Role of Cytoskeleton Structure in The Transformation of Endocytosis Pathways of Vascular Endothelial Cadherin after Lipopolysaccharide Treatment_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

 ZHANGYe ,  ZHANGLian-yang , TANHao , SUNShi-jin , LIYang

State Key Laboratory of Trauma, Burns and Combined Injury, Trauma Center of PLA, Institute of Surgery Research, Daping Hospital, The Third Military Medical University, Chongqing 400042, China;

Corresponding?author：

ZHANGLian-yang, Email: hpzhangly@163.com

Keywords：

Lipopolysaccharide; Vascular endothelial cadherin; Clathrin; Caveolae; Actin cytoskeleton; Vascular hyperpermeability

DOI：

10.7507/1007-9424.20150073

Video：

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Objective To explore the effects of cytoskeleton depolymerizing agent and stabilizer on the clathrin/caveolae-mediated endocytosis, the expression of membrane vascular endothelial cadherin (VE-cad), and the vascular permeability by the transformation of cytoskeleton structure after lipopolysaccharide (LPS) treatment. Methods CRL-2922 cells were used in the experiments. Indexes were tested at corresponding time point according to name of group, but in blank control group indexes could be tested at any time point. CRL-2922 cells were divided into blank control group, LPS-1 h group, and LPS-4 h group to observe cytoskeleton structure; CRL-2922 cells were divided into LPS-1 h group, Cyt D+LPS-1 h group, LPS-4 h group, and Jasp+LPS-4 h group to determine the expression of membrane VE-cad, and to determine the expression of its co-immunoprecipitation with clathrin and caveolin-1 (Cav1); besides, CRL-2922 cells were divided into blank control group, LPS-1 h group, Cyt D+LPS-1 h group, LPS-4 h group, and Jasp+LPS-4 h group to detect the cumulative infiltration rate. Results ①The cytoskeleton showed a dynamic change after LPS treat-ment, the F-actin polymerized and stress fibers formed at 1 hour after LPS treatment, but depolymerized at 4 hours after LPS treatment. ②Compared with LPS-1 h group, the level of co-immunoprecipitation of VE-cad with clathrin in Cyt D+ LPS-1 h group decreased (P<0.05), the level of co-immunoprecipitation of VE-cad with Cav1 increased (P<0.05), and expression level of VE-cad in plasma membrane decreased (P<0.05); compared with LPS-4 h group, there was no significant difference in the level of co-immunoprecipitation of VE-cad with clathrin of Jasp+LPS-4 h group (P>0.05), but the level of co-immunoprecipitation of VE-cad with Cav1 decreased in Jasp+LPS-4 h group (P<0.05), and expression level of VE-cad in plasma membrane increased (P<0.05). ③Compared with blank control group, the cumulative infiltration rates of LPS-1 h group and LPS-4 h group were both higher (P<0.05); compared with LPS-1 h group, the cumulative infiltration rate of Cyt D+LPS-1 h group was higher (P<0.05); compared with LPS-4 h group, the cumulative infiltration rate of Jasp+LPS-4 h group was lower (P<0.05). Conclusion Actin cytoskeleton shifts from polymerization to depoly-merization after LPS treatment, the structural change of actin cytoskeleton is an important reason for the transformation of VE-cad endocytosis pathway from clathrin-mediated to caveolae-mediated after LPS treatment.

Citation： ZHANGYe, ZHANGLian-yang, TANHao, SUNShi-jin, LIYang. Role of Cytoskeleton Structure in The Transformation of Endocytosis Pathways of Vascular Endothelial Cadherin after Lipopolysaccharide Treatment. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2015, 22(3): 269-273. doi: 10.7507/1007-9424.20150073 Copy

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2.	Hamidian Jahromi A, Freeland K, Youssef AM. Intra-abdominal hypertension causes disruption of the blood-brain barrier in mice, which is increased with added severe head trauma. J Trauma Acute Care Surg, 2012, 73(5):1175-1179.
3.	中華醫學會創傷學分會創傷急救與多發傷學組. 創傷后腹腔高壓癥/腹腔間隙綜合征診治規范. 中華創傷雜志, 2012, 28(11):961-964.
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5.	Lundblad C, Axelberg H, Grande PO. Treatment with the sphingo-sine-1-phosphate analogue FTY 720 reduces loss of plasma volume during experimental sepsis in the rat. Acta Anaesthesiol Scand, 2013, 57(6):713-718.
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9.	Shen L, Turner JR. Actin depolymerization disrupts tight junctions via caveolae-mediated endocytosis. Mol Biol Cell, 2005, 16(9):3919-3936.
10.	Czupalla CJ, Liebner S, Devraj K. In vitro models of the blood-brain barrier. Methods Mol Biol, 2014, 1135:415-437.
11.	Hayakawa K, Pham LD, Arai K, et al. Reactive astrocytes promote adhesive interactions between brain endothelium and endothelial progenitor cells via HMGB1 and beta-2 integrin signaling. Stem Cell Res, 2014, 12(2):531-538.
12.	Xiaolu D, Jing P, Fang H, et al. Role of p115RhoGEF in lipopoly-saccharide-induced mouse brain microvascular endothelial barrier dysfunction. Brain Res, 2011, 1387:1-7.
13.	Shivanna M, Rajashekhar G, Srinivas SP. Barrier dysfunction of the corneal endothelium in response to TNF-alpha:role of p38 MAP kinase. Invest Ophthalmol Vis Sci, 2010, 51(3):1575-1582.
14.	Giusti B, Margheri F, Rossi L, et al. Desmoglein-2-integrin beta-8 interaction regulates actin assembly in endothelial cells:deregulation in systemic sclerosis. PLoS One, 2013, 8(7):e68117.
15.	Li L, Wang L, Song P, et al. Critical role of histone demethylase RBP2in human gastric cancer angiogenesis. Mol Cancer, 2014, 13:81.
16.	Sánchez FA, Rana R, González FG, et al. Functional significance of cytosolic endothelial nitric-oxide synthase (eNOS):regulation of hyperpermeability. J Biol Chem, 2011, 286(35):30409-30414.
17.	Stagg HW, Bowen KA, Sawant DA, et al. Tumor necrosis factor-related apoptosis-inducing ligand promotes microvascular endothelial cell hyperpermeability through phosphatidylinositol 3-kinase pathway. Am J Surg, 2013, 205(4):419-425.
18.	Ochoa CD, Stevens T. Studies on the cell biology of interendothelial cell gaps. Am J Physiol Lung Cell Mol Physiol, 2012, 302(3):L275-L286.
19.	Tiruppathi C, Shimizu J, Miyawaki-Shimizu K, et al. Role of NF-kappaB-dependent caveolin-1 expression in the mechanism of increased endothelial permeability induced by lipopolysaccharide. J Biol Chem, 2008, 283(7):4210-4218.
20.	Dubrovskyi O, Birukova AA, Birukov KG. Measurement of local permeability at subcellular level in cell models of agonist-and ventilator-induced lung injury. Lab Invest, 2013, 93(2):254-263.
21.	Kumar P, Shen Q, Pivetti CD, et al. Molecular mechanisms of endothelial hyperpermeability:implications in inflammation. Expert Rev Mol Med, 2009, 11:e19.
22.	Desclozeaux M, Venturato J, Wylie FG, et al. Active Rab11 and functional recycling endosome are required for E-cadherin traffic-king and lumen formation during epithelial morphogenesis. Am J Physiol Cell Physiol, 2008, 295(2):C545-C556.
23.	D'Souza-Schorey C. Disassembling adherens junctions:breaking up is hard to do. Trends Cell Biol, 2005, 15(1):19-26.
24.	Palacios F, Tushir JS, Fujita Y, et al. Lysosomal targeting of E-cadherin:a unique mechanism for the down-regulation of cell-cell adhesion during epithelial to mesenchymal transitions. Mol Cell Biol, 2005, 25(1):389-402.
25.	Sounni NE, Paye A, Host L, et al. MT-MMPS as regulators of vessel stability associated with angiogenesis. Front Pharmacol, 2011, 2:111.

1. ?Carrillo-Esper R, Sosa-García JO, Carrillo-Córdova JR, et al. Synd-rome of abdominal compartment in trauma. Cir Cir, 2012, 80(6):550-555.
2. Hamidian Jahromi A, Freeland K, Youssef AM. Intra-abdominal hypertension causes disruption of the blood-brain barrier in mice, which is increased with added severe head trauma. J Trauma Acute Care Surg, 2012, 73(5):1175-1179.
3. 中華醫學會創傷學分會創傷急救與多發傷學組. 創傷后腹腔高壓癥/腹腔間隙綜合征診治規范. 中華創傷雜志, 2012, 28(11):961-964.
4. Rolando M, Munro P, Stefani C, et al. Injection of staphylococcus aureus EDIN by the bacillus anthracis protective antigen machinery induces vascular permeability. Infect Immun, 2009, 77(9):3596-3601.
5. Lundblad C, Axelberg H, Grande PO. Treatment with the sphingo-sine-1-phosphate analogue FTY 720 reduces loss of plasma volume during experimental sepsis in the rat. Acta Anaesthesiol Scand, 2013, 57(6):713-718.
6. Engqvist-Goldstein AE, Drubin DG. Actin assembly and endocy-tosis: from yeast to mammals. Annu Rev Cell Dev Biol, 2003, 19:287-332.
7. Yarar D, Waterman-Storer CM, Schmid SL. A dynamic actin cytoskeleton functions at multiple stages of clathrin-mediated endocytosis. Mol Biol Cell, 2005, 16(2):964-975.
8. Engqvist-Goldstein AE, Warren RA, Kessels MM, et al. The actin-binding protein Hip1R associates with clathrin during early stages of endocytosis and promotes clathrin assembly in vitro. J Cell Biol, 2001, 154(6):1209-1223.
9. Shen L, Turner JR. Actin depolymerization disrupts tight junctions via caveolae-mediated endocytosis. Mol Biol Cell, 2005, 16(9):3919-3936.
10. Czupalla CJ, Liebner S, Devraj K. In vitro models of the blood-brain barrier. Methods Mol Biol, 2014, 1135:415-437.
11. Hayakawa K, Pham LD, Arai K, et al. Reactive astrocytes promote adhesive interactions between brain endothelium and endothelial progenitor cells via HMGB1 and beta-2 integrin signaling. Stem Cell Res, 2014, 12(2):531-538.
12. Xiaolu D, Jing P, Fang H, et al. Role of p115RhoGEF in lipopoly-saccharide-induced mouse brain microvascular endothelial barrier dysfunction. Brain Res, 2011, 1387:1-7.
13. Shivanna M, Rajashekhar G, Srinivas SP. Barrier dysfunction of the corneal endothelium in response to TNF-alpha:role of p38 MAP kinase. Invest Ophthalmol Vis Sci, 2010, 51(3):1575-1582.
14. Giusti B, Margheri F, Rossi L, et al. Desmoglein-2-integrin beta-8 interaction regulates actin assembly in endothelial cells:deregulation in systemic sclerosis. PLoS One, 2013, 8(7):e68117.
15. Li L, Wang L, Song P, et al. Critical role of histone demethylase RBP2in human gastric cancer angiogenesis. Mol Cancer, 2014, 13:81.
16. Sánchez FA, Rana R, González FG, et al. Functional significance of cytosolic endothelial nitric-oxide synthase (eNOS):regulation of hyperpermeability. J Biol Chem, 2011, 286(35):30409-30414.
17. Stagg HW, Bowen KA, Sawant DA, et al. Tumor necrosis factor-related apoptosis-inducing ligand promotes microvascular endothelial cell hyperpermeability through phosphatidylinositol 3-kinase pathway. Am J Surg, 2013, 205(4):419-425.
18. Ochoa CD, Stevens T. Studies on the cell biology of interendothelial cell gaps. Am J Physiol Lung Cell Mol Physiol, 2012, 302(3):L275-L286.
19. Tiruppathi C, Shimizu J, Miyawaki-Shimizu K, et al. Role of NF-kappaB-dependent caveolin-1 expression in the mechanism of increased endothelial permeability induced by lipopolysaccharide. J Biol Chem, 2008, 283(7):4210-4218.
20. Dubrovskyi O, Birukova AA, Birukov KG. Measurement of local permeability at subcellular level in cell models of agonist-and ventilator-induced lung injury. Lab Invest, 2013, 93(2):254-263.
21. Kumar P, Shen Q, Pivetti CD, et al. Molecular mechanisms of endothelial hyperpermeability:implications in inflammation. Expert Rev Mol Med, 2009, 11:e19.
22. Desclozeaux M, Venturato J, Wylie FG, et al. Active Rab11 and functional recycling endosome are required for E-cadherin traffic-king and lumen formation during epithelial morphogenesis. Am J Physiol Cell Physiol, 2008, 295(2):C545-C556.
23. D'Souza-Schorey C. Disassembling adherens junctions:breaking up is hard to do. Trends Cell Biol, 2005, 15(1):19-26.
24. Palacios F, Tushir JS, Fujita Y, et al. Lysosomal targeting of E-cadherin:a unique mechanism for the down-regulation of cell-cell adhesion during epithelial to mesenchymal transitions. Mol Cell Biol, 2005, 25(1):389-402.
25. Sounni NE, Paye A, Host L, et al. MT-MMPS as regulators of vessel stability associated with angiogenesis. Front Pharmacol, 2011, 2:111.

CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Role of Cytoskeleton Structure in The Transformation of Endocytosis Pathways of Vascular Endothelial Cadherin after Lipopolysaccharide Treatment

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