OBJECTIVE: Vascular endothelial zinc finger 1 (Vezf1) is a recently identified zinc finger transcription factor that is expressed in endothelial cells (ECs) during vascular development in mouse embryo. Here, we present that Vezf1 was expressed in ECs at the site of postnatal angiogenesis. We therefore examined whether Vezf1 was involved in the regulation of angiogenesis. METHODS AND RESULTS: The specific downregulation of Vezf1 by antisense oligodeoxynucleotide (AS-ODN) significantly inhibited the proliferation, migration, and network formation of cultured ECs as well as angiogenesis in vivo. Vezf1 AS-ODN downregulated the expression of stathmin/oncoprotein18 (OP18), a microtubule-destabilizing protein, in ECs, whereas transient transfection of Vezf1 cDNA increased the expression of stathmin/OP18 in ECs. To explore the relationship between Vezf1 and stathmin/OP18, we specifically downregulated stathmin/OP18. We found that stathmin/OP18 AS-ODN inhibited the proliferation, migration, and network formation of ECs as Vezf1 AS-ODN did. Moreover, Vezf1 AS-ODN decreased G2/M population of ECs and increased apoptosis, which reproduced the characteristic feature of stathmin/OP18 inhibition. CONCLUSIONS: These results suggest that Vezf1 is involved in the regulation of angiogenesis, at least in part, through the expression of stathmin/OP18 in ECs.
OBJECTIVE:Vascular endothelial zinc finger 1 (Vezf1) is a recently identified zinc finger transcription factor that is expressed in endothelial cells (ECs) during vascular development in mouse embryo. Here, we present that Vezf1 was expressed in ECs at the site of postnatal angiogenesis. We therefore examined whether Vezf1 was involved in the regulation of angiogenesis. METHODS AND RESULTS: The specific downregulation of Vezf1 by antisense oligodeoxynucleotide (AS-ODN) significantly inhibited the proliferation, migration, and network formation of cultured ECs as well as angiogenesis in vivo. Vezf1AS-ODN downregulated the expression of stathmin/oncoprotein18 (OP18), a microtubule-destabilizing protein, in ECs, whereas transient transfection of Vezf1 cDNA increased the expression of stathmin/OP18 in ECs. To explore the relationship between Vezf1 and stathmin/OP18, we specifically downregulated stathmin/OP18. We found that stathmin/OP18AS-ODN inhibited the proliferation, migration, and network formation of ECs as Vezf1AS-ODN did. Moreover, Vezf1AS-ODN decreased G2/M population of ECs and increased apoptosis, which reproduced the characteristic feature of stathmin/OP18 inhibition. CONCLUSIONS: These results suggest that Vezf1 is involved in the regulation of angiogenesis, at least in part, through the expression of stathmin/OP18 in ECs.
Authors: Amudhan Venkateswaran; David B Friedman; Alexandra J Walsh; Melissa C Skala; Soumya Sasi; Girish Rachakonda; Peter A Crooks; Michael L Freeman; Konjeti R Sekhar Journal: Invest New Drugs Date: 2012-10-09 Impact factor: 3.850
Authors: Andrea Caporali; Elisabetta Pani; Anton J G Horrevoets; Nicolle Kraenkel; Atsuhiko Oikawa; Graciela B Sala-Newby; Marco Meloni; Brunella Cristofaro; Gallia Graiani; Aurelie S Leroyer; Chantal M Boulanger; Gaia Spinetti; Sung Ok Yoon; Paolo Madeddu; Costanza Emanueli Journal: Circ Res Date: 2008-06-19 Impact factor: 17.367
Authors: Cheen P Khoo; Maria G Roubelakis; Jack B Schrader; Grigorios Tsaknakis; Rebecca Konietzny; Benedikt Kessler; Adrian L Harris; Suzanne M Watt Journal: Sci Rep Date: 2017-03-09 Impact factor: 4.379