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Bone morphogenetic protein-2 upregulates expression and function of voltage-gated K+ channels in human pulmonary

Ivana Fantozzi1, Oleksandr Platoshyn, Ada H Wong

  • 1Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California San Diego, 9500 Gilman Drive, MC 0725, La Jolla, 92093-0725, USA.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|July 4, 2006
PubMed

Insights

Bone morphogenetic protein-2 (BMP-2) alters voltage-gated potassium (K(V)) channel expression and function in human pulmonary artery smooth muscle cells (PASMC). BMP-2 increases K(V) channel activity, potentially mediating its anti-proliferative and pro-apoptotic effects.

Area of Science:

  • Cardiovascular Biology
  • Ion Channel Physiology
  • Cell Signaling

Background:

  • Voltage-gated potassium (K(V)) channels regulate membrane potential, apoptosis, and proliferation in pulmonary artery smooth muscle cells (PASMC).
  • Dysfunctional BMP signaling and reduced K(V) channels are implicated in pulmonary hypertension and vascular remodeling.
  • Bone morphogenetic proteins (BMPs) typically inhibit PASMC proliferation and promote apoptosis.

Purpose of the Study:

  • To investigate the impact of BMP-2 on K(V) channel function and expression in normal human PASMC.
  • To elucidate the role of BMP-2 in regulating K(V) channel subunits and overall channel activity.

Main Methods:

  • Human PASMC were treated with BMP-2 (100 nM for 18-24 hours).
  • Quantitative real-time PCR was used to assess K(V) channel mRNA expression.
  • Whole-cell patch-clamp electrophysiology was employed to measure K(V) currents.

Main Results:

  • BMP-2 significantly upregulated mRNA for several K(V) channel alpha-, beta-, and gamma-subunits (e.g., KCNA5, KCNC4, KCNS3).
  • BMP-2 markedly downregulated KCNG2 and KCNV2 (gamma-subunits) by over 10-fold.
  • BMP-2 treatment led to a significant increase in whole-cell K(V) current amplitude and density.
  • BMP-2 attenuated c-Myc expression, potentially linking it to K(V) channel regulation.

Conclusions:

  • BMP-2 differentially regulates K(V) channel subunit expression in human PASMC.
  • BMP-2 enhances K(V) channel activity, likely by downregulating inhibitory gamma-subunits (KCNG2, KCNV2).
  • Increased K(V) channel activity induced by BMP-2 may contribute to its antiproliferative and pro-apoptotic effects in PASMC.

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