Effects of dexamethasone on angiotensin II‑induced changes of monolayer permeability and F-actin distribution in glomerular endothelial cells

Fang,Junyan; Wang,Miao; Zhang,Wei; Wang,Yingdeng

doi:10.3892/etm.2013.1278

Effects of dexamethasone on angiotensin II‑induced changes of monolayer permeability and F-actin distribution in glomerular endothelial cells

Authors:
- Junyan Fang
- Miao Wang
- Wei Zhang
- Yingdeng Wang
View Affiliations

Affiliations: Department of Clinical Nephrology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, P.R. China
Published online on: August 30, 2013 https://doi.org/10.3892/etm.2013.1278
Pages: 1131-1136

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

The aim of this study was to investigate the changes in monolayer permeability and F-actin distribution caused by angiotensin II (Ang II)‑induced injury in glomerular endothelial cells (GENCs) and the effects of dexamethasone on these changes. GENCs isolated and cultured from Wistar rats were used to examine the changes in monolayer permeability and F-actin distribution induced by Ang II. GENC permeability was evaluated by measuring the diffusion of biotin‑conjugated bovine serum albumin (biotin-BSA) across a cell monolayer. The expression levels and distribution of F-actin were assessed by flow cytometry. The biotin-BSA concentrations were measured by capture enzyme‑linked immunosorbent assay. Ang II at a concentration of 10 mg/l increased the permeability of the GENC monolayer at 6 h and 12 h (P<0.05 and P<0.01, respectively) and caused F-actin depolymerisation at 6 h and 12 h (P<0.01). The two effects attributed to Ang II were significantly inhibited by dexamethasone treatment (P<0.01). The increased permeability of the GENC monolayer induced by Ang II was significantly correlated with the depolymerisation of F-actin. Dexamethasone abrogated the Ang II-mediated damage to GENCs indicating that it may play an important role in protecting GENCs from injury.

View Figures

View References

1.	Vianna HR, Soares CM, Tavares MS, Teixeira MM and Silva AC: Inflammation in chronic kidney disease: the role of cytokines. J Bras Nefrol. 33:351–364. 2011.(In Portuguese).
2.	Cheung WW, Paik KH and Mak RH: Inflammation and cachexia in chronic kidney disease. Pediatr Nephrol. 25:711–724. 2010. View Article : Google Scholar : PubMed/NCBI
3.	Sun YB, Qu X, Zhang X, Caruana G, Bertram JF and Li J: Glomerular endothelial cell injury and damage precedes that of podocytes in adriamycin-induced nephropathy. PLoS One. 8:e550272013. View Article : Google Scholar : PubMed/NCBI
4.	Stehouwer CD: Endothelial dysfunction in diabetic nephropathy: state of the art and potential significance for non-diabetic renal disease. Nephrol Dial Transplant. 18:778–781. 2004. View Article : Google Scholar : PubMed/NCBI
5.	Birukova AA, Birukov KG, Adyshev D, et al: Involvement of microtubules and Rho pathway in TGF-beta1-induced lung vascular barrier dysfunction. J Cell Physiol. 204:934–947. 2005. View Article : Google Scholar : PubMed/NCBI
6.	Dudek SM and Garcia JG: Cytoskeletal regulation of pulmonary vascular permeability. J Appl Physiol. 91:1487–1500. 2001.PubMed/NCBI
7.	Waschke J, Curry FE, Adamson RH and Drenckhahn D: Regulation of actin dynamics is critical for endothelial barrier functions. Am J Physiol Heart Circ Physiol. 288:H1296–H1305. 2005. View Article : Google Scholar : PubMed/NCBI
8.	You QH, Sun GY, Wang N, Chen S and Luo QL: Role of src-suppressed C kinase substrate in rat pulmonary microvascular endothelial hyperpermeability stimulated by inflammatory cytokines. Inflamm Res. 59:949–958. 2010. View Article : Google Scholar
9.	Woolf AS, Gnudi L and Long DA: Roles of angiopoietins in kidney development and disease. J Am Soc Nephrol. 20:239–244. 2009. View Article : Google Scholar : PubMed/NCBI
10.	Navar LG and Nishiyama A: Why are angiotensin concentrations so high in the kidney? Curr Opin Nephrol Hypertens. 13:107–115. 2004. View Article : Google Scholar : PubMed/NCBI
11.	Yao Y, Wang L, Zhang H, et al: A novel anticancer therapy that simultaneously targets aberrant p53 and Notch activities in tumors. PLoS One. 7:e466272012. View Article : Google Scholar : PubMed/NCBI
12.	Akis N and Madaio MP: Isolation, culture, and characterization of endothelial cells from mouse glomeruli. Kidney Int. 65:2223–2227. 2004. View Article : Google Scholar : PubMed/NCBI
13.	Rops AL, van der Vlag J, Jacobs CW, et al: Isolation and characterization of conditionally immortalized mouse glomerular endothelial cell lines. Kidney Int. 66:2193–2201. 2004. View Article : Google Scholar : PubMed/NCBI
14.	Zhao JH, Huang L, Wang JP, et al: Culture of endothelial cells from rat glomeruli and the effects of high glucose concentration on its nitric oxide secretion. Immunol J. 23:13–15. 2007.(In Chinese).
15.	Green DF, Hwang KH, Ryan US and Bourgoignie JJ: Culture of endothelial cells from baboon and human glomeruli. Kidney Int. 41:1506–1516. 1992. View Article : Google Scholar : PubMed/NCBI
16.	Johnston AP, Baker J, Bellamy LM, et al: Regulation of muscle satellite cell activation and chemotaxis by angiotensin II. PLoS One. 5:e152122010. View Article : Google Scholar : PubMed/NCBI
17.	Li Y, Wu Y, Gong X, et al: Low molecular weight heparin decreases the permeability of glomerular endothelial cells when exposed to pre-eclampsia serum in vitro. Nephrology (Carlton). 17:754–759. 2012. View Article : Google Scholar : PubMed/NCBI
18.	Cooper JA, Del Vecchio PJ, Minnear FL, et al: Measurement of albumin permeability across endothelial monolayers in vitro. J Appl Physiol. 62:1076–1083. 1987.PubMed/NCBI
19.	Xu X, Jia R, Zhou Y, et al: Microarray-based analysis: identification of hypoxia-regulated microRNAs in retinoblastoma cells. Int J Oncol. 38:1385–1393. 2011.PubMed/NCBI
20.	Annuk M, Zilmer M, Lind L, Linde T and Fellström B: Oxidative stress and endothelial function in chronic renal failure. J Am Soc Nephrol. 12:2747–2752. 2001.PubMed/NCBI
21.	Garcia JG and Schaphorst KL: Regulation of endothelial cell gap formation and paracellular permeability. J Investig Med. 43:117–126. 1995.PubMed/NCBI
22.	Miura S, Saku K and Karnik SS: Molecular analysis of the structure and function of the angiotensin II type 1 receptor. Hypertens Res. 26:937–943. 2003. View Article : Google Scholar : PubMed/NCBI
23.	Davis B, Dei Cas A, Long DA, et al: Podocyte-specific expression of angiopoietin-2 causes proteinuria and apoptosis of glomerular endothelia. J Am Soc Nephrol. 18:2320–2329. 2007. View Article : Google Scholar : PubMed/NCBI
24.	Cheng ZJ, Vapaatalo H and Mervaala E: Angiotensin II and vascular inflammation. Med Sci Monit. 11:RA194–R205. 2005.PubMed/NCBI
25.	Kim J, Ahn S, Ren XR, et al: Functional antagonism of different G protein-coupled receptor kinases for beta-arrestin-mediated angiotensin II receptor signaling. Proc Natl Acad Sci USA. 102:1442–1447. 2005. View Article : Google Scholar : PubMed/NCBI
26.	Yan M, Cheng C, Jiang J, et al: Essential role of SRC suppressed C kinase substrates in Schwann cells adhesion, spreading and migration. Neurochem Res. 34:1002–1010. 2009. View Article : Google Scholar : PubMed/NCBI
27.	Suzuki Y, Ruiz-Ortega M, Lorenzo O, Ruperez M, Esteban V and Egido J: Inflammation and angiotensin II. Int J Biochem Cell Biol. 35:881–900. 2003. View Article : Google Scholar
28.	Lv J, Xu D, Perkovic V, Ma X, et al: Corticosteroid therapy in IgA nephropathy. J Am Soc Nephrol. 23:1108–1116. 2012. View Article : Google Scholar
29.	Hodson EM, Willis NS and Craig J: Corticosteroid therapy for nephrotic syndrome in children. Cochrane Database Syst Rev. 4:CD0015332007.