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Articles by T Thorne
Total Records ( 2 ) for T Thorne
  J Zhou , Y Zhu , M Cheng , D Dinesh , T Thorne , K. K Poh , D Liu , C Botros , Y. L Tang , N Reisdorph , R Kishore , D. W Losordo and G. Qin
 

Background— Recent studies have identified a polymorphism in the endothelin-converting enzyme (ECE)–1b promoter (–338C/A) that is strongly associated with hypertension in women. The polymorphism is located in a consensus binding sequence for the E2F family of transcription factors. E2F proteins are crucially involved in cell-cycle regulation, but their roles in cardiovascular function are poorly understood. Here, we investigated the potential role of E2F2 in blood pressure regulation.

Methods and Results— Tail-cuff measurements of systolic and diastolic blood pressures were significantly higher in E2F2-null (E2F2–/–) mice than in their wild-type littermates, and in ex vivo ring assays, aortas from the E2F2–/– mice exhibited significantly greater contractility in response to big endothelin-1. Big endothelin-1 is activated by ECE-1, and mRNA levels of ECE-1b, the repressive ECE-1 isoform, were significantly lower in E2F2–/– mice than in wild-type mice. In endothelial cells, chromatin immunoprecipitation assays confirmed that E2F2 binds the ECE-1b promoter, and promoter-reporter assays indicated that E2F2 activates ECE-1b transcription. Furthermore, loss or downregulation of E2F2 led to a decline in ECE-1b levels, to higher levels of the membranous ECE-1 isoforms (ie, ECE-1a, -1c, and -1d), and to deregulated ECE-1 activity. Finally, Sam68 coimmunoprecipitated with E2F2, occupied the ECE-1b promoter (chromatin immunoprecipitation), and repressed E2F2-mediated ECE-1b promoter activity (promoter-reporter assays).

Conclusion— Our results identify a cell-cycle–independent mechanism by which E2F2 regulates endothelial function, arterial contractility, and blood pressure.

  M Ii , K Takeshita , K Ibusuki , C Luedemann , A Wecker , E Eaton , T Thorne , T Asahara , J. K Liao and D. W. Losordo
 

Background— Little is known about the role of endothelial progenitor cells (EPCs) in atherosclerosis. Accordingly, we performed a series of assessments with hypercholesterolemic (apolipoprotein E–null [ApoE–/–]) and wild-type (WT) mice to evaluate how cholesterol influences reendothelialization, atherosclerosis, and EPC function after arterial injury.

Methods and Results— Unexpectedly, reendothelialization (assessed by resistance to Evans blue staining) and circulating EPC counts (EPC culture assay) were greater in ApoE–/– mice than in WT mice, and transplantation of ApoE–/– bone marrow in WT mice accelerated endothelial recovery and increased recruitment of bone marrow–derived EPCs to the neoendothelium. Cholesterol concentration-dependently promoted the proliferation (MTS assay) of both ApoE–/– and WT EPCs, and the concentration dependence of EPC adhesion (to vitronectin-, collagen type I–, fibronectin-, and laminin-coated plates), migration (modified Boyden chamber assay), and antiapoptotic (terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling stain) activity was biphasic. Cholesterol enhanced the messenger RNA expression (quantitative, real-time reverse-transcription polymerase chain reaction) of vascular endothelial growth factor and inhibited Notch1 messenger RNA expression in both ApoE–/– and WT EPCs, whereas endothelial nitric oxide synthase messenger RNA expression increased in ApoE–/– EPCs and declined in WT EPCs after cholesterol exposure. EPC activity was greater in Notch1+/– EPCs than in WT EPCs, and transplantation of Notch1+/– bone marrow accelerated endothelial recovery after arterial injury in WT mice.

Conclusion— The results presented here provide novel insights into the role of EPCs during atherosclerosis and suggest that cholesterol and Notch1 may be involved in the regulation of EPC activity.

 
 
 
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