翼状胬肉上皮细胞基质金属蛋白酶Ⅱ的表达

翼状胬肉是眼科常见病，对其病变本质及发病机制仍有争论。病理学研究认为，胬肉上皮细胞在其形成中起关键作用。本研究以人翼状胬肉上皮细胞为研究对象，同时检测培养的结膜及翼状胬肉上皮细胞MMP2表达水平，探讨其与翼状胬肉形成、发展的关系。     

翼状胬肉发病机制及治疗研究新进展

翼状胬肉是眼科常见病,其确切的发病机制直今还没有一致的观点,该病的发病率及复发率较高。多数研究表明,翼状胬肉的主要诱因是环境因素,紫外线过强刺激与其发病密切相关,还有风沙、粉尘等,现受到国内外许多学者的关注。近年来,随着生物技术的发展,对该病的发病机制及治疗的研究有了较新的认识,本文就翼状胬肉的发病机制及治疗现状作一综述。     

翼状胬肉发病机制研究进展

翼状胬肉是常见的眼表疾病之一,其确切病因和发病机制至今尚未完全清楚,目前认为其发生、发展是多种因素协同作用的结果。现有研究表明,翼状胬肉的发生与环境因素有密切关系。眼部长期遭到阳光照射及风沙、花粉、粉尘等长期慢性刺激是主要诱因。多种因素促使角膜缘屏障功能障碍,诱发各种生长因子及炎症因子,使结膜组织变性增生向角膜生长形成胬肉。我们对翼状胬肉发病机制的研究进展进行综述。     

翼状胬肉发病机制的研究进展

翼状胬肉是眼科临床常见的眼表疾病,该病发病率高,切除后复发率高。目前其发病机制仍然不甚明确,学者们一致认为与多种因素共同作用有关。近年来随着分子生物学的发展,有关翼状胬肉基于基因与分子水平的研究取得了突破性的进展。现将翼状胬肉发病机制的研究状况作一综述。     

原发性与复发性翼状胬肉的临床指标及实验室指标差异

翼状胬肉是一种临床常见的人眼表结膜疾病,目前主要归因于慢性紫外线暴露。以往研究主要集中于翼状胬肉的临床特点、外科治疗和发病机制,而对原发性翼状胬肉和复发性翼状胬肉的区别归纳较少。本文总结了关于原发性和复发性胬肉的差异性研究的最新发现,对原发性和复发性翼状胬肉的临床表现、组织病理学、实验室研究差异进行一综述。     

翼状胬肉的流行病学研究现状(英文)

翼状胬肉为常见的一种眼表疾病,其病因及病理遗传学机制不明。国内外文献关于翼状胬肉的流行病学研究显示患病率由0.3%到37.46%不等。翼状胬肉发病与地理位置、阳光及紫外线的照射、年龄、性别及经济条件、干眼症等相关。本文就翼状胬肉的流行病学研究现状做一综述,重点在其患病率与危险因素的调查研究方面。     

翼状胬肉发病机制的研究进展

翼状胬肉是眼科常见病,其病因及发病机制有多种不同的解释,而确切机制尚不清楚,但多数研究表明,翼状胬肉的主要诱因是环境因素,紫外线过强刺激与翼状胬肉的发生密切相关,还有如眼部长期受到风沙、烟尘、热、花粉等过度刺激,遗传因素、营养缺乏、泪液分泌不足、过敏反应及解剖因素等等,种种诱因使角膜缘上皮屏障破坏,继而结膜变性与增生而发生本病,在此过程中,免疫因素参与的成纤维细胞转化起重要作用。对翼状胬肉的病因及发病机制进行综述。     

翼状胬肉发病机制研究进展

翼状胬肉是仅见于人类的常见的眼表疾病之一。对其发病机制的了解仍十分有限,治疗效果也欠满意。有关翼状胬肉发病机制众说纷纭。免疫机制、角膜缘干细胞移行机制、细胞凋亡与增生异常机制及基质金属蛋白酶作用机制均是近几年研究的重点,遗传的易感性也被众多学者强调,但尚无统一定论,对此尚需进一步研究。     

原发性翼状胬肉发病机制和治疗新进展

原发性翼状胬肉是常见的眼表疾病之一。关于它的发病机制尚未达成共识。最近的研究发现翼状胬肉是一个增殖性而不是以变性为特征的病变,并与紫外线的照射有关。翼状胬肉的治疗目前还是以手术治疗为主,同时联合使用抗代谢类药物,最近关于翼状胬肉的发病机制在分子及生化方面有了进一步的认识,也许能够发现更小创伤的治疗方法。     

翼状胬肉发病机制研究进展

翼状胬肉是仅见于人类的常见的眼表疾病之一。对其发病机制的了解仍十分有限，治疗效果也欠满意。有关翼状胬肉发病机制众说纷纭。免疫机制、角膜缘干细胞移行机制、细胞凋亡与增生异常机制及基质金属蛋白酶作用机制均是近几年研究的重点，遗传的易感性也被众多学强调，但尚无统一定论，对此尚需进一步研究。     

Molecular Basis of Pterygium Development

Pterygium pathogenesis is mainly related to UV light exposure. However, the exact mechanisms by which it is formed have not been elucidated. Clinical advances in surgical treatment use conjunctival autografts and amniotic membranes in combination with adjuvant therapies, including mitomycin C, β-radiation, and 5-fluoroacil, to reduce recurrence. Several studies aim to unveil the molecular mechanisms underlying pterygium growth and proliferation. They demonstrate the role of different factors, such as viruses, oxidative stress, DNA methylation, apoptotic and oncogenic proteins, loss of heterozygosity, microsatellite instability, inflammatory mediators, extracellular matrix modulators, lymphangiogenesis, cell epithelial-mesenchymal transition, and alterations in cholesterol metabolism in pterygium development. Understanding the molecular basis of pterygium provides new potential therapeutic targets for its prevention and elimination. This review focuses on providing a broad overview of what is currently known regarding molecular mechanisms of pterygium pathogenesis.     

Temporary amniotic membrane patch for the treatment of primary pterygium: mechanisms of reducing the recurrence rate

Purpose The purpose of the study was to evaluate the outcome of the use of the temporary amniotic membrane patch (TAMP) for the treatment of primary pterygium and to investigate the mechanisms of reducing the recurrence rate.Methods Twenty eyes in 20 patients with primary pterygium underwent pterygium excision followed by TAMP for 5 days. Removed amniotic membrane (AM) was immunostained with primary antibodies CD34, c-Kit, STRO-1 and AC133.Results Within the period of follow-up (53.3±13.8 months), all the eyes showed a smooth ocular surface without recurrence of pterygium. Different grades of CD34, c-Kit, STRO-1and AC133 positive stem and progenitor cells infiltrated or attached to the stroma of patched AM, with more spindle-shaped c-Kit cells than ovoid-shaped CD34 and AC133 cells.Conclusion The temporary amniotic membrane patch is an effective and safe procedure for the treatment of primary pterygium. Absorbing excessive stem and progenitor cells may be one of the mechanisms of reducing the recurrence rate using AM.     

Bcl-2、Bax、Ki67在原发性翼状胬肉组织中的表达研究

目的：观察Bcl-2、Bax、Ki67在原发性翼状胬肉和正常球结膜组织中的表达。

方法：将手术切除的原发性翼状胬肉和正常球结膜组织进行固定、石蜡包埋、切片,利用免疫组织化学染色方法分析Bcl-2(B细胞淋巴瘤-2)、Bax(与Bcl-2相关的X蛋白)、Ki67(细胞核相关抗原)在其中的表达情况。

结果：Bcl-2、Bax、Ki67在原发性翼状胬肉组织中的阳性表达率分别为14.73%、7.00%、12.73%,在正常球结膜组织阳性表达率分别为4.00%、6.00%、0,其中Bcl-2、Ki67在原发性翼状胬肉组织头部上皮中的表达明显高于颈部和体部。

结论：Bcl-2、Ki67在原发性翼状胬肉组织中呈高表达,且在胬肉头部表达最高,在正常球结膜组织中呈低表达; Bax在原发性翼状胬肉和正常球结膜组织中表达无明显差异,提示细胞凋亡失衡和异常增殖可能是原发性翼状胬肉发生发展的机制之一。     

Aberrant expression of genes and proteins in pterygium and their implications in the pathogenesis

Pterygium is a common ocular surface disease induced by a variety of factors. The exact pathogenesis of pterygium remains unclear. Numbers of genes and proteins are discovered in pterygium and they function differently in the occurrence and development of this disease. We searched the Web of Science and PubMed throughout history for literatures about the subject. The keywords we used contain pterygium, gene, protein, angiogenesis, fibrosis, proliferation, inflammation, pathogenesis and therapy. In this review, we summarize the aberrant expression of a range of genes and proteins in pterygium compared with normal conjunctiva or cornea, including growth factors, matrix metalloproteinases and tissue inhibitors of metalloproteinases, interleukins, tumor suppressor genes, proliferation related proteins, apoptosis related proteins, cell adhesion molecules, extracellular matrix proteins, heat shock proteins and tight junction proteins. We illustrate their possible mechanisms in the pathogenesis of pterygium as well as the related intervention based on them for pterygium therapy.     

The pathogenesis of pterygium: current concepts and their therapeutic implications

Pterygium is a disease of the ocular surface that is associated with chronic UV exposure and is characterized by proliferation, inflammatory infiltrates, fibrosis, angiogenesis and extracellular matrix breakdown. Although pterygium is not fully understood, significant progress has been made toward understanding the mechanisms involved in its pathogenesis. In this review, we provide an update on the signaling pathways activated by UV light that result in induction of mediators responsible for the growth of pterygium. We also review the recent genetic studies on hereditary factors and provide a brief overview of the role of epithelial mesenchymal transition, bone marrow progenitor cells, and neuronal signals that may also contribute to the pathogenesis of pterygium. Therapeutic options for pterygium are discussed based on the mechanisms that perpetuate its growth.     

Expression of p27(KIP1) and cyclin D1, and cell proliferation in human pterygium

BACKGROUND: The pterygium is a growth onto the cornea of fibrovascular tissue that is continuous with the conjunctiva, whereas the mechanisms of cell proliferation in pterygium epithelium are unknown. AIM: To analyse the histopathology and the expression of cell cycle-related molecules in pterygium tissues. METHODS: Seven pterygia were surgically removed using the bare-sclera procedure, and three normal bulbar conjunctivas were also obtained. Formalin-fixed, paraffin-wax-embedded tissues were analysed by immunohistochemistry with anti-p27(KIP1), cyclin D1 and Ki-67 antibodies. RESULTS: Conjunctival epithelium consisted of several layers of round cells with a few goblet cells. Nuclear immunoreactivity for p27(KIP1) was noted in many normal epithelial cells, where cyclin D1 and Ki-67-positive nuclei were intermingled. A variety of goblet cells were located in the superficial layer of the pterygium head as well as those of the body epithelia. Several pterygium epithelial cells were p27(KIP1) positive, whereas nuclear immunoreactivity for cyclin D1 and Ki-67 was detected in many epithelial cells. By contrast, immunoreactivity for p27(KIP1), cyclin D1 and Ki-67 was hardly detected in the pterygium stroma. CONCLUSION: It is suggested that pterygium growth and development are associated with the proliferation of epithelium, which is possibly involved in the expression of cell cycle-related molecules.     

Pathogenesis of pterygia: role of cytokines, growth factors, and matrix metalloproteinases

Pterygium is a common ocular surface disease apparently only observed in humans. Chronic UV exposure is a widely accepted aetiological factor in the pathogenesis of this disease and this concept is supported by epidemiological data, ray tracing models and histopathological changes that share common features with UV damaged skin. The mechanism(s) of pterygium formation is incompletely understood. Recent data have provided evidence implicating a genetic component, anti-apoptotic mechanisms, cytokines, growth factors, extracellular matrix remodelling (through the actions of matrix metalloproteinases), immunological mechanisms and viral infections in the pathogenesis of this disease. In this review, the current knowledge on pterygium pathogenesis is summarised, highlighting recent developments. In addition, we provide novel data further demonstrating the complexity of this intriguing disease.     

Connective tissue growth factor in pterygium: simultaneous presence with vascular endothelial growth factor – possible contributing factor to conjunctival scarring

BACKGROUND: Various growth factors have been detected in pterygium and been associated with its vasculogenesis. The basic pathophysiological mechanisms responsible especially for the fibrotic activity in pterygium are, however, not yet known. Connective tissue growth factor (CTGF) has been shown to be substantially involved in various processes of fibrosis. We report on the presence of CTGF in pterygium and its simultaneous presence with vascular endothelial growth factor (VEGF). METHODS: Samples of pterygium were collected during surgery with informed consent of the patients. Specific, non-commercial primary antibodies against CTGF were used to detect CTGF using immunohistochemistry. Specificity of antibodies was confirmed with Western-blot analysis. The same specimens were stained with commercial antibodies for VEGF. Additionally RT-PCR analysis was performed from pterygium samples. RESULTS: CTGF was detected in the epithelium of all samples as well as in some stromal keratocytes. The RT-PCR confirmed the identity of CTGF in these samples. The staining pattern differed slightly from that of VEGF, which was detected in all samples. The control sections were negative. CONCLUSION: CTGF is present in the epithelium of a majority of pterygia and probably contributes to fibrosis. Simultaneous presence with VEGF suggests growth factor interaction and possible involvement in apoptotic dysregulation.     

Immunolocalisation of E-cadherin and beta-catenin in human pterygium

AIM: The pterygium represents an invasion of a wing of altered ocular surface tissue into the normal cornea. The head itself is slightly elevated and white, which is the only site of firm adhesion to the globe. The mechanisms of cell proliferation and adhesion in pterygium epithelium, however, are unknown. The aim of this study was to analyse the expression of cell adhesion molecules in pterygium tissues. METHODS: Six pterygia were surgically removed using the bare-sclera procedure, and two normal corneas and a normal bulbar conjunctiva were also obtained. Formalin-fixed, paraffin-embedded tissues were analysed by immunohistochemistry with anti-E-cadherin and beta-catenin antibodies. RESULTS: Immunoreactivity for E-cadherin was not detected in the normal cornea and conjunctiva. In contrast, all corneal and conjunctival epithelial cells showed a weak homogeneous immunoreaction for beta-catenin on the cell membrane. In the pterygium head, the thickness was relatively marked compared with the body, and normal conjunctival and corneal epithelia. E-cadherin as well as beta-catenin was heterogeneously expressed in the cell membrane and cytoplasm of a variety of epithelial cells, whereas the expression was less marked in the body. Several epithelial cells showed intense nuclear immunoreactivity for beta-catenin. Immunoreactivity of beta-catenin, but not E-cadherin, was detected in only a few stromal cells, which were less marked than in epithelial cells. CONCLUSION: It is suggested that E-cadherin and beta-catenin are concentrated in pterygium tissue, and are possibly involved with epithelial proliferation and adhesion.     

IL-1 α在初发与复发性翼状胬肉中的异常表达

目的 该研究的目的 是了解白细胞介素1α(interleukin-1α,IL-1α)在初发与复发翼状胬肉中的异常表达,探讨翼状胬肉复发的机制.方法 用免疫组织化学方法对30例初发翼状胬肉和30例复发翼状胬肉患者切除的翼状胬肉组织中的IL-1α进行检测,并与正常人角巩膜缘组织中的IL-1α进行对照.结果 免疫组织化学染色显示IL-1α主要定位于初发和复发翼状胬肉上皮和基质内的血管旁炎症细胞浆内;正常结膜、初发胬肉、复发胬肉中的IL-1α的含量差异有统计学意义(P=0.000).结论 此研究首次将初发翼状胬肉与复发翼状胬肉中的IL-1α进行对照性研究.认为翼状胬肉切除术后长期处于非感染性炎症状态是翼状胬肉复发的主要因素.