肺微血管内皮细胞屏障功能调控与修复机制研究进展
摘要
<正>肺水肿是重症肺炎、脓毒血症以及急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)等呼吸危重症的主要病理特点,其发病机制是肺微血管屏障功能下降而导致的微血管通透性增高和肺泡内液体清除率的降低。目前对各种原因引起的ALI仍然缺乏有效的治疗手段。因此,充分认识肺微血管内皮细胞(PMVEC)屏障功能的调节及损伤修复机制,对于肺水肿的防治具有重要意义。本文就PMVEC屏障功能调控与修复机制进行综述。
引文
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[3]孙喜家,王键,冯娅妮.七氟烷对脂多糖诱导小鼠肺损伤的保护作用及与Toll样受体[O2][O3]4表达的关系[J].广东医学,2016,37(1):59-61.
[4]Minamino T,Komuro I.Regeneration of the endothelium as a novel therapeutic strategy for acute lung injury[J].J Clin Invest,2006,116(9):2316-2319.
[5]Shimizu Y,Camp SM,Sun X,et al.Sp1-mediated nonmuscle myosin light chain kinase expression and enhanced activity in vascular endothelial growth factor-induced vascular permeability[J].Pulm Circ,2015,5(4):707-715.
[6]Sawant DA,Wilson RL,Tharakan B,et al.Tumor necrosis factor-α-induced microvascular endothelial cell hyperpermeability:role of intrinsic apoptotic signaling[J].J Physiol Biochem,2014,70(4):971-980.
[7]Seybold J,Thomas D,Witzenrath M,et al.Tumor necrosis factoralpha-dependent expression of phosphodiesterase 2:role in endothelial hyperpermeability[J].Blood,2005,105(9):3569-3576.
[8]Goodman RB,Pugin J,Lee JS,et al.Cytokine-mediated inflammation in acute lung injury[J].Cytokine Growth Factor Rev,2003,14(6):523-535.
[9]Donnelly SC,Strieter RM,Kunkel SL,et al.Interleukin-8 and development of adult respiratory distress syndrome in at-risk patient groups[J].Lancet,1993,341(8846):643-647.
[10]Frank JA,Matthay MA.TGF-beta and lung fluid balance in ARDS[J].Proc Natl Acad Sci U S A,2014,111(3):885-886.
[11]Troyanovsky B,Alvarez DF,King JA,et al.Thrombin enhances the barrier function of rat microvascular endothelium in a PAR-1-dependent manner[J].Am J Physiol Lung Cell Mol Physiol,2008,294(2):L266-L275.
[12]Adamson RH,Zeng M,Adamson GN,et al.PAF-and bradykinin-induced hyperpermeability of rat venules is independent of actin-myosin contraction[J].Am J Physiol Heart Circ Physiol,2003,285(1):H406-H417.
[13]Mikelis CM,Simaan M,Ando K,et al.Rho A and ROCK mediate histamine-induced vascular leakage and anaphylactic shock[J].Nat Commun,2015,6:6725.
[14]Bedard K,Krause KH.The NOX Family of ROS-Generating NADPH Oxidases:Physiology and Pathophysiology[J].Physiological Reviews,2007,87(1):245-313.
[15]Pollard TD,Borisy GG.Cellular motility driven by assembly and disassembly of actin filaments[J].Cell,2003,112(4):453-465.
[16]Borisy GG,Svitkina TM.Actin machinery:pushing the envelope[J].Curr Opin Cell Biol,2000,12(1):104-112.
[17]Gorovoy M,Han J,Pan H,et al.LIM kinase 1 promotes endothelial barrier disruption and neutrophil infiltration in mouse lungs[J].Circ Res,2009,105(6):549-556.
[18]Mirzapoiazova T,Kolosova IA,Moreno L,et al.Suppression of endotoxin-induced inflammation by taxol[J].Eur Respir J,2007,30(3):429-435.
[19]Spindler V,Schlegel N,Waschke J.Role of GTPases in control of microvascular permeability[J].Cardiovasc Res,2010,87(2):243-253.
[20]Kasa A,Csortos C,Verin AD.Cytoskeletal mechanisms regulating vascular endothelial barrier function in response to acute lung injury[J].Tissue Barriers,2015,3(1-2):e974448.
[21]Ward DT.Calcium receptor-mediated intracellular signalling[J].Cell Calcium,2004,35(3):217-228.
[22]Kandasamy K,Bezavada L,Escue RB,et al.Lipopolysaccharide induces endoplasmic store Ca2+-dependent inflammatory responses in lung microvessels[J].PLo S One,2013,8(5):e63465.
[23]Waschke J,Burger S,Curry FR,et al.Activation of Rac-1 and Cdc42 stabilizes the microvascular endothelial barrier[J].Histochem Cell Biol,2006,125(4):397-406.
[24]Wan H,Liu C,Wert SE,et al.CDC42 is required for structural patterning of the lung during development[Z].2013:374,46-57.
[25]Zhao YD,Ohkawara H,Rehman J,et al.Bone marrow progenitor cells induce endothelial adherens junction integrity by sphingosine-1-phosphate-mediated Rac1 and Cdc42 signaling[J].Circ Res,2009,105(7):696-704.