Endothelial STAT3 Activation Increases Vascular Leakage Through Downregulating Tight Junction Proteins: Implications for Diabetic Retinopathy

2016 ◽  
Vol 232 (5) ◽  
pp. 1123-1134 ◽  
Author(s):  
Jang-Hyuk Yun ◽  
Sung Wook Park ◽  
Kyung-Jin Kim ◽  
Jong-Sup Bae ◽  
Eun Hui Lee ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Tight Junction ◽  
Vascular Leakage ◽  
Tight Junction Proteins ◽  
Junction Proteins

scholarly journals Dendrobium chrysotoxumLindl. Alleviates Diabetic Retinopathy by Preventing Retinal Inflammation and Tight Junction Protein Decrease

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Zengyang Yu ◽  
Chenyuan Gong ◽  
Bin Lu ◽  
Li Yang ◽  
Yuchen Sheng ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Tight Junction ◽  
Diabetic Rats ◽  
Intercellular Adhesion Molecule ◽  
Tight Junction Proteins ◽  
Intercellular Adhesion Molecule 1 ◽  
Traditional Chinese Herbal Medicine ◽  
Junction Protein ◽  
Retinal Inflammation ◽  
Junction Proteins

Diabetic retinopathy (DR) is a serious complication of diabetes mellitus. This study aimed to observe the alleviation of the ethanol extract ofDendrobium chrysotoxumLindl. (DC), a traditional Chinese herbal medicine, on DR and its engaged mechanism. After DC (30 or 300 mg/kg) was orally administrated, the breakdown of blood retinal barrier (BRB) in streptozotocin- (STZ-) induced diabetic rats was attenuated by DC. Decreased retinal mRNA expression of tight junction proteins (including occludin and claudin-1) in diabetic rats was also reversed by DC. Western blot analysis and retinal immunofluorescence staining results further confirmed that DC reversed the decreased expression of occludin and claudin-1 proteins in diabetic rats. DC reduced the increased retinal mRNA expressions of intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factorα(TNFα), interleukin- (IL-) 6, and IL-1βin diabetic rats. In addition, DC alleviated the increased 1 and phosphorylated p65, IκB, and IκB kinase (IKK) in diabetic rats. DC also reduced the increased serum levels of TNFα, interferon-γ(IFN-γ), IL-6, IL-1β, IL-8, IL-12, IL-2, IL-3, and IL-10 in diabetic rats. Therefore, DC can alleviate DR by inhibiting retinal inflammation and preventing the decrease of tight junction proteins, such as occludin and claudin-1.

scholarly journals Blockade of Angiotensin II Attenuates VEGF-Mediated Blood—Retinal Barrier Breakdown in Diabetic Retinopathy

2008 ◽  
Vol 29 (3) ◽  
pp. 621-628 ◽  
Author(s):  
Jeong Hun Kim ◽  
Jin Hyoung Kim ◽  
Young Suk Yu ◽  
Chang Sik Cho ◽  
Kyu-Won Kim
Keyword(s):  
Diabetic Retinopathy ◽  
Angiotensin Ii ◽  
Tight Junction ◽  
Vascular Permeability ◽  
Ace Inhibitor ◽  
Ang Ii ◽  
Tight Junction Proteins ◽  
Blood Retinal Barrier ◽  
Brb Breakdown ◽  
Junction Proteins

Diabetic retinopathy (DR) is the leading cause of vision loss as a major complication of diabetes mellitus. The blood—retinal barrier (BRB) breakdown is a critical early event in the pathogenesis of DR. It has been known that the rennin-angiotensin system (RAS) is important in the progression of the DR via angiotensin II (Ang II), the effector of RAS. In this study, we showed that blockade of Ang II attenuates vascular endothelial growth factor (VEGF)-mediated BRB breakdown in DR. In streptozotocin-induced diabetes, retinal vascular permeability increased with upregulation of VEGF, where Ang II and its receptors were upregulated. Ang II induced VEGF expression in retinal endothelial cells accompanied by loss of tight junction proteins. However, the blockade of Ang II by perindopril, an angiotensin converting enzyme (ACE) inhibitor, inhibited upregulation of VEGF, and prevented the loss of tight junction proteins. Moreover, inhibition of Ang II by perindopril attenuated increased vascular permeability of diabetic retina accompanied by recovery of tight junction proteins in retinal vessels. Therefore, we suggest that the RAS involves in increased vascular permeability during early stage of DR, which is mediated by VEGF. Furthermore, the ACE inhibitor may have a therapeutic potential in the treatment of diabetic BRB breakdown.

Tight junction proteins in HCC and metastatic liver tumours

2005 ◽  
Vol 43 (05) ◽  
Author(s):  
Cs Páska ◽  
E Orbán ◽  
A Kiss ◽  
Zs Schaff ◽  
A Szijjártó ◽  
...  
Keyword(s):  
Tight Junction ◽  
Tight Junction Proteins ◽  
Liver Tumours ◽  
Metastatic Liver ◽  
Junction Proteins

Evidence that gene expression of ovarian follicular tight junction proteins is regulated in vivo and in vitro in cattle

2017 ◽  
Vol 95 (3) ◽  
pp. 1313 ◽  
Author(s):  
L. Zhang ◽  
L. F. Schütz ◽  
C. L. Robinson ◽  
M. L. Totty ◽  
L. J. Spicer
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Tight Junction Proteins ◽  
Junction Proteins

New insights in gut-liver axis in wild-type murine imiquimod-induced lupus

Lupus ◽  
2021 ◽  
Vol 30 (6) ◽  
pp. 926-936
Author(s):  
Georges Maalouly ◽  
Joelle Hajal ◽  
Charbel Noujeim ◽  
Michel Choueiry ◽  
Hussein Nassereddine ◽  
...  
Keyword(s):  
Tight Junction ◽  
Fecal Calprotectin ◽  
Liver Inflammation ◽  
Tight Junction Proteins ◽  
Wild Type ◽  
Imiquimod Cream ◽  
E Coli ◽  
Intestinal Pathology ◽  
Nfκb Pathway ◽  
Junction Proteins

Background Intestinal and hepatic manifestations of lupus seem to be underestimated in comparison to other major organ lesions. Although recent data point to gut-liver axis involvement in lupus, gut permeability dysfunction and liver inflammation need to be more investigated. Objective This study aims to assess fecal calprotectin, intestinal tight junction proteins and liver inflammation pathway in wild-type murine imiquimod- induced lupus. Methods C57BL/6 mice were topically treated on their right ears with 1.25 mg of 5% imiquimod cream, three times per week for six weeks. Fecal calprotectin was collected at day 0, 22 and 45. Renal, liver and intestinal pathology, as well as inflammatory markers, intestinal tight junction proteins, and E. coli protein in liver were assessed at sacrifice. Results At six weeks, lupus nephritis was confirmed on histopathology and NGAL and KIM-1 expression. Calprotectin rise started at day 22 and persists at day 45. Protein expression of Claudine, ZO-1 and occludin was significantly decreased. E. coli protein was significantly increased in liver with necro-inflammation and increased TLR4, TLR7, and pNFκB/NFκB liver expression. Conclusion This study is the first to demonstrate early fecal calprotectin increase and liver activation of TLR4- NFκB pathway in wild-type murine imiquimod-induced lupus.

Sign in / Sign up

Export Citation Format

Share Document