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Title: Nuclear translocation of phosphorylated STAT3 regulates VEGF-A-induced lymphatic endothelial cell migration and tube formation

Abstract

Highlights: {yields} VEGF-A enhanced lymphatic endothelial cell migration and increased tube formation. {yields} VEGF-A treated lymphatic endothelial cell showed activation of STAT3. {yields} Dominant-negative STAT3 inhibited VEGF-A-induced lymphatic endothelial cell migration and tube formation. -- Abstract: Vascular endothelial growth factor (VEGF) is an endothelial cell-specific growth factor that regulates endothelial functions, and signal transducers and activators of transcription (STATs) are known to be important during VEGF receptor signaling. The aim of this study was to determine whether STAT3 regulates VEGF-induced lymphatic endothelial cell (LEC) migration and tube formation. VEGF-A (33 ng/ml) enhanced LEC migration by 2-fold and increased tube length by 25% compared with the control, as analyzed using a Boyden chamber and Matrigel assay, respectively. Western blot analysis and immunostaining revealed that VEGF-A induced the nuclear translocation of phosphorylated STAT3 in LECs, and this translocation was blocked by the transfection of LECs with an adenovirus vector expressing a dominant-negative mutant of STAT3 (Ax-STAT3F). Transfection with Ax-STAT3F also almost completely inhibited VEGF-A-induced LEC migration and tube formation. These results indicate that STAT3 is essential for VEGF-A-induced LEC migration and tube formation and that STAT3 regulates LEC functions.

Authors:
; ; ; ; ; ; ; ;  [1];  [1]
  1. Department of Dermatology, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295 (Japan)
Publication Date:
OSTI Identifier:
22207476
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 412; Journal Issue: 3; Other Information: Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ADENOVIRUS; GROWTH FACTORS; MUTANTS; RECEPTORS; TRANSCRIPTION; TRANSDUCERS; TRANSLOCATION

Citation Formats

Okazaki, Hideki, Tokumaru, Sho, Hanakawa, Yasushi, Shiraishi, Ken, Shirakata, Yuji, Dai, Xiuju, Yang, Lijun, Tohyama, Mikiko, Hashimoto, Koji, and Sayama, Koji. Nuclear translocation of phosphorylated STAT3 regulates VEGF-A-induced lymphatic endothelial cell migration and tube formation. United States: N. p., 2011. Web. doi:10.1016/J.BBRC.2011.07.111.
Okazaki, Hideki, Tokumaru, Sho, Hanakawa, Yasushi, Shiraishi, Ken, Shirakata, Yuji, Dai, Xiuju, Yang, Lijun, Tohyama, Mikiko, Hashimoto, Koji, & Sayama, Koji. Nuclear translocation of phosphorylated STAT3 regulates VEGF-A-induced lymphatic endothelial cell migration and tube formation. United States. https://doi.org/10.1016/J.BBRC.2011.07.111
Okazaki, Hideki, Tokumaru, Sho, Hanakawa, Yasushi, Shiraishi, Ken, Shirakata, Yuji, Dai, Xiuju, Yang, Lijun, Tohyama, Mikiko, Hashimoto, Koji, and Sayama, Koji. 2011. "Nuclear translocation of phosphorylated STAT3 regulates VEGF-A-induced lymphatic endothelial cell migration and tube formation". United States. https://doi.org/10.1016/J.BBRC.2011.07.111.
@article{osti_22207476,
title = {Nuclear translocation of phosphorylated STAT3 regulates VEGF-A-induced lymphatic endothelial cell migration and tube formation},
author = {Okazaki, Hideki and Tokumaru, Sho and Hanakawa, Yasushi and Shiraishi, Ken and Shirakata, Yuji and Dai, Xiuju and Yang, Lijun and Tohyama, Mikiko and Hashimoto, Koji and Sayama, Koji},
abstractNote = {Highlights: {yields} VEGF-A enhanced lymphatic endothelial cell migration and increased tube formation. {yields} VEGF-A treated lymphatic endothelial cell showed activation of STAT3. {yields} Dominant-negative STAT3 inhibited VEGF-A-induced lymphatic endothelial cell migration and tube formation. -- Abstract: Vascular endothelial growth factor (VEGF) is an endothelial cell-specific growth factor that regulates endothelial functions, and signal transducers and activators of transcription (STATs) are known to be important during VEGF receptor signaling. The aim of this study was to determine whether STAT3 regulates VEGF-induced lymphatic endothelial cell (LEC) migration and tube formation. VEGF-A (33 ng/ml) enhanced LEC migration by 2-fold and increased tube length by 25% compared with the control, as analyzed using a Boyden chamber and Matrigel assay, respectively. Western blot analysis and immunostaining revealed that VEGF-A induced the nuclear translocation of phosphorylated STAT3 in LECs, and this translocation was blocked by the transfection of LECs with an adenovirus vector expressing a dominant-negative mutant of STAT3 (Ax-STAT3F). Transfection with Ax-STAT3F also almost completely inhibited VEGF-A-induced LEC migration and tube formation. These results indicate that STAT3 is essential for VEGF-A-induced LEC migration and tube formation and that STAT3 regulates LEC functions.},
doi = {10.1016/J.BBRC.2011.07.111},
url = {https://www.osti.gov/biblio/22207476}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 3,
volume = 412,
place = {United States},
year = {Fri Sep 02 00:00:00 EDT 2011},
month = {Fri Sep 02 00:00:00 EDT 2011}
}