, Seelige, R, Pallerla, SR, Moon, AM, Lawrence, R, Esko, JD, Zhang, X & Grobe, K 2014, 'Heparan sulfate expression in the neural crest is essential for mouse cardiogenesis', MATRIX BIOL, Jg. 35, S. 253-65. https://doi.org/10.1016/j.matbio.2013.10.013

APA

Pan, Y., Carbe, C., Kupich, S., Pickhinke, U., Ohlig, S., Frye, M., Seelige, R., Pallerla, S. R., Moon, A. M., Lawrence, R., Esko, J. D., Zhang, X., & Grobe, K. (2014). Heparan sulfate expression in the neural crest is essential for mouse cardiogenesis. MATRIX BIOL, 35, 253-65. https://doi.org/10.1016/j.matbio.2013.10.013

Vancouver

Pan Y, Carbe C, Kupich S, Pickhinke U, Ohlig S, Frye M et al. Heparan sulfate expression in the neural crest is essential for mouse cardiogenesis. MATRIX BIOL. 2014 Apr;35:253-65. https://doi.org/10.1016/j.matbio.2013.10.013

Bibtex

@article{b85e64ab64c1400a893b9402ea29f56e,
title = "Heparan sulfate expression in the neural crest is essential for mouse cardiogenesis",
abstract = "Impaired heparan sulfate (HS) synthesis in vertebrate development causes complex malformations due to the functional disruption of multiple HS-binding growth factors and morphogens. Here, we report developmental heart defects in mice bearing a targeted disruption of the HS-generating enzyme GlcNAc N-deacetylase/GlcN N-sulfotransferase 1 (NDST1), including ventricular septal defects (VSD), persistent truncus arteriosus (PTA), double outlet right ventricle (DORV), and retroesophageal right subclavian artery (RERSC). These defects closely resemble cardiac anomalies observed in mice made deficient in the cardiogenic regulator fibroblast growth factor 8 (FGF8). Consistent with this, we show that HS-dependent FGF8/FGF-receptor2C assembly and FGF8-dependent ERK-phosphorylation are strongly reduced in NDST1(-/-) embryonic cells and tissues. Moreover, WNT1-Cre/LoxP-mediated conditional targeting of NDST function in neural crest cells (NCCs) revealed that their impaired HS-dependent development contributes strongly to the observed cardiac defects. These findings raise the possibility that defects in HS biosynthesis may contribute to congenital heart defects in humans that represent the most common type of birth defect. ",
keywords = "Animals, DNA Primers/genetics, Double Outlet Right Ventricle/genetics, Fibroblast Growth Factor 8/genetics, Heart/embryology, Heart Defects, Congenital/genetics, Heart Septal Defects, Ventricular/genetics, Heparitin Sulfate/biosynthesis, Immunohistochemistry, Mice, Mice, Knockout, Neural Crest/embryology, Organogenesis/physiology, Reverse Transcriptase Polymerase Chain Reaction, Subclavian Artery/abnormalities, Sulfotransferases/genetics, Truncus Arteriosus, Persistent/genetics",
author = "Yi Pan and Christian Carbe and Sabine Kupich and Ute Pickhinke and Stefanie Ohlig and Maike Frye and Ruth Seelige and Pallerla, {Srinivas R} and Moon, {Anne M} and Roger Lawrence and Esko, {Jeffrey D} and Xin Zhang and Kay Grobe",
note = "Copyright {\textcopyright} 2013 International Society of Matrix Biology. All rights reserved.",
year = "2014",
month = apr,
doi = "10.1016/j.matbio.2013.10.013",
language = "English",
volume = "35",
pages = "253--65",
journal = "MATRIX BIOL",
issn = "0945-053X",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Heparan sulfate expression in the neural crest is essential for mouse cardiogenesis

AU - Pan, Yi

AU - Carbe, Christian

AU - Kupich, Sabine

AU - Pickhinke, Ute

AU - Ohlig, Stefanie

AU - Frye, Maike

AU - Seelige, Ruth

AU - Pallerla, Srinivas R

AU - Moon, Anne M

AU - Lawrence, Roger

AU - Esko, Jeffrey D

AU - Zhang, Xin

AU - Grobe, Kay

N1 - Copyright © 2013 International Society of Matrix Biology. All rights reserved.

PY - 2014/4

Y1 - 2014/4

N2 - Impaired heparan sulfate (HS) synthesis in vertebrate development causes complex malformations due to the functional disruption of multiple HS-binding growth factors and morphogens. Here, we report developmental heart defects in mice bearing a targeted disruption of the HS-generating enzyme GlcNAc N-deacetylase/GlcN N-sulfotransferase 1 (NDST1), including ventricular septal defects (VSD), persistent truncus arteriosus (PTA), double outlet right ventricle (DORV), and retroesophageal right subclavian artery (RERSC). These defects closely resemble cardiac anomalies observed in mice made deficient in the cardiogenic regulator fibroblast growth factor 8 (FGF8). Consistent with this, we show that HS-dependent FGF8/FGF-receptor2C assembly and FGF8-dependent ERK-phosphorylation are strongly reduced in NDST1(-/-) embryonic cells and tissues. Moreover, WNT1-Cre/LoxP-mediated conditional targeting of NDST function in neural crest cells (NCCs) revealed that their impaired HS-dependent development contributes strongly to the observed cardiac defects. These findings raise the possibility that defects in HS biosynthesis may contribute to congenital heart defects in humans that represent the most common type of birth defect.

AB - Impaired heparan sulfate (HS) synthesis in vertebrate development causes complex malformations due to the functional disruption of multiple HS-binding growth factors and morphogens. Here, we report developmental heart defects in mice bearing a targeted disruption of the HS-generating enzyme GlcNAc N-deacetylase/GlcN N-sulfotransferase 1 (NDST1), including ventricular septal defects (VSD), persistent truncus arteriosus (PTA), double outlet right ventricle (DORV), and retroesophageal right subclavian artery (RERSC). These defects closely resemble cardiac anomalies observed in mice made deficient in the cardiogenic regulator fibroblast growth factor 8 (FGF8). Consistent with this, we show that HS-dependent FGF8/FGF-receptor2C assembly and FGF8-dependent ERK-phosphorylation are strongly reduced in NDST1(-/-) embryonic cells and tissues. Moreover, WNT1-Cre/LoxP-mediated conditional targeting of NDST function in neural crest cells (NCCs) revealed that their impaired HS-dependent development contributes strongly to the observed cardiac defects. These findings raise the possibility that defects in HS biosynthesis may contribute to congenital heart defects in humans that represent the most common type of birth defect.

KW - Animals

KW - DNA Primers/genetics

KW - Double Outlet Right Ventricle/genetics

KW - Fibroblast Growth Factor 8/genetics

KW - Heart/embryology

KW - Heart Defects, Congenital/genetics

KW - Heart Septal Defects, Ventricular/genetics

KW - Heparitin Sulfate/biosynthesis

KW - Immunohistochemistry

KW - Mice

KW - Mice, Knockout

KW - Neural Crest/embryology

KW - Organogenesis/physiology

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Subclavian Artery/abnormalities

KW - Sulfotransferases/genetics

KW - Truncus Arteriosus, Persistent/genetics

U2 - 10.1016/j.matbio.2013.10.013

DO - 10.1016/j.matbio.2013.10.013

M3 - SCORING: Journal article

C2 - 24200809

VL - 35

SP - 253

EP - 265

JO - MATRIX BIOL

JF - MATRIX BIOL

SN - 0945-053X

ER -