Reverse Regulation of Endothelial Cells and Myointimal Hyperplasia on Cell Proliferation by a Heatshock Protein-Coinducer After Hypoxia
| Autor: | László Entz, Zoltan K. Nagy, Laszlo Denes, Zoltán Bori, Éva Csonka |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Pathology
medicine.medical_specialty Vascular smooth muscle Endothelium Flow cytometry Piperidines Oxazines medicine Humans Hypoxia Cells Cultured Heat-Shock Proteins Aged Cell Proliferation Advanced and Specialized Nursing Hyperplasia medicine.diagnostic_test Cell growth business.industry Brain Endothelial Cells Middle Aged Cell cycle Hypoxia (medical) medicine.disease Capillaries Endothelial stem cell medicine.anatomical_structure Cancer research Neurology (clinical) medicine.symptom Tunica Intima Cardiology and Cardiovascular Medicine business |
| Zdroj: | Stroke. 39:1022-1024 |
| ISSN: | 1524-4628 0039-2499 |
| DOI: | 10.1161/strokeaha.107.495754 |
| Popis: | 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 P 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. |
| Databáze: | OpenAIRE |
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