Lack of circulating autoantibodies to bone morphogenetic protein receptor-II or activin receptor-like kinase 1 in mixed connective tissue disease patients with pulmonary arterial hypertension

T. Satoh, K. Kimura, Y. Okano, Michito Hirakata, Yutaka Kawakami, M. Kuwana

Research output: Contribution to journalArticle

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Abstract

Objectives. To examine whether autoantibodies against bone morphogenetic protein receptor-II (BMPR-II) or activin receptor-like kinase 1 (ALK-1) are associated with pulmonary arterial hypertension (PAH) in patients with mixed connective tissue disease (MCTD). Methods. We studied sera from 37 MCTD patients with or without PAH, six patients with idiopathic PAH, and 30 healthy controls. Circulating anti-BMPR-II and anti-ALK-1 antibodies were detected using immunoprecipitation of recombinant antigens generated by in vitro transcription/translation and indirect immunofluorescence of cultured cells that were induced to express these antigens by gene transfer. Anti-BMPR-II antibodies were further examined by immunoprecipitation and immunoblotting using a recombinant fragment of the extracellular domain of BMPR-II. Results. Serum anti-BMPR-II and anti-ALK-1 autoantibodies were not detected in MCTD patients irrespective of the presence or absence of PAH, or in patients with idiopathic PAH. Conclusions. Our finding does not support the hypothesis that autoantibody-mediated dysregulation of signals through BMPR-II or ALK-1 contributes to the development of PAH in patients with connective tissue diseases.

Original languageEnglish
Pages (from-to)192-196
Number of pages5
JournalRheumatology
Volume44
Issue number2
DOIs
Publication statusPublished - 2005 Feb

Fingerprint

Type II Bone Morphogenetic Protein Receptors
Activin Receptors
Mixed Connective Tissue Disease
Pulmonary Hypertension
Autoantibodies
Immunoprecipitation
Antigens
Connective Tissue Diseases
Antibodies
Indirect Fluorescent Antibody Technique
Serum
Immunoblotting
Cultured Cells

Keywords

  • Activin receptor-like kinase 1
  • Autoantibody
  • Bone morphogenetic protein receptor-II
  • Mixed connective tissue disease
  • Pulmonary arterial hypertension

ASJC Scopus subject areas

  • Neuroscience(all)
  • Rheumatology

Cite this

Lack of circulating autoantibodies to bone morphogenetic protein receptor-II or activin receptor-like kinase 1 in mixed connective tissue disease patients with pulmonary arterial hypertension. / Satoh, T.; Kimura, K.; Okano, Y.; Hirakata, Michito; Kawakami, Yutaka; Kuwana, M.

In: Rheumatology, Vol. 44, No. 2, 02.2005, p. 192-196.

Research output: Contribution to journalArticle

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AU - Kimura, K.

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AU - Hirakata, Michito

AU - Kawakami, Yutaka

AU - Kuwana, M.

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N2 - Objectives. To examine whether autoantibodies against bone morphogenetic protein receptor-II (BMPR-II) or activin receptor-like kinase 1 (ALK-1) are associated with pulmonary arterial hypertension (PAH) in patients with mixed connective tissue disease (MCTD). Methods. We studied sera from 37 MCTD patients with or without PAH, six patients with idiopathic PAH, and 30 healthy controls. Circulating anti-BMPR-II and anti-ALK-1 antibodies were detected using immunoprecipitation of recombinant antigens generated by in vitro transcription/translation and indirect immunofluorescence of cultured cells that were induced to express these antigens by gene transfer. Anti-BMPR-II antibodies were further examined by immunoprecipitation and immunoblotting using a recombinant fragment of the extracellular domain of BMPR-II. Results. Serum anti-BMPR-II and anti-ALK-1 autoantibodies were not detected in MCTD patients irrespective of the presence or absence of PAH, or in patients with idiopathic PAH. Conclusions. Our finding does not support the hypothesis that autoantibody-mediated dysregulation of signals through BMPR-II or ALK-1 contributes to the development of PAH in patients with connective tissue diseases.

AB - Objectives. To examine whether autoantibodies against bone morphogenetic protein receptor-II (BMPR-II) or activin receptor-like kinase 1 (ALK-1) are associated with pulmonary arterial hypertension (PAH) in patients with mixed connective tissue disease (MCTD). Methods. We studied sera from 37 MCTD patients with or without PAH, six patients with idiopathic PAH, and 30 healthy controls. Circulating anti-BMPR-II and anti-ALK-1 antibodies were detected using immunoprecipitation of recombinant antigens generated by in vitro transcription/translation and indirect immunofluorescence of cultured cells that were induced to express these antigens by gene transfer. Anti-BMPR-II antibodies were further examined by immunoprecipitation and immunoblotting using a recombinant fragment of the extracellular domain of BMPR-II. Results. Serum anti-BMPR-II and anti-ALK-1 autoantibodies were not detected in MCTD patients irrespective of the presence or absence of PAH, or in patients with idiopathic PAH. Conclusions. Our finding does not support the hypothesis that autoantibody-mediated dysregulation of signals through BMPR-II or ALK-1 contributes to the development of PAH in patients with connective tissue diseases.

KW - Activin receptor-like kinase 1

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