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Compartmentalization of hnRNP-K during cell cycle progression and its interaction with calponin in the cytoplasm

Lisa D Laury-Kleintop1, Maria Tresini, Olivia Hammond

  • 1Lankenau Institute for Medical Research, 100 E. Lancaster Avenue, Wynnewood, Pennsylvania 19096, USA. KleintopL@mlhs.org

Journal of Cellular Biochemistry
|June 18, 2005
PubMed

Insights

Heterogeneous nuclear ribonucleoprotein K (hnRNP-K) protein accumulates in smooth muscle cells during cardiovascular disease, potentially driving cell proliferation and impacting treatment outcomes.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cell Biology
  • Biochemistry

Background:

  • Coronary artery blockage, a consequence of cardiovascular disease, is commonly addressed by angioplasty or bypass surgery.
  • Smooth muscle cell (SMC) proliferation is a key factor limiting the success of these interventions.
  • Heterogeneous nuclear ribonucleoprotein K (hnRNP-K), a protein primarily studied in cancer, is implicated in cell cycle progression.

Purpose of the Study:

  • To investigate the role and regulation of hnRNP-K in SMC proliferation within the context of cardiovascular disease.
  • To determine the sub-cellular localization and potential signaling functions of hnRNP-K in SMCs.

Main Methods:

  • Analysis of hnRNP-K protein levels in SMCs stimulated with serum in vitro.
  • Examination of hnRNP-K in aortic tissue from an animal atherosclerosis model and human occluded vein segments.
  • Cell cycle analysis of hnRNP-K sub-cellular localization using cycloheximide to assess protein synthesis and translocation.

Main Results:

  • hnRNP-K protein levels were elevated in SMCs in response to serum stimulation, in atherosclerotic aortas, and in human vein segments.
  • In cultured SMCs, hnRNP-K localization shifted between the nucleus and cytoplasm during the cell cycle.
  • Cytoplasmic accumulation of hnRNP-K correlated with decreased nuclear levels, suggesting translocation, and appeared to involve new protein synthesis.
  • Cytoplasmic hnRNP-K formed a complex with calponin and ERK1/2.

Conclusions:

  • hnRNP-K protein expression and localization are altered in SMCs during cardiovascular disease progression.
  • Cytoplasmic hnRNP-K in SMCs may participate in a signaling complex regulating growth and post-transcriptional events.
  • Targeting hnRNP-K could offer a novel therapeutic strategy for cardiovascular diseases driven by SMC proliferation.

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