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首页> 外文期刊>Journal of Cellular Physiology >Vertebrate Lonesome Kinase Regulated Extracellular Matrix Protein Phosphorylation, Cell Shape, and Adhesion in Trabecular Meshwork Cells
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Vertebrate Lonesome Kinase Regulated Extracellular Matrix Protein Phosphorylation, Cell Shape, and Adhesion in Trabecular Meshwork Cells

机译：脊椎动物寂寞激酶调节细胞外基质蛋白磷酸化、细胞形状和在小梁网细胞粘附

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Glaucoma, a leading cause of irreversible blindness, is commonly associated with elevated intraocular pressure (IOP) due to impaired aqueous humor (AH) drainage through the trabecular meshwork (TM). Although dysregulated production and organization of extracellular matrix (ECM) is presumed to increase resistance to AH outflow and elevate IOP by altering TM cell contractile and adhesive properties, it is not known whether regulation of ECM protein phosphorylation via the secretory vertebrate lonesome kinase (VLK) influences TM cellular characteristics. Here, we tested this possibility. Experiments carried out in this study reveal that the 32 kDa protein is a prominent VLK isoform detectable in lysates and conditioned media (CM) of human TM cells. Increased levels of VLK were observed in CM of TM cells subjected to cyclic mechanical stretch, or treated with dexamethasone, TGF-beta 2, and TM cells expressing constitutively active RhoA GTPase. Downregulation of VLK expression in TM cells using siRNA decreased tyrosine phosphorylation (TyrP) of ECM proteins and focal adhesions, and induced changes in cell shape in association with reduced levels of actin stress fibers and phospho-paxillin. VLK was also demonstrated to regulate TGF-beta 2-induced TyrP of ECM proteins. Taken together, these results suggest that VLK secretion can be regulated by external cues, intracellular signal proteins, and mechanical stretch, and VLK can in turn regulate TyrP of ECM proteins secreted by TM cells and control cell shape, actin stress fibers, and focal adhesions. These observations indicate a potential role for VLK in homeostasis of AH outflow and IOP, and in the pathobiology of glaucoma. (C) 2016 Wiley Periodicals, Inc.
机译：青光眼,不可逆转的主要原因失明,通常与升高有关由于受损的眼内压(IOP)房水排水通过(啊)小梁网(TM)。生产和组织细胞外矩阵(ECM)认为增加阻力啊流出和提升IOP细胞通过改变TM收缩和胶粘剂属性,它不是知道ECM调节蛋白质通过分泌脊椎动物磷酸化寂寞的小梁网细胞激酶(VLK)影响特征。的可能性。研究显示,32 kDa的蛋白质突出VLK同种型检测溶菌产物和人类小梁网细胞的条件媒体(CM)。水平的提高VLK是TM的观察在CM中细胞受循环机械拉伸,或用地塞米松治疗,及2,TM细胞表达RhoA持续活跃GTPase。使用核细胞减少酪氨酸ECM蛋白质的磷酸化(TyrP)和焦点粘连,诱导细胞形状的变化协会肌动蛋白水平降低的压力纤维和phospho-paxillin。了规范及2-induced TyrPECM的蛋白质。建议可以由VLK分泌外部线索,细胞内信号蛋白,和机械拉伸,VLK可以调节TyrP ECM的小梁网细胞分泌的蛋白质压力控制细胞形状,肌动蛋白纤维局部粘连。潜在作用VLK体内平衡啊病理学的流出和眼压,青光眼。

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