Identification of a New Intronic BMPR2-Mutation and Early Diagnosis of Heritable Pulmonary Arterial Hypertension in a Large Family with Mean Clinical Follow-Up of 12 Years
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{"title"=>"Identification of a new intronic BMPR2-mutation and early diagnosis of heritable pulmonary arterial hypertension in a large family with mean clinical follow-up of 12 years", "type"=>"journal", "authors"=>[{"first_name"=>"Katrin", "last_name"=>"Hinderhofer", "scopus_author_id"=>"6507583558"}, {"first_name"=>"Christine", "last_name"=>"Fischer", "scopus_author_id"=>"7402486599"}, {"first_name"=>"Nicole", "last_name"=>"Pfarr", "scopus_author_id"=>"6508017394"}, {"first_name"=>"Justyna", "last_name"=>"Szamalek-Hoegel", "scopus_author_id"=>"36106400800"}, {"first_name"=>"Mona", "last_name"=>"Lichtblau", "scopus_author_id"=>"36523425000"}, {"first_name"=>"Christian", "last_name"=>"Nagel", "scopus_author_id"=>"25646624600"}, {"first_name"=>"Benjamin", "last_name"=>"Egenlauf", "scopus_author_id"=>"36451872400"}, {"first_name"=>"Nicola", "last_name"=>"Ehlken", "scopus_author_id"=>"14830085800"}, {"first_name"=>"Ekkehard", "last_name"=>"Grünig", "scopus_author_id"=>"6603702994"}], "year"=>2014, "source"=>"PLoS ONE", "identifiers"=>{"issn"=>"19326203", "pui"=>"372799620", "doi"=>"10.1371/journal.pone.0091374", "sgr"=>"84897980984", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)", "pmid"=>"24621962", "scopus"=>"2-s2.0-84897980984"}, "id"=>"8e65de9f-40e1-3ee8-a9ad-206188ebd8c3", "abstract"=>"BACKGROUND: Mutations in the bone morphogenetic protein receptor 2 (BMPR2) gene can lead to hereditary pulmonary arterial hypertension (HPAH) and are detected in more than 80% of cases with familial aggregation of the disease. Factors determining disease penetrance are largely unknown.\\n\\nMETHODS: A mean clinical follow-up of 12 years was accomplished in 46 family members including echocardiography, stress-Dopplerechocardiography and genetic analysis of TGF-β pathway genes. Right heart catheterization and RNA-analysis was performed in members with pathological findings.\\n\\nRESULTS: Manifest HPAH was diagnosed in 8 members, 4 were already deceased, two died during the follow-up, two are still alive. Normal pulmonary artery systolic pressure at rest but hypertensive response to exercise has been identified in 19 family members. Analysis of BMPR2 transcripts revealed aberrant splicing due to an insertion of an intronic Alu element adjacent to exon 6. All HPAH patients and 12 further asymptomatic family members carried this insertion. During follow-up two family members carrying hypertensive response and the Alu insertion developed manifest HPAH.\\n\\nCONCLUSION: This is the first report of an intronic BMPR2 mutation due to an Alu element insertion causing HPAH in a large family which has been confirmed on RNA-level. Only those members that carried both hypertensive response and the mutation developed manifest HPAH during follow-up. Our findings highlight the importance of including further methods such as RNA analysis into the molecular genetic diagnostic of PAH patients. They suggest that at least in some families hypertensive response may be an additional risk factor for disease manifestation and penetrance.", "link"=>"http://www.mendeley.com/research/identification-new-intronic-bmpr2mutation-early-diagnosis-heritable-pulmonary-arterial-hypertension", "reader_count"=>14, "reader_count_by_academic_status"=>{"Professor > Associate Professor"=>1, "Researcher"=>4, "Student > Ph. D. Student"=>5, "Student > Master"=>1, "Student > Bachelor"=>2, "Student > Postgraduate"=>1}, "reader_count_by_user_role"=>{"Professor > Associate Professor"=>1, "Researcher"=>4, "Student > Ph. D. Student"=>5, "Student > Master"=>1, "Student > Bachelor"=>2, "Student > Postgraduate"=>1}, "reader_count_by_subject_area"=>{"Nursing and Health Professions"=>1, "Medicine and Dentistry"=>7, "Agricultural and Biological Sciences"=>4, "Sports and Recreations"=>1, "Computer Science"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>7}, "Sports and Recreations"=>{"Sports and Recreations"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>4}, "Computer Science"=>{"Computer Science"=>1}, "Nursing and Health Professions"=>{"Nursing and Health Professions"=>1}}, "reader_count_by_country"=>{"Italy"=>1, "Germany"=>1}, "group_count"=>1}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/1417158"], "description"=>"<p>The genomic amplification with forward primer located in intron 5 and a reverse primer located in intron 6 resulted in two products of different length identified in several family members (shown is the result of 15 family members). Sequencing analysis of the larger products revealed the insertion of an AluYb8 element with an adjacent duplicated sequence motive in antisense orientation to <i>BMPR2</i> in intron 5 (adjacent to exon 6). A schematic representation of the region and the insertion of the Alu element on one allele and the complete sequence of the Alu element, the duplicated sequence and the beginning of exon 6 are shown.</p>", "links"=>[], "tags"=>["cardiovascular", "Heart failure", "hemodynamics", "Pulmonary vascular diseases", "Clinical genetics", "Pulmonology", "intronic"], "article_id"=>959653, "categories"=>["Medicine"], "users"=>["Katrin Hinderhofer", "Christine Fischer", "Nicole Pfarr", "Justyna Szamalek-Hoegel", "Mona Lichtblau", "Christian Nagel", "Benjamin Egenlauf", "Nicola Ehlken", "Ekkehard Grünig"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0091374.g004", "stats"=>{"downloads"=>0, "page_views"=>3, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Genomic_analysis_of_the_intronic_region_/959653", "title"=>"Genomic analysis of the intronic region.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-03-12 03:32:12"}
  • {"files"=>["https://ndownloader.figshare.com/files/1417159"], "description"=>"<p>f =  female, m =  male, n =  no, y =  yes, n.m. =  not measurable, HR =  hypertensive response, NR =  normal response, PAH =  pulmonary arterial hypertension, sec. PH =  secondary pulmonary hypertension, RHC =  right heart catheterization.</p>", "links"=>[], "tags"=>["cardiovascular", "Heart failure", "hemodynamics", "Pulmonary vascular diseases", "Clinical genetics", "Pulmonology"], "article_id"=>959654, "categories"=>["Medicine"], "users"=>["Katrin Hinderhofer", "Christine Fischer", "Nicole Pfarr", "Justyna Szamalek-Hoegel", "Mona Lichtblau", "Christian Nagel", "Benjamin Egenlauf", "Nicola Ehlken", "Ekkehard Grünig"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0091374.t001", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Clinical_and_genetic_assessment_in_family_members_/959654", "title"=>"Clinical and genetic assessment in family members.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2014-03-12 03:32:12"}
  • {"files"=>["https://ndownloader.figshare.com/files/1417156"], "description"=>"<p>This figure shows the genotype-phenotype correlation between Alu insertion and PASP during exercise, classified as HR and NR. Only patients who carried both HR and Alu insertion developed manifest PAH during follow-up. Patients with the Alu insertion in the <i>BMPR2</i> gene show significantly more frequent Hypertensive response to exercise (10/13 vs. 8/25; Fishers exact test p = 0.016).</p>", "links"=>[], "tags"=>["cardiovascular", "Heart failure", "hemodynamics", "Pulmonary vascular diseases", "Clinical genetics", "Pulmonology", "correlations", "alu", "carriers", "pasp"], "article_id"=>959651, "categories"=>["Medicine"], "users"=>["Katrin Hinderhofer", "Christine Fischer", "Nicole Pfarr", "Justyna Szamalek-Hoegel", "Mona Lichtblau", "Christian Nagel", "Benjamin Egenlauf", "Nicola Ehlken", "Ekkehard Grünig"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0091374.g002", "stats"=>{"downloads"=>3, "page_views"=>11, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Genotype_phenotype_correlations_of_Alu_carriers_and_PASP_during_exercise_/959651", "title"=>"Genotype-phenotype correlations of Alu carriers and PASP during exercise.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-03-12 03:32:12"}
  • {"files"=>["https://ndownloader.figshare.com/files/1417157"], "description"=>"<p>A) Schematic representation of the genomic region from 5′-untranslated Region (5′-UTR) to exon 7 of <i>BMPR2</i>. Indicated are the identified polymorphisms (c.-212_-211insC and c.600A>C) used as markers for the analysis of the <i>BMPR2</i> transcript in the index patient, the primer used for the amplification, the location of the inserted Alu element, the duplicated 13 bp region and a potential cryptic splice site (marked by a star with four spikes). B) The upper part of this figure shows the amplified product using the forward primer located in exon 5 with the reverse primer located at the beginning of exon 6. The PCR with primers F1 and R1 resulted in amplification of a single transcript with the polymorphism in exon 5 in apparently homozygous state (c.600A). The other PCR with the same forward primer in exon 5 as above but with another reverse primer located in exon 7 (R2) resulted in amplification of at least five products of different length. Product #3 corresponds to the normally spliced wild type sequence with an apparently homozygous c.600A polymorphism in exon 5; the two larger products (#1 and #2) contained a complete and partial (only left arm) incorporated AluYb8 element, respectively. Furthermore, two smaller products were identified in which the 5′ part of exon 6 (product #4) and the complete exon 6 (product #5) are missing. All aberrant spliced products (#1, 2, 4, and 5) contained apparently homozygous the C-allele of the polymorphism located in exon 5 (c.600C).</p>", "links"=>[], "tags"=>["cardiovascular", "Heart failure", "hemodynamics", "Pulmonary vascular diseases", "Clinical genetics", "Pulmonology", "rna"], "article_id"=>959652, "categories"=>["Medicine"], "users"=>["Katrin Hinderhofer", "Christine Fischer", "Nicole Pfarr", "Justyna Szamalek-Hoegel", "Mona Lichtblau", "Christian Nagel", "Benjamin Egenlauf", "Nicola Ehlken", "Ekkehard Grünig"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0091374.g003", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Results_of_the_analysis_on_RNA_level_/959652", "title"=>"Results of the analysis on RNA level.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-03-12 03:32:12"}
  • {"files"=>["https://ndownloader.figshare.com/files/1417155"], "description"=>"<p>This figure represents the pedigree tree of the German family analysed in this study. The index patient of the family is marked by an arrow. All family members with manifest PAH are shown in black. Healthy family members have open symbols and those who were heterozygous for the identified mutation are marked with “Alu”. Those family members with hypertensive response due to exercise have half-filled symbols. Family members with unknown hemodynamic status have open symbols with a question mark inside. A question mark below the pedigree ID indicates that the genetic status in this family member is unknown. An open blue square marks the family members which presented at the beginning of the follow-up with hypertensive response due to exercise and changed their status to manifest PAH (II:12 and III:28). All family members who participated in the clinical and/or genetic analysis are marked by a star. The numbering of the individuals in the pedigree corresponds to the IDs of the family members in <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0091374#pone-0091374-t001\" target=\"_blank\">table 1</a>.</p>", "links"=>[], "tags"=>["cardiovascular", "Heart failure", "hemodynamics", "Pulmonary vascular diseases", "Clinical genetics", "Pulmonology", "german"], "article_id"=>959650, "categories"=>["Medicine"], "users"=>["Katrin Hinderhofer", "Christine Fischer", "Nicole Pfarr", "Justyna Szamalek-Hoegel", "Mona Lichtblau", "Christian Nagel", "Benjamin Egenlauf", "Nicola Ehlken", "Ekkehard Grünig"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0091374.g001", "stats"=>{"downloads"=>3, "page_views"=>3, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Pedigree_of_the_large_German_family_/959650", "title"=>"Pedigree of the large German family.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-03-12 03:32:12"}

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