Knockdown of Bone Morphogenetic Protein Type II Receptor Leads to Decreased Aquaporin 1 Expression and Function in Human Pulmonary Microvascular Endothelial Cells.

Bone morphogenetic proteins (BMPs) were once considered only to have a role in bone formation. It is now known that they have pivotal roles in other organ diseases, including heritable pulmonary arterial hypertension (PAH), where genetic mutations in the type II BMP receptor (BMPR2) are the commonest cause of receptor dysfunction. However, it has also recently been demonstrated that aquaporin 1 (Aqp1) dysfunction may contribute to PAH, highlighting that PAH development may involve more than one pathogenic pathway. Whether reduction in BMPR2 affects Aqp1 is unknown. We therefore studied Aqp1 in BMPR2-silenced human pulmonary microvascular endothelial cells (HPMECs). We demonstrated reduced Aqp1 mRNA, protein and function in the BMPR2-silenced cells. Additionally, BMPR2-silenced cells exhibited lower expression of BMP-signalling molecules. In conclusion, decreased BMPR2 appears to affect Aqp1 at mRNA, protein, and functional levels. This observation may identify a contributory mechanism for PAH.

• Publication year

  2020

• Venue

  Canadian Journal of Physiology and Pharmacology

• Publication date

  2020-07-20

• Fields of study

  Biology, Medicine, Chemistry, Environmental Science

• Identifiers
  DOI 10.1139/cjpp-2020-0185PMID 32687728
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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