Bone morphogenetic protein signaling is required for RAD51-mediated maintenance of genome integrity in vascular endothelial cells

The integrity of blood vessels is fundamental to vascular homeostasis. Inactivating mutations in the bone morphogenetic protein (BMP) receptor type II (BMPR2) gene cause hereditary vascular disorders, including pulmonary arterial hypertension and hereditary hemorrhagic telangiectasia, suggesting tha...

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Published inCommunications biology Vol. 1; no. 1; p. 149
Main Authors Vattulainen-Collanus, Sanna, Southwood, Mark, Yang, Xu Dong, Moore, Stephen, Ghatpande, Prajakta, Morrell, Nicholas W., Lagna, Giorgio, Hata, Akiko
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.01.2018
Nature Publishing Group
Subjects
13/106
13/109
13/51
13/89
38/39
38/90
631/337/1427/2566
631/80/86/2370
692/4019/592/75/593/1920
82/80
Animal models
Biology
Biomedical and Life Sciences
Blood vessels
Bone morphogenetic protein receptor type II
Bone morphogenetic proteins
Cell culture
Cell death
Deoxyribonucleic acid
DNA
DNA biosynthesis
DNA damage
DNA repair
Endothelial cells
Genomes
Hemorrhage
Hereditary hemorrhagic telangiectasia
Homeostasis
Hypertension
Life Sciences
Mutation
Phenotypes
Pulmonary hypertension
Replication
Signal transduction
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Abstract The integrity of blood vessels is fundamental to vascular homeostasis. Inactivating mutations in the bone morphogenetic protein (BMP) receptor type II (BMPR2) gene cause hereditary vascular disorders, including pulmonary arterial hypertension and hereditary hemorrhagic telangiectasia, suggesting that BMPR2 and its downstream signaling pathway are pivotal to the maintenance of vascular integrity through an unknown molecular mechanism. Here we report that inactivation of BMPR2 in pulmonary vascular endothelial cells results in a deficit of RAD51, an enzyme essential for DNA repair and replication. Loss of RAD51, which causes DNA damage and cell death, is also detected in animal models and human patients with pulmonary arterial hypertension. Restoration of BMPR2 or activation of the BMP signaling pathway rescues RAD51 and prevents DNA damage. This is an unexpected role of BMP signaling in preventing the accumulation of DNA damage and the concomitant loss of endothelial integrity and vascular remodeling associated with vascular disorders. Sanna Vattulainen-Collanus et al. report that mutations in the BMPR2 gene, which is associated with pulmonary arterial hypertension, result in a deficit of RAD51 and altered DNA repair and replication. They were able to rescue the RAD51-deficient phenotype by restoring BMPR2 activity in cell culture.
AbstractList The integrity of blood vessels is fundamental to vascular homeostasis. Inactivating mutations in the bone morphogenetic protein (BMP) receptor type II (BMPR2) gene cause hereditary vascular disorders, including pulmonary arterial hypertension and hereditary hemorrhagic telangiectasia, suggesting that BMPR2 and its downstream signaling pathway are pivotal to the maintenance of vascular integrity through an unknown molecular mechanism. Here we report that inactivation of BMPR2 in pulmonary vascular endothelial cells results in a deficit of RAD51, an enzyme essential for DNA repair and replication. Loss of RAD51, which causes DNA damage and cell death, is also detected in animal models and human patients with pulmonary arterial hypertension. Restoration of BMPR2 or activation of the BMP signaling pathway rescues RAD51 and prevents DNA damage. This is an unexpected role of BMP signaling in preventing the accumulation of DNA damage and the concomitant loss of endothelial integrity and vascular remodeling associated with vascular disorders.Sanna Vattulainen-Collanus et al. report that mutations in the BMPR2 gene, which is associated with pulmonary arterial hypertension, result in a deficit of RAD51 and altered DNA repair and replication. They were able to rescue the RAD51-deficient phenotype by restoring BMPR2 activity in cell culture.
The integrity of blood vessels is fundamental to vascular homeostasis. Inactivating mutations in the bone morphogenetic protein (BMP) receptor type II (BMPR2) gene cause hereditary vascular disorders, including pulmonary arterial hypertension and hereditary hemorrhagic telangiectasia, suggesting that BMPR2 and its downstream signaling pathway are pivotal to the maintenance of vascular integrity through an unknown molecular mechanism. Here we report that inactivation of BMPR2 in pulmonary vascular endothelial cells results in a deficit of RAD51, an enzyme essential for DNA repair and replication. Loss of RAD51, which causes DNA damage and cell death, is also detected in animal models and human patients with pulmonary arterial hypertension. Restoration of BMPR2 or activation of the BMP signaling pathway rescues RAD51 and prevents DNA damage. This is an unexpected role of BMP signaling in preventing the accumulation of DNA damage and the concomitant loss of endothelial integrity and vascular remodeling associated with vascular disorders. Sanna Vattulainen-Collanus et al. report that mutations in the BMPR2 gene, which is associated with pulmonary arterial hypertension, result in a deficit of RAD51 and altered DNA repair and replication. They were able to rescue the RAD51-deficient phenotype by restoring BMPR2 activity in cell culture.
Abstract The integrity of blood vessels is fundamental to vascular homeostasis. Inactivating mutations in the bone morphogenetic protein (BMP) receptor type II (BMPR2) gene cause hereditary vascular disorders, including pulmonary arterial hypertension and hereditary hemorrhagic telangiectasia, suggesting that BMPR2 and its downstream signaling pathway are pivotal to the maintenance of vascular integrity through an unknown molecular mechanism. Here we report that inactivation of BMPR2 in pulmonary vascular endothelial cells results in a deficit of RAD51, an enzyme essential for DNA repair and replication. Loss of RAD51, which causes DNA damage and cell death, is also detected in animal models and human patients with pulmonary arterial hypertension. Restoration of BMPR2 or activation of the BMP signaling pathway rescues RAD51 and prevents DNA damage. This is an unexpected role of BMP signaling in preventing the accumulation of DNA damage and the concomitant loss of endothelial integrity and vascular remodeling associated with vascular disorders.
The integrity of blood vessels is fundamental to vascular homeostasis. Inactivating mutations in the bone morphogenetic protein (BMP) receptor type II (BMPR2) gene cause hereditary vascular disorders, including pulmonary arterial hypertension and hereditary hemorrhagic telangiectasia, suggesting that BMPR2 and its downstream signaling pathway are pivotal to the maintenance of vascular integrity through an unknown molecular mechanism. Here we report that inactivation of BMPR2 in pulmonary vascular endothelial cells results in a deficit of RAD51, an enzyme essential for DNA repair and replication. Loss of RAD51, which causes DNA damage and cell death, is also detected in animal models and human patients with pulmonary arterial hypertension. Restoration of BMPR2 or activation of the BMP signaling pathway rescues RAD51 and prevents DNA damage. This is an unexpected role of BMP signaling in preventing the accumulation of DNA damage and the concomitant loss of endothelial integrity and vascular remodeling associated with vascular disorders.
ArticleNumber 149
Author Moore, Stephen
Hata, Akiko
Vattulainen-Collanus, Sanna
Yang, Xu Dong
Ghatpande, Prajakta
Morrell, Nicholas W.
Southwood, Mark
Lagna, Giorgio
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  email: akiko.hata@ucsf.edu
  organization: Cardiovascular Research Institute, University of California, San Francisco, Department of Biochemistry and Biophysics, University of California, San Francisco
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Snippet The integrity of blood vessels is fundamental to vascular homeostasis. Inactivating mutations in the bone morphogenetic protein (BMP) receptor type II (BMPR2)...
Abstract The integrity of blood vessels is fundamental to vascular homeostasis. Inactivating mutations in the bone morphogenetic protein (BMP) receptor type II...
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SubjectTerms 13/106
13/109
13/51
13/89
38/39
38/90
631/337/1427/2566
631/80/86/2370
692/4019/592/75/593/1920
82/80
Animal models
Biology
Biomedical and Life Sciences
Blood vessels
Bone morphogenetic protein receptor type II
Bone morphogenetic proteins
Cell culture
Cell death
Deoxyribonucleic acid
DNA
DNA biosynthesis
DNA damage
DNA repair
Endothelial cells
Genomes
Hemorrhage
Hereditary hemorrhagic telangiectasia
Homeostasis
Hypertension
Life Sciences
Mutation
Phenotypes
Pulmonary hypertension
Replication
Signal transduction
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Title Bone morphogenetic protein signaling is required for RAD51-mediated maintenance of genome integrity in vascular endothelial cells
URI https://link.springer.com/article/10.1038/s42003-018-0152-1
https://www.ncbi.nlm.nih.gov/pubmed/30272025
https://www.proquest.com/docview/2389699296
https://search.proquest.com/docview/2115271141
https://pubmed.ncbi.nlm.nih.gov/PMC6155317
Volume 1
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