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近年来研究表明近视的发生发展与巩膜细胞外基质(ECM)的重塑关系密切,基质金属蛋白酶(MMPs)作为调控巩膜ECM动态平衡最重要的一大酶系,也受到越来越多的重视,其中对于MMP-2的研究最为广泛,作为探讨近视发病机制及治疗的靶因子,不仅有大量研究证明其活性增加与近视发展明显相关,很多通过抑制MMP-2来防治近视的研究也取得了丰硕的成果.现就MMP-2多年来在近视方面的研究进展做一综述. 相似文献
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巩膜细胞外基质及基质金属蛋白酶在近视发展中作用的研究进展 总被引:3,自引:0,他引:3
近视是眼科发病率最高的疾病,目前尚无明确有效的防治方法。近年来研究表明:近视的发生发展与巩膜细胞外基质(ECM)的重塑有密切关系,而基质金属蛋白酶(MMPs)作为调节巩膜ECM动态平衡最重要的一大酶系,其活性增加与近视发展明显相关。本文就目前巩膜ECM及MMPs在近视发展中作用的研究进展进行综述。 相似文献
3.
巩膜作为近视过程中的最后一层靶组织,其细胞外基质(ECM)的生物分子及生物力学特性在近视的形成和发展过程中发生重要变化。大量研究证实巩膜ECM的主动重塑是近视过程中的关键环节,近几年,探索巩膜ECM的重塑机制以及通过调控ECM的重塑过程来防治近视已成为屈光领域的研究热点。现就近年来有关巩膜ECM在近视发生发展中的作用做一综述。 相似文献
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外源性基质金属蛋白酶抑制剂GM6001对FDM形成的抑制作用 总被引:1,自引:1,他引:0
目的研究非特异性基质金属蛋白酶(MMPs)抑制剂GM6001对小鸡形觉剥夺性近视眼(FDM)形成的影响。方法150只ld龄来亨雏鸡采用半透明塑料眼罩单眼遮盖制备FDM动物模型,同时每日球后注射不同剂量GM6001连续4d、14d。检测眼轴长度及屈光度,观察后极部巩膜组织病理学变化及检测MMP-2蛋白质、酶活性及其mRNA的表达。结果GM6001明显抑制遮盖4d眼FDM的形成,对遮盖14d眼仅部分抑制,对正常鸡无作用。GM6001干预后,遮盖14d眼后极部巩膜组织病理学改变与FDM相似,后极部巩膜MMP-2表达显著降低,而遮盖4d组均与正常小鸡眼相似。GM6001干预眼明胶酶谱图未检测到透亮带。GM6001对后极部巩膜MMP-2mRNA表达无影响。结论MMP。2活性增高为小鸡细胞外基质(ECM)后极部巩膜ECM重塑的关键因素之一。 相似文献
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目的探讨豚鼠形觉剥夺性近视(form-deprivation myopia, FDM )早期后极部巩膜基质金属蛋白酶2(matrix metalloproteinase-2, MMP-2)及基质金属蛋白酶抑制剂2(tissue inhibitor of matrix metalloproteinase-2,TIMP-2)mRNA的表达。方法4周龄三色豚鼠50只,随机分成实验组和正常对照组各25只,实验组又随机分为5组,单眼形觉剥夺(monocular deprivation, MD)右眼1、4、7、14、21d制备FDM动物模型,未遮盖眼为自身对照组。各组豚鼠进行检影验光和A超测量眼轴长度。提取后极部巩膜总RNA,二步法逆转录聚合酶链反应检测各组后极部巩膜MMP-2及TIMP-2mRNA的表达水平。结果除1d外,各组MD后极部巩膜MMP-2mRNA的表达与正常对照组、自身对照组差异均有统计学意义(P〈0,05),MD组间差异也有统计学意义(P〈0.01);而TIMP-2mRNA的表达则逐渐下降。各自身对照组MMP-2、TIMP-2mRNA的表达与MD组变化趋势大致相同。结论MMP-2/TIMP-2之间动态平衡失调可能是启动豚鼠FDM巩膜细胞外基质早期主动重塑的重要因素。(中国跟耳鼻喉科杂志,2010,10:75—78) 相似文献
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目的观察形觉剥夺性近视眼后极部巩膜组织细胞外基质的改变以及基质金属蛋白酶-2(matrix melallopro-teniases,MMP-2)表达的变化,以揭示其与形觉剥夺性近视眼后极部巩膜组织改变的关系。方法采用形觉剥夺方法建立豚鼠的近视动物模型。分别测量后极部巩膜组织厚度和干重,应用免疫组化技术研究MMP-2在形觉剥夺8周后的豚鼠处理眼与对照眼后极部巩膜中表达的差异。结果形觉剥夺后处理眼较对侧眼及正常对照眼有明显近视形成(P<0.001),形成的近视度数分别为(-8.20±1.21)DS和(-7.00±1.03)DS;剥夺后后极部巩膜厚度明显变薄(P<0.01),剥夺前后厚度差为(13.8±8.2)μm;干重减轻(P<0.05),剥夺前后干重差为(0.13±0.07)mg。MMP-2在形觉剥夺后的豚鼠处理眼、对侧眼及正常对照眼后极部巩膜的表达定位于成纤维细胞胞浆和细胞外基质中。处理眼后极部巩膜中MMP-2表达量明显高于对侧眼及正常对照眼(P<0.001)。结论形觉剥夺眼后极部巩膜组织细胞外基质有显著降解趋势,同时MMP-2表达升高。MMP-2可能参与了形觉剥夺性近视发生过程中巩膜的重塑。 相似文献
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病理性近视巩膜细胞外基质中胶原蛋白的研究进展 总被引:2,自引:0,他引:2
病理性近视(pathological myopia),亦称高度进行性近视,属近视的一种亚型;常伴发眼后极部的变性改变,包括巩膜变薄、脉络膜萎缩变薄及眼轴的增长。在所有屈光不正中,病理性近视危害最大,多导致视力不佳,甚至最终失明。近年来研究表明:病理性近视的发展与巩膜组织细胞外基质的生物化学特性改变有密切关系,而胶原作为巩膜组织细胞外基质的重要组成部分,其表达和积聚的改变与病理性近视的发展明显相关。本文就目前病理性近视发展中巩膜组织细胞外基质中胶原改变的研究进展进行综述。 相似文献
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近视是世界最常见眼病之一,其发病机制尚不完全清楚。有研究发现,细胞生长因子与近视的发生发展密切相关,其中碱性成纤维细胞生长因子(bFGF)与转化生长因子β(TGF-β)作为关键的信号分子可以通过调控巩膜细胞外基质的合成与降解参与近视眼巩膜重塑,但具体转导途径和机制还不十分清楚。现就bFGF和TGF-β在近视眼巩膜中的表达及其调控巩膜重塑的可能机制进行综述。 相似文献
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目的观察透镜诱导豚鼠近视眼巩膜基质中基质金属蛋白酶2(matrix metalloproteinases 2,MMP-2)、金属蛋白酶2组织抑制剂ftissue inhibitor of metaloproteinase 2,TIMP-2)和转化生长因子B2(transforming growth factorβ2,TGF—β2)和成纤维细胞生长因子(fibroblast growth factor,bFGF)的变化.探讨透镜诱导与形觉剥夺在近视眼发生机制上的异同点。方法 11只豚鼠于诱导前后分别验光、测量眼轴长度.用-6D的透镜诱导右眼作为诱导眼,左眼作为对照眼,诱导成功后,将豚鼠处死,摘除眼球,取后极部巩膜分别进行MMP-2和TIMP-2、TGF—β2和bFGF的免疫组织化学染色.观察它们在巩膜组织成纤维细胞胞浆中表达的阳性率和阳性细胞所占面积的百分比,并与对侧眼进行比较。结果11只豚鼠诱导眼成功诱导出(-3.31±1.04)D近视,诱导眼巩膜中MMP-2的阳性率为81.8%,对照眼为45.5%,差异有显著性;TIMP-2的阳性率36.4%,对照眼为72.7%;MMP-2染色阳性细胞面积百分比为0.22±0.15.对照眼为0.06±0.08(P〈0.05);TIMP-2为0.05±0.08,对照眼为0.13±0.10。巩膜中TGF—β2阳性率为81.8%,对照眼为36.4%(P〈0.05),bFGF的阳性率为45.5%,明显低于对照眼(63.6%)。诱导眼TGF—β2染色阳性细胞面积百分比为0.21±0.14.对照眼为0.06±0.10,差异有显著性:bFGF为0.07±0.09,对照眼为0.15±0.14。结论透镜可以成功地诱导出豚鼠近视眼.透镜诱导近视眼巩膜基质中MMP-2活性增强,TIMP-2活性降低,TGF—β2表达增加,bFGF表达减少,MMP-2和TIMP-2、TGF—β2和bFGF之间存在平衡失调.它们的改变与形觉剥夺性近视的变化相似,表明透镜诱导近视眼与形觉剥夺性近视眼在巩膜基质的改变和生长因子的变化上存在相似的机制。 相似文献
11.
高度近视眼是目前为止全球范围内主要的不可逆性致盲性眼部疾病之一。高度近视眼在发生和发展的过程中,眼球后部巩膜可能异常薄变或扩展。巩膜薄变、脉络膜萎缩性薄变及不同程度的眼轴延长,且伴有巩膜细胞外基质(ECM)的过度降解是高度近视眼不断发展的根本原因。近年来,随着相关研究的不断深入,国内外学者发现巩膜ECM生化特性的改变与近视眼的发展有着十分密切的关系,而胶原作为巩膜ECM的重要组成部分,其表达和积聚的改变与病理性近视眼的发展呈显著正相关的关系。目前,临床医学领域对此尚无有效的治疗方法,常用的药物及手术疗法的疗效尚未确定且毒副作用较大,并不适合在临床上进行大范围的推广和使用。本文就目前高度近视眼巩膜ECM中胶原分子机制的研究进展进行综述。 相似文献
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With the increasing prevalence in recent years, myopia has become an essential global health concern. In most instances, an increased axial length of the eye is the structural cause of nearsightedness. The scleral remodeling, primarily dependent on the scleral extracellular matrix (ECM) changes, is significantly linked to eye lengthening. Scleral remodeling plays a critical function in the incidence and progression of myopia. This mini-review will focus on recent research progress of scleral remodeling in the hope of providing new ideas for the prophylaxis and treatment of myopia. 相似文献
13.
The sclera and myopia 总被引:12,自引:0,他引:12
Myopia is a very common ocular problem, affecting perhaps one billion people worldwide. Most myopia is produced by lengthening of the vitreous chamber of the ocular globe. High myopia is characterized by scleral thinning and localized ectasia of the posterior sclera. The sclera is a dense, fibrous, viscoelastic connective tissue that forms the outer coat of the eye and consists of irregularly arranged lamellae of collagen fibrils interspersed with proteoglycans and non-collagenous glycoproteins. Scleral fibroblasts are located between scleral lamellae, and are responsible for synthesizing the extracellular matrix in which they reside. Research highlighted in this review clearly demonstrates that the sclera is not a static container of the eye, but rather is a dynamic tissue, capable of altering extracellular matrix composition and its biomechanical properties in response to changes in the visual environment to regulate ocular size and refraction. Based on these studies, a strategy directed at reversing myopia-associated scleral extracellular matrix remodeling events would be warranted, particularly in cases of high myopia in humans. 相似文献
14.
Expression of collagen-binding integrin receptors in the mammalian sclera and their regulation during the development of myopia 总被引:2,自引:0,他引:2
McBrien NA Metlapally R Jobling AI Gentle A 《Investigative ophthalmology & visual science》2006,47(11):4674-4682
PURPOSE: The sclera has a collagen-rich extracellular matrix that undergoes significant biochemical and biomechanical remodeling during myopic eye growth. The integrin family of cell surface receptors play critical roles in extracellular matrix and biomechanical remodeling in connective tissues. This study identified the major collagen-binding integrin receptors in the mammalian sclera and investigated their mRNA expression during the development of and recovery from experimental myopia. METHODS: The presence of the alpha1, alpha2, and beta1 integrin subunits was examined by using tree-shrew-specific primers and RT-PCR. Scleral expression of alpha1beta1 and alpha2beta1 receptor proteins was further investigated by using Western blot analysis and immunocytochemistry. Myopia was induced monocularly by occluding pattern vision and scleral tissue collected after 24 hours and 5 days. In a subset of the 5-day treatment group, vision was restored for 24 hours before tissue was isolated. Total RNA was extracted, and integrin subunit expression levels were assessed with quantitative real-time PCR. RESULTS: The presence of the major collagen-binding integrin subunits alpha1, alpha2, and beta1 was confirmed by RT-PCR in both scleral tissue and cultured scleral fibroblasts. Both the alpha1 and alpha2 integrin subunit proteins were identified in tree shrew scleral tissues, and integrin receptor expression was localized to scleral fibroblast focal adhesions. After only 24 hours of myopia induction, a time when no structural elongation has occurred, significant decreases were observed in the expression of the alpha1 (-36%) and beta1 (-44%) integrin subunits. After 5 days of myopia induction, alpha1 integrin expression had returned to baseline levels, whereas the alpha2 subunit showed a significant decrease in expression (-52%). The 5-day integrin profiles were maintained during recovery from the induced myopia, with only alpha2 integrin showing a statistically significant relative decrease in expression (-41%). CONCLUSIONS: The mammalian sclera expresses the major collagen-binding integrin subunits. The alpha1 and beta1 subunit expression was decreased early during the development of myopia, whereas the regulation of alpha2 integrin occurred at a later time point. The differential regulation of alpha1beta1 and alpha2beta1 during the development of myopia may reflect specific roles for these receptors in the scleral extracellular matrix and biomechanical remodeling that accompanies myopic eye growth. 相似文献
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近视严重威胁着儿童的视力健康,高度近视可以导致多种并发症,甚至视力完全丧失。近年来随着近视发病率的持续增加,人们对近视认知水平的持续提升,儿童近视问题受到了广泛关注。目前近视发生和发展的具体机制尚不清楚,人们普遍认为巩膜是近视发生的效应器。随着近视不断发展,眼轴逐渐拉长,眼球的结构和功能随之发生改变,其中,眼轴过度延长导致巩膜重塑,后极部巩膜加速变薄,巩膜的组织结构和生物力学特性发生了重要改变,而相关基因表达的调控则是视觉信号引起巩膜重塑的关键。大量研究者借助于近视动物模型和基因测序技术发现,巩膜细胞外基质重塑与近视的发生和发展密切相关。文章就目前巩膜在近视发生发展中组织结构及相关基因的变化进行综述,为深入探究近视的巩膜重塑机制和寻找新的近视治疗靶点提供思路。 相似文献
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近视是发生率最高的屈光不正,已经成为世界范围内的公共卫生问题。我国有约6亿的近视患者,其中高度近视(high myopia,HM)患者超过8000万。目前近视的发生趋于年轻化、高度化,HM眼底病变尤其黄斑病变是东亚国家主要的致盲原因。迄今为止,HM的具体发病机制尚未阐明。越来越多的研究表明,其发生与遗传基因、环境因素、分子生物学和巩膜生物力学变化等有密切关系,氧化应激(oxidative stress,OS)在其中起重要作用。OS过程中能产生活性氧自由基和活性氮自由基,聚集在视网膜和脉络膜中,通过多种机制诱导巩膜细胞凋亡、细胞外基质降解等。本文对OS介导HM发病机制的研究进行综述,以期推进HM发病机制与防治的深入研究。 相似文献