Repression of Sox9 by Jag1 is continuously required to suppress the default chondrogenic fate of vascular smooth muscle cells
| Autor: | Carsten Rudat, Matteo Pellegrini, Marlin Touma, Jennifer J. Hofmann, Carmen M. Warren, Rannar Airik, Karen M. Lyons, Andreas Kispert, Jing Lu, M. Luisa Iruela-Arispe, Gerry Weinmaster, Yibin Wang, Anaïs Briot, Artur Jaroszewicz |
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| Rok vydání: | 2014 |
| Předmět: |
Male
Vascular smooth muscle Time Factors Cardiovascular Ligands Medical and Health Sciences Muscle Smooth Vascular Mice Smooth Muscle Receptors Myocyte Developmental Serrate-Jagged Proteins Receptors Notch Gene Expression Regulation Developmental SOX9 Transcription Factor Biological Sciences musculoskeletal system Active Transport Cell biology Heart Disease cardiovascular system Muscle Intercellular Signaling Peptides and Proteins Female Smooth Sequence Analysis Chondrogenesis Signal Transduction Muscle Contraction medicine.medical_specialty JAG1 Notch 1.1 Normal biological development and functioning Myocytes Smooth Muscle Notch signaling pathway Active Transport Cell Nucleus Cartilage metabolism Biology General Biochemistry Genetics and Molecular Biology Article Chondrocytes Internal medicine Vascular medicine Animals Cell Lineage Molecular Biology Transcription factor Heart Disease - Coronary Heart Disease Cell Nucleus Myocytes Sequence Analysis RNA Calcium-Binding Proteins Membrane Proteins Cell Biology Endocrinology Cartilage Gene Expression Regulation Jagged-1 Protein RNA Transcription Factors Developmental Biology |
| Zdroj: | Developmental cell, vol 31, iss 6 Briot, A; Jaroszewicz, A; Warren, CM; Lu, J; Touma, M; Rudat, C; et al.(2014). Repression of Sox9 by Jag1 is continuously required to suppress the default chondrogenic fate of vascular smooth muscle cells. Developmental Cell, 31(6), 707-721. doi: 10.1016/j.devcel.2014.11.023. UCLA: Retrieved from: http://www.escholarship.org/uc/item/66x666mp |
| DOI: | 10.1016/j.devcel.2014.11.023. |
| Popis: | © 2014 Elsevier Inc. Acquisition and maintenance of vascular smooth muscle fate are essential for the morphogenesis and function of the circulatory system. Loss of contractile properties or changes in the identity of vascular smooth muscle cells (vSMCs) can result in structural alterations associated with aneurysms and vascular wall calcification. Here we report that maturation of sclerotome-derived vSMCs depends on a transcriptional switch between mouse embryonic days 13 and 14.5. At this time, Notch/Jag1-mediated repression of sclerotome transcription factors Pax1, Scx, and Sox9 is necessary tofully enable vSMC maturation. Specifically, Notch signaling in vSMCs antagonizes sclerotome and cartilage transcription factors and promotes upregulation of contractile genes. In the absence of the Notch ligand Jag1, vSMCs acquire a chondrocytic transcriptional repertoire that can lead to ossification. Importantly, our findings suggest that sustained Notch signaling is essential throughout vSMC life to maintain contractile function, prevent vSMC reprogramming, and promote vascular wall integrity. |
| Databáze: | OpenAIRE |
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