原创力文档the plk1 inhibitor bi 2536 temporarily arrests primary cardiac fibroblasts in mitosis and generates aneuploidy in vitroplk1抑制剂bi 2536临时逮捕主要心脏成纤维细胞在有丝分裂和产生非整倍性体外.pdfVIP
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the plk1 inhibitor bi 2536 temporarily arrests primary cardiac fibroblasts in mitosis and generates aneuploidy in vitroplk1抑制剂bi 2536临时逮捕主要心脏成纤维细胞在有丝分裂和产生非整倍性体外
The Plk1 Inhibitor BI 2536 Temporarily Arrests Primary
Cardiac Fibroblasts in Mitosis and Generates Aneuploidy
In Vitro
1 1 1 2 1 1
Bo Lu , Hasan Mahmud , Alexander H. Maass , Bo Yu , Wiek H. van Gilst , Rudolf A. de Boer ,
´ 1*
Herman H. W. Sillje
1 Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands, 2 Department of Cardiology, The Second
Affiliated Hospital of Harbin Medical University, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Harbin, China
Abstract
BI 2536 is a new anti-mitotic drug that targets polo-like kinase 1 (Plk1) and is currently under clinical development for cancer
therapy. The effect of this drug on cancer cells has been extensively investigated, but information about the effects on
primary dividing cells and differentiated non-dividing cells is scarce. We have investigated the effects of this drug on
primary neonatal rat cardiac fibroblasts and on differentiated cardiomyocytes and explored the possibility to use this drug
to enrich differentiated cell populations in vitro. BI 2536 had a profound effect on cardiac fibroblast proliferation in vitro and
arrested these cells in mitosis with an IC50 of about 43 nM. Similar results were observed with primary human cells (HUVEC,
IC50 = 30 nM), whereas the cancer cell line HeLa was more sensitive (IC50 of 9 nM). Further analysis revealed that
prolonged mitotic arrest resulted in cell death for about 40% of cardiac fibroblasts. The remaining cells showed an
interphase morphology with mostly multi- and micro-nucleated nuclei. This indicates that a significant n
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