MAFB modulates the maturation of lymphatic vascular networks in mice.


Journal

Developmental dynamics : an official publication of the American Association of Anatomists
ISSN: 1097-0177
Titre abrégé: Dev Dyn
Pays: United States
ID NLM: 9201927

Informations de publication

Date de publication:
10 2020
Historique:
received: 23 04 2020
accepted: 18 05 2020
pubmed: 12 6 2020
medline: 3 11 2021
entrez: 12 6 2020
Statut: ppublish

Résumé

Lymphatic vessels play key roles in tissue fluid homeostasis, immune cell trafficking and in diverse disease settings. Lymphangiogenesis requires lymphatic endothelial cell (LEC) differentiation, proliferation, migration, and co-ordinated network formation, yet the transcriptional regulators underpinning these processes remain to be fully understood. The transcription factor MAFB was recently identified as essential for lymphangiogenesis in zebrafish and in cultured human LECs. MAFB is activated in response to VEGFC-VEGFR3 signaling and acts as a downstream effector. However, it remains unclear if the role of MAFB in lymphatic development is conserved in the mammalian embryo. We generated a Mafb loss-of-function mouse using CRISPR/Cas9 gene editing. Mafb mutant mice presented with perinatal lethality associated with cyanosis. We identify a role for MAFB in modifying lymphatic network morphogenesis in the developing dermis, as well as developing and postnatal diaphragm. Furthermore, mutant vessels displayed excessive smooth muscle cell coverage, suggestive of a defect in the maturation of lymphatic networks. This work confirms a conserved role for MAFB in murine lymphatics that is subtle and modulatory and may suggest redundancy in MAF family transcription factors during lymphangiogenesis.

Sections du résumé

BACKGROUND
Lymphatic vessels play key roles in tissue fluid homeostasis, immune cell trafficking and in diverse disease settings. Lymphangiogenesis requires lymphatic endothelial cell (LEC) differentiation, proliferation, migration, and co-ordinated network formation, yet the transcriptional regulators underpinning these processes remain to be fully understood. The transcription factor MAFB was recently identified as essential for lymphangiogenesis in zebrafish and in cultured human LECs. MAFB is activated in response to VEGFC-VEGFR3 signaling and acts as a downstream effector. However, it remains unclear if the role of MAFB in lymphatic development is conserved in the mammalian embryo.
RESULTS
We generated a Mafb loss-of-function mouse using CRISPR/Cas9 gene editing. Mafb mutant mice presented with perinatal lethality associated with cyanosis. We identify a role for MAFB in modifying lymphatic network morphogenesis in the developing dermis, as well as developing and postnatal diaphragm. Furthermore, mutant vessels displayed excessive smooth muscle cell coverage, suggestive of a defect in the maturation of lymphatic networks.
CONCLUSIONS
This work confirms a conserved role for MAFB in murine lymphatics that is subtle and modulatory and may suggest redundancy in MAF family transcription factors during lymphangiogenesis.

Identifiants

pubmed: 32525258
doi: 10.1002/dvdy.209
doi:

Substances chimiques

MafB Transcription Factor 0
Mafb protein, mouse 0
RNA, Messenger 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1201-1216

Subventions

Organisme : National Health and Medical Research Council
ID : 1083811
Pays : International
Organisme : National Health and Medical Research Council
ID : 1107755
Pays : International

Informations de copyright

© 2020 Wiley Periodicals LLC.

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Auteurs

Maria Rondon-Galeano (M)

Division of Genomics of Development and Disease, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland, Australia.
Organogenesis and Cancer Program, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.

Renae Skoczylas (R)

Division of Genomics of Development and Disease, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland, Australia.
Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.

Neil I Bower (NI)

Division of Genomics of Development and Disease, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland, Australia.

Cas Simons (C)

Division of Genomics of Development and Disease, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland, Australia.
Murdoch Children's Research Institute, Parkville, Victoria, Australia.

Emma Gordon (E)

Division of Genomics of Development and Disease, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland, Australia.

Mathias Francois (M)

Division of Genomics of Development and Disease, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland, Australia.
Centenary Institute, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia.

Katarzyna Koltowska (K)

Division of Genomics of Development and Disease, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland, Australia.
Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.

Benjamin M Hogan (BM)

Division of Genomics of Development and Disease, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland, Australia.
Organogenesis and Cancer Program, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
Department of Anatomy and Neuroscience and Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Victoria, Australia.

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