OBJECTIVE: SOX18, a member of the SOX gene family (SRY-like 3-hydroxy-3-methylglutaryl box gene), is a transcription factor expressed in the development of blood vessels during embryogenesis. We analyzed SOX18 expression in human coronary atherosclerotic lesions and investigated its potential function in vascular cells. METHODS AND RESULTS: In advanced human coronary atherosclerotic lesions, SOX18 immunostaining was localized in endothelial cells (on the luminal surface, in vasa vasorum, and in intimal neovessels) and in vascular smooth muscle cells (VSMCs) scattered in the intima, colocalizing with proliferating cell nuclear antigen. In cell cultures, SOX18 was mainly localized in subconfluent and denuded areas. Significant SOX18 mRNA levels (by Northern blot analysis and reverse transcription-polymerase chain reaction) were detected in cell cultures from human umbilical vein endothelial cells and human VSMCs. Antisense SOX18 inhibited DNA synthesis ([3H]thymidine incorporation) and vascular cell growth. Antisense SOX18 also significantly reduced VSMC regrowth after injury in an in vitro model of wound repair. CONCLUSIONS: Our results indicate that SOX18 is involved in vascular cell growth and suggest that this transcription factor may play a role in atherosclerosis.
OBJECTIVE:SOX18, a member of the SOX gene family (SRY-like 3-hydroxy-3-methylglutaryl box gene), is a transcription factor expressed in the development of blood vessels during embryogenesis. We analyzed SOX18 expression in humancoronary atherosclerotic lesions and investigated its potential function in vascular cells. METHODS AND RESULTS: In advanced humancoronary atherosclerotic lesions, SOX18 immunostaining was localized in endothelial cells (on the luminal surface, in vasa vasorum, and in intimal neovessels) and in vascular smooth muscle cells (VSMCs) scattered in the intima, colocalizing with proliferating cell nuclear antigen. In cell cultures, SOX18 was mainly localized in subconfluent and denuded areas. Significant SOX18 mRNA levels (by Northern blot analysis and reverse transcription-polymerase chain reaction) were detected in cell cultures from human umbilical vein endothelial cells and human VSMCs. Antisense SOX18 inhibited DNA synthesis ([3H]thymidine incorporation) and vascular cell growth. Antisense SOX18 also significantly reduced VSMC regrowth after injury in an in vitro model of wound repair. CONCLUSIONS: Our results indicate that SOX18 is involved in vascular cell growth and suggest that this transcription factor may play a role in atherosclerosis.
Authors: Mahyar Heydarpour; Julius Ejiofor; Michael Gilfeather; Gregory Stone; Josh Gorham; Christine E Seidman; Jon G Seidman; Maroun Yammine; Simon C Body; Sary F Aranki; Jochen D Muehlschlegel Journal: Ann Thorac Surg Date: 2018-07-17 Impact factor: 4.330
Authors: James R Springstead; B Gabriel Gugiu; Sangderk Lee; Seung Cha; Andrew D Watson; Judith A Berliner Journal: J Lipid Res Date: 2012-05-01 Impact factor: 5.922
Authors: Martina Hoeth; Heide Niederleithner; Renate Hofer-Warbinek; Martin Bilban; Herbert Mayer; Ulrike Resch; Christof Lemberger; Oswald Wagner; Erhard Hofer; Peter Petzelbauer; Rainer de Martin Journal: PLoS One Date: 2012-01-23 Impact factor: 3.240