Next Article in Journal
New Is Old, and Old Is New: Recent Advances in Antibiotic-Based, Antibiotic-Free and Ethnomedical Treatments against Methicillin-Resistant Staphylococcus aureus Wound Infections
Next Article in Special Issue
Hypercholesterolemia Tunes Hematopoietic Stem/Progenitor Cells for Inflammation and Atherosclerosis
Previous Article in Journal
Piperlongumine Suppresses Proliferation of Human Oral Squamous Cell Carcinoma through Cell Cycle Arrest, Apoptosis and Senescence
Previous Article in Special Issue
Comparison of Topical Hemostatic Agents in a Swine Model of Extremity Arterial Hemorrhage: BloodSTOP iX Battle Matrix vs. QuikClot Combat Gauze
Article Menu
Issue 5 (May) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2016, 17(5), 615; doi:10.3390/ijms17050615

TNFSF15 Inhibits Blood Retinal Barrier Breakdown Induced by Diabetes

Department of Ophthalmology, Tianjin Medical University General Hospital, Tianjin 300052, China
*
Author to whom correspondence should be addressed.
Academic Editors: Shaker A. Mousa and Lu Cai
Received: 3 January 2016 / Revised: 7 April 2016 / Accepted: 11 April 2016 / Published: 25 April 2016
(This article belongs to the Special Issue Vascular Biology and Therapeutics)
View Full-Text   |   Download PDF [3440 KB, uploaded 25 April 2016]   |  

Abstract

Tumor necrosis factor superfamily 15 (TNFSF15) is an endogenous neovascularization inhibitor and an important negative regulator of vascular homeostasis. This study aimed to explore the potential role of TNFSF15 in diabetic retinopathy. Vitreous TNFSF15 and VEGF levels in proliferative diabetic retinopathy (PDR) patients were detected by ELISA. Retinal expression of TNFSF15 and the content of tight junction proteins (TJPs) in rats were detected by immunohistochemistry and Western blot, respectively. The blood retinal barrier (BRB) permeability was evaluated using Evans Blue (EB) dye. The TNFSF15/VEGF ratio was decreased in the vitreous fluid of patients with PDR relative to the controls, even though the expression levels of TNFSF15 were higher. TNFSF15 was dramatically decreased one month later after diabetes induction (p < 0.001), and then increased three months later and thereafter. TNFSF15 treatment significantly protected the BRB in the diabetic animals. Diabetes decreased TJPs levels in the retina, and these changes were inhibited by TNFSF15 treatment. Moreover, TNFSF15 decreased activation of VEGF both in mRNA and protein levels caused by diabetes. These results indicate that TNFSF15 is an important inhibitor in the progression of DR and suggest that the regulation of TNFSF15 shows promise for the development of diabetic retinopathy treatment strategies. View Full-Text
Keywords: tumor necrosis factor superfamily 15; vascular endothelial growth factor; blood retinal barrier; vascular permeability; diabetic retinopathy tumor necrosis factor superfamily 15; vascular endothelial growth factor; blood retinal barrier; vascular permeability; diabetic retinopathy
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Jiang, F.; Chen, Q.; Huang, L.; Wang, Y.; Zhang, Z.; Meng, X.; Liu, Y.; Mao, C.; Zheng, F.; Zhang, J.; Yan, H. TNFSF15 Inhibits Blood Retinal Barrier Breakdown Induced by Diabetes. Int. J. Mol. Sci. 2016, 17, 615.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top