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TGF-β2-mediated ocular hypertension is attenuated in SPARC-null mice.基质细胞衍生因子 2 介导的眼内高压在 SPARC 基因敲除小鼠中减轻。
Invest Ophthalmol Vis Sci. 2014 Jun 6;55(7):4084-97. doi: 10.1167/iovs.13-12463.
2
AMP-activated protein kinase regulates intraocular pressure, extracellular matrix, and cytoskeleton in trabecular meshwork.AMP激活的蛋白激酶调节小梁网中的眼压、细胞外基质和细胞骨架。
Invest Ophthalmol Vis Sci. 2014 Apr 8;55(5):3127-39. doi: 10.1167/iovs.13-12755.
3
The prostaglandin f2α analog fluprostenol attenuates the fibrotic effects of connective tissue growth factor on human trabecular meshwork cells.前列腺素 F2α 类似物氟前列醇可减轻结缔组织生长因子对人眼小梁细胞的纤维增生作用。
J Ocul Pharmacol Ther. 2014 Mar-Apr;30(2-3):237-45. doi: 10.1089/jop.2013.0205. Epub 2014 Feb 27.
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Pharmacological regulation of SPARC by lovastatin in human trabecular meshwork cells.洛伐他汀通过基质细胞衍生因子 1 调节人眼小梁细胞。
Invest Ophthalmol Vis Sci. 2014 Mar 19;55(3):1657-65. doi: 10.1167/iovs.13-12712.
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Anti-connective tissue growth factor antibody treatment reduces extracellular matrix production in trabecular meshwork and lamina cribrosa cells.抗结缔组织生长因子抗体治疗可减少小梁网和筛板细胞细胞外基质的产生。
Invest Ophthalmol Vis Sci. 2013 Dec 2;54(13):7836-48. doi: 10.1167/iovs.13-12494.
6
Adenovirus conducted connective tissue growth factor on extracellular matrix in trabecular meshwork and its role on aqueous humor outflow facility.腺病毒对小梁网细胞外基质中结缔组织生长因子的作用及其对房水流出通道的影响。
Mol Biol Rep. 2013 Nov;40(11):6091-6. doi: 10.1007/s11033-013-2720-2. Epub 2013 Sep 20.
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Wounded embryonic corneas exhibit nonfibrotic regeneration and complete innervation.受伤的胚胎角膜表现出非纤维性再生和完全神经支配。
Invest Ophthalmol Vis Sci. 2013 Sep 24;54(9):6334-44. doi: 10.1167/iovs.13-12504.
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Matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, B⁺ tenascin-C and ED-A⁺ fibronectin in dilated cardiomyopathy: potential impact on disease progression and patients' prognosis.基质金属蛋白酶-9、金属蛋白酶组织抑制剂-1、B⁺ tenascin-C 和 ED-A⁺ 纤维连接蛋白在扩张型心肌病中的作用:对疾病进展和患者预后的潜在影响。
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Lipopolysaccharide increases the incidence of collagen-induced arthritis in mice through induction of protease HTRA-1 expression.脂多糖通过诱导蛋白酶HTRA-1的表达增加小鼠胶原诱导性关节炎的发病率。
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Tenascin-C is expressed by human glioma in vivo and shows a strong association with tumor blood vessels.人神经胶质瘤中存在 tenascin-C 的表达,并与肿瘤血管有很强的相关性。
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小梁网中的基质细胞蛋白:综述与更新

Matricellular proteins in the trabecular meshwork: review and update.

作者信息

Chatterjee Ayan, Villarreal Guadalupe, Rhee Douglas J

机构信息

Department of Ophthalmology and Visual Sciences, University Hospitals Eye Institute, Case Western Reserve University School of Medicine , Cleveland, Ohio.

出版信息

J Ocul Pharmacol Ther. 2014 Aug;30(6):447-63. doi: 10.1089/jop.2014.0013. Epub 2014 Jun 5.

DOI:10.1089/jop.2014.0013
PMID:24901502
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4074754/
Abstract

Abstract Primary open-angle glaucoma (POAG) is a leading cause of blindness worldwide, and intraocular pressure (IOP) is an important modifiable risk factor. IOP is a function of aqueous humor production and aqueous humor outflow, and it is thought that prolonged IOP elevation leads to optic nerve damage over time. Within the trabecular meshwork (TM), the eye's primary drainage system for aqueous humor, matricellular proteins generally allow cells to modulate their attachments with and alter the characteristics of their surrounding extracellular matrix (ECM). It is now well established that ECM turnover in the TM affects outflow facility, and matricellular proteins are emerging as significant players in IOP regulation. The formalized study of matricellular proteins in TM has gained increased attention. Secreted protein acidic and rich in cysteine (SPARC), myocilin, connective tissue growth factor (CTGF), and thrombospondin-1 and -2 (TSP-1 and -2) have been localized to the TM, and a growing body of evidence suggests that these matricellular proteins play an important role in IOP regulation and possibly the pathophysiology of POAG. As evidence continues to emerge, these proteins are now seen as potential therapeutic targets. Further study is warranted to assess their utility in treating glaucoma in humans.

摘要

摘要 原发性开角型青光眼(POAG)是全球失明的主要原因,而眼压(IOP)是一个重要的可调节风险因素。眼压是房水生成和房水流出的函数,长期眼压升高被认为会随着时间的推移导致视神经损伤。在小梁网(TM)中,眼睛房水的主要引流系统,基质细胞蛋白通常允许细胞调节它们与周围细胞外基质(ECM)的附着并改变其特性。现在已经明确,小梁网中的细胞外基质周转会影响房水流出率,并且基质细胞蛋白正在成为眼压调节中的重要参与者。对小梁网中基质细胞蛋白的正式研究越来越受到关注。富含半胱氨酸的酸性分泌蛋白(SPARC)、肌纤蛋白、结缔组织生长因子(CTGF)以及血小板反应蛋白-1和-2(TSP-1和TSP-2)已定位到小梁网,越来越多的证据表明这些基质细胞蛋白在眼压调节以及可能在原发性开角型青光眼的病理生理学中起重要作用。随着证据不断出现,这些蛋白现在被视为潜在的治疗靶点。有必要进一步研究以评估它们在治疗人类青光眼方面的效用。