Publication Name	World Journal of Transplantation
Manuscript ID	26201
Country	Germany

Received	2016-03-30 09:07
Peer-Review Started	2016-03-31 10:55
To Make the First Decision	2016-05-16 10:57
Return for Revision	2016-05-17 16:19
Revised	2016-06-24 14:28
Second Decision	2016-07-05 17:38
Accepted by Journal Editor-in-Chief	2016-07-05 23:52
Accepted by Company Editor-in-Chief	2016-07-18 10:42
Articles in Press	2016-07-18 10:42
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2016-09-19 10:13
Publish the Manuscript Online	2016-09-23 15:41

ISSN	2220-3230 (online)
Open Access	This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Copyright	© The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
Article Reprints	For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
Permissions	For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
Publisher	Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Website	http://www.wjgnet.com

Category	Transplantation
Manuscript Type	Basic Study
Article Title	Pharmacological Tie2 activation in kidney transplantation
Manuscript Source	Invited Manuscript
All Author List	Kristina Thamm, Florence Njau, Paul Van Slyke, Daniel J Dumont, Joon-Keun Park, Hermann Haller and Sascha David
Funding Agency and Grant Number	Funding Agency Grant Number Else-Kröner Fresenius Stiftung 2013_A154 German Research Foundation DA 1209/4-1 (to David S)
Corresponding Author	Sascha David, MD, Department of Nephrology and Hypertension, Medical School Hannover, Carl Neuberg-Straße 1, 30625 Hannover, Germany. david.sascha@mh-hannover.de
Key Words	Vasculotide; Tie2; Kidney transplantation; Endothelium; Angiopoietin
Core Tip	Activation of the Tie2 receptor has been shown to be beneficial in different models of disease. Here, we demonstrate that agonistic stimulation of Tie2 via the drug-like putative therapeutic termed “vasculotide” (VT) ameliorates outcome in a murine MHC-mismatched kidney transplant model. VT treatment (i.e., activation of endothelial Tie2) prevented inflammation and fibrosis thereby preserving graft function. Moreover, single administration at the time of transplantation was also sufficient to prolong survival compared to control group.
Publish Date	2016-09-23 15:41
Citation	Thamm K, Njau F, Van Slyke P, Dumont DJ, Park JK, Haller H, David S. Pharmacological Tie2 activation in kidney transplantation. World J Transplant 2016; 6(3): 573-582
URL	http://www.wjgnet.com/2220-3230/full/v6/i3/573.htm
DOI	http://dx.doi.org/10.5500/wjt.v6.i3.573

Full Article (PDF)	WJT-6-573.pdf
Full Article (Word)	WJT-6-573.doc
Manuscript File	26201-Review.docx
Answering Reviewers	26201-Answering reviewers.pdf
Audio Core Tip	26201-Audio core tip.mp3
Biostatistics Review Certificate	26201-Biostatistics statement.pdf
Conflict-of-Interest Disclosure Form	26201-Conflict-of-interest statement.pdf
Copyright License Agreement	26201-Copyright assignment.pdf
Approved Grant Application Form(s) or Funding Agency Copy of any Approval Document(s)	26201-Grant application form(s).pdf
Institutional Animal Care and Use Committee Approval Form or Document	26201-Institutional animal care and use committee statement.pdf
Institutional Review Board Approval Form or Document	26201-Institutional review board statement.pdf
Peer-review Report	26201-Peer-review(s).pdf
Journal Editor-in-Chief Review Report	26201-Journal editor-in-chief review report.pdf
Scientific Misconduct Check	26201-Scientific misconduct check.pdf
Scientific Editor Work List	26201-Scientific editor work list.pdf