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on January 31, 2008

Stroke. 2008
Published online before print January 31, 2008, doi: 10.1161/STROKEAHA.107.495754
A more recent version of this article appeared on March 1, 2008
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Right arrow Smooth muscle proliferation and differentiation

Submitted on June 13, 2007
Revised on July 28, 2007
Accepted on August 1, 2007

Reverse Regulation of Endothelial Cells and Myointimal Hyperplasia on Cell Proliferation by a Heatshock Protein-Coinducer After Hypoxia

Laszlo Denes PhD*; Zoltan Bori MS; Eva Csonka DSc; Laszlo Entz MD, PhD; and Zoltan Nagy MD, DSc

From the National Stroke Centre (L.D., Z.B., E.C., Z.N.), National Institute of Psychiatry and Neurology, Section of Vascular Neurology; Department of Vascular Surgery (L.E.), Semmelweis University, Budapest, Hungary.

* To whom correspondence should be addressed. E-mail: dr.denes{at}gmail.com.

Background and Purpose—Myointimal hyperplasia (MIH) cells are related to permanent upregulated proliferation as tumor-like cells. The aim of this study is to assess whether treatment of cells after hypoxia by Iroxanadine heat-shock protein (HSP-coinducer) predicts recovery through cell proliferation.

Methods—Vascular smooth muscle cells (VSMC) and brain capillary endothelial cells (HBEC) were isolated from human origin and MIH-cells from early carotid restenosis after surgery. Cell proliferation was quantified by bromuridine (BrdU) incorporation after hypoxia/reoxygenation. HSP72 and cyclin-dependent kinase (CDKN1A) mRNA expression was assessed by reverse transcription-polymerase chain reaction (PCR) and cell cycle distribution by flow cytometry (FACS) analysis.

Results—After hypoxia/reoxygenation, the proliferation of MIH-cells increased, whereas endothelial cells decreased (MIH: 0.266±0.016 versus 0.336±0.024; P<0.05; HBEC: 1.249±0.10 versus 0.878±0.11; P<0.05). Whereas augmented proliferation of MIH-cells was reduced (40% to 45%) by HSP-coinducer, diminished HBEC proliferation increased (46.2%). Stress-activated-protein-kinase (SAPK)p38-dependent cell cycle redistribution was generated by an increase in HSP72 and CDKN1A mRNA levels in MIH-cells.

Conclusions—The 2 key players of early restenosis (MIH, EC) were oppositely regulated and correspondingly after treatment by HSP-coinducer reverse recovered. Drug candidate may have therapeutic potential in (re)restenosis.
Key words: carotid stenosis • endothelium • heatshock-protein • proliferation • smooth muscle cells






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