细胞凋亡与角膜损伤修复

角膜基质细胞凋亡影响着包括屈光知识性角膜手术在内的损伤修复过程。本就角膜损伤修复过程中细胞凋亡的概况,相关基因以及影响细胞凋亡发生的局部微环境,细胞凋亡的意义进行了综述。     

血小板源生长因子与角膜的损伤及修复

角膜损伤是眼科常见病,常致视力严重损害。角膜损伤的修复是一个复杂的过程,多种细胞因子参与其中。血小板源生长因子可能在角膜损伤的修复过程中起重要作用。研究血小板源生长因子与角膜的关系,特别是其在角膜损伤后修复过程中的作用及机制,可能会对角膜疾病的防治开辟一条崭新的有效途径。     

角膜缘干细胞缺乏对角膜上皮损伤修复的影响

目的探讨角膜缘干细胞的功能。方法采用生物医学图像分析系统,计算切除角膜缘上皮组织的兔眼的角膜上皮愈合速率;用光学显微镜观察角膜上皮损伤修复过程的组织学变化。结果在角膜上皮损伤８～３２小时内,实验组与对照组角膜上皮愈合速率分别为１．２２±０．１９ｍｍ２／ｈ和１．４５±０．２０ｍｍ２／ｈ（ｔ＝３．８９,Ｐ＜０．０１）,实验组角膜上皮损伤愈合速度明显比对照组慢。实验组角膜可见大量的杯状细胞和新生血管,并随时间而逐渐向中央区发展。结论实验结果进一步证实了角膜上皮干细胞存在于角膜缘,角膜缘干细胞缺失,可使角膜上皮增殖能力丧失,角膜缘屏障功能下降,导致持续性角膜上皮糜烂、结膜组织长入和新生血管形成。     

生长因子对角膜上皮细胞损伤修复的作用

角膜上皮细胞是维持角膜正常生理功能的重要细胞。角膜上皮缺损,一般修复较快,但也有些角膜疾患可导致持续性角膜上皮缺损,从而此起一系列并发症,一些生长因子可促进角膜上皮的修复,开创了治疗角膜上皮持续缺损的新方法,本着重介绍与角膜上皮细胞关系密切的表皮生长因子（EGF）、血小板源性生长因子（PDGF）、成纤维细胞生长因子（FGF）、转化生长因子（TGF）、肝细胞生长因子（HGF）和角质细胞生长因子（KGF）的结构及其在角膜上皮细胞修复中的作用。     

微小RNA与眼底疾病

微小RNA (miRNAs)是一类内源性的非编码小分子RNA,广泛存在于真核生物细胞中.miRNAs通过抑制mRNA翻译或降解mRNA的方式下调目的基因的表达水平,被认为是基因转录后表达调控的主要方式,参与调节细胞的增生、分化、死亡等生物学过程.近年来的研究表明,miRNAs的表达水平和/或功能的改变与糖尿病视网膜病变(DR)、年龄相关性黄斑变性(AMD)、视网膜母细胞瘤(RB)等多种严重致盲性眼底疾病的发生、发展、治疗和预后密切相关.就近年来miRNAs与眼底疾病的研究进展进行综述.     

血小板源性生长因子与角膜损伤修复

血小板源性生长因子(PDGF)在机体伤口愈合过程中具有重要的调节作用。由于角膜的特殊结构和功能,其伤口愈合的调节显得至关重要。本文简述PDGF的结构、受体、生物学活性及其在角膜伤口愈合中的作用。     

表皮生长因子促角膜损伤修复的研究进展

EGF是促生长因子家族成员之一，呈单链多肽结构，通过与靶细胞上的受体结合而发挥促细胞生长发育及组织损伤修复等作用。随着基因工程技术的进展，EGF重组蛋白已广泛用于组织损伤修复的研究。本就EGF促进组织损伤愈合机制的研究进展作一综述。     

表皮生长因子促进猫角膜内皮损伤修复

角膜内皮细胞的屏障和泵功能对于维持角膜的透明性起着关键的作用，研究促进角膜内皮细胞生长的药物非常重要。本实验的目的是观察EGF对角膜内皮损伤修复的影响。     

微小RNA及其与眼相关性疾病的研究进展

微小RNA是一种长约22个核苷酸的非编码小分子RNA,它可通过阻断蛋白质翻译或降解信使RNA来调控基因表达。近年来发现,多种微小RNA分别存在于角膜、晶状体、视网膜中,并且广泛参与眼部多种疾病的发生、发展,如视网膜母细胞瘤、脉络膜黑色素瘤、眼部新生血管性疾病、葡萄膜炎、眼部神经退行性疾病、视网膜色素变性、眼部发育异常等。     

ECM,MMP与角膜结构和角膜损伤修复

细胞外基质是角膜的主要结构成分,赋予角膜特殊的生理功能。基质金属蛋白酶是调节细胞外基质降解代谢的主要酶类。本文概述了成熟角膜细胞外基质的组成及基质金属蛋白酶在角膜损伤修复过程中的作用。     

表皮生长因子对家兔角膜内皮损伤修复作用的实验研究

目的 研究表皮生长因子对家兔角膜内皮损伤的修复作用。方法 将溶于透明持酸钠的ＥＧＦ注入角膜内皮已损伤的兔眼前房,对照眼只注入ＮａＨＡ。结果 １０μｇ和５μｇ的ＥＧＦ均可使角膜内皮缺损面积显著缩小,并可使再生的角膜中央内皮细胞密度,六边形细胞出现率显著上升及细胞面积变异系数明显减小。     

飞秒激光制瓣LASIK手术后的角膜伤口愈合反应

任何屈光手术都会对角膜组织造成损伤,发生伤口愈合过程。飞秒激光作为新兴技术逐渐成为角膜屈光手术的主流方法,其伤口愈合过程直接影响术后早期炎症刺激及远期临床疗效。此前国内外对准分子激光引起的愈合反应已有详细的研究,但飞秒激光造成的角膜损伤及愈合过程报道较少。飞秒激光制瓣LASIK手术后早期炎症反应较机械刀制瓣LASIK术后重,并有其特点。（国际跟科纵览,2012,36：323—327）     

Removal of the basement membrane enhances corneal wound healing

Recurrent corneal erosions are painful and put patients’ vision at risk. Treatment typically begins with debridement of the area around the erosion site followed by more aggressive treatments. An in vivo mouse model has been developed that reproducibly induces recurrent epithelial erosions in wild-type mice spontaneously within two weeks after a single 1.5 mm corneal debridement wound created using a dulled-blade. This study was conducted to determine whether 1) inhibiting MMP9 function during healing after dulled-blade wounding impacts erosion development and 2) wounds made with a rotating-burr heal without erosions. Oral or topical inhibition of MMPs after dulled-blade wounding does not improve healing. Wounds made by rotating-burr heal with significantly fewer erosions than dulled-blade wounds. The localization of MMP9, β4 integrin and basement membrane proteins (LN332 and type VII collagen), immune cell influx, and reinnervation of the corneal nerves were compared after both wound types. Rotating-burr wounds remove the anterior basement membrane centrally but not at the periphery near the wound margin, induce more apoptosis of corneal stromal cells, and damage more stromal nerve fibers. Despite the fact that rotating-burr wounds do more damage to the cornea, fewer immune cells are recruited and significantly more wounds resolve completely.     

Bone marrow-derived progenitor cells promote corneal wound healing following alkali injury

Purpose To determine whether bone marrow-derived progenitor cells can be stimulated by inflammatory mediators and play a role in corneal wound healing following alkali injury. Methods Sixty rabbits were divided into two groups( Group I and Group II). Group I served as a bone marrow-suppression model, and received 200 mg/kg cyclophosphamide. Corneal alkali injury was created in one eye of each rabbit in each group; the other eye served as control. Three days after corneal burn, inflammatory cells in peripheral blood were counted. At the end of 4 weeks follow-up, corneas of all rabbits were subjected to histochemical examination to assess infiltrated CD34 and C-kit positive cells. Clinical outcome was determined at the end of 4 weeks. Results Cyclophosphamide suppressed bone marrow function in Group I by reducing cellularity by more than 30% and neutrophil distribution by 3.18 ± 1.83%. The number of bone marrow hematopoietic and mesenchymal progenitor cells were all suppressed by cyclophophamide, as demonstrated by statistically significant differences between Group I and Group II of CD34+ cells (t = −21.62, P < 0.01) and C-Kit cells (t = −21.62, P < 0.01). Fewer inflammatory cells were released into circulation in Group I (14.42 ± 5.70%) than in Group II (44.36 ± 8.64%). Clinical observation revealed that Group II rabbits had much greater reepithelization (t = 6.999, P < 0.01) and clearer corneas (X ² = 4.417, P < 0.01) than Group I. Conclusions Corneal alkali injury is a stimulus that induces a rapid bone marrow reaction to release not only inflammatory cells but also progenitor cells into circulation. Migrated bone marrow-derived progenitor cells can home to local sites to promote wound healing. Authors have no financial interest in any product or concept discussed in article. Grant: China National Scientific Fund 30500552. Research Fund of Health Bureau of Zhejiang Province, PR China. 2005QN006.     

Aquaporin-1-facilitated keratocyte migration in cell culture and in vivo corneal wound healing models

Aquaporin-1 (AQP1) water channels are expressed in corneal keratocytes, which become activated and migrate following corneal wounding. The purpose of this study was to investigate the role of AQP1 in keratocyte migration. Keratocyte primary cell cultures from wildtype and AQP1-null mice were compared, as well as keratocyte cultures from pig cornea in which AQP1 expression was modulated by RNAi knockdown and adenovirus-mediated overexpression. AQP1 expression was found in a plasma membrane pattern in corneal stromal and cultured keratocytes. Osmotic water permeability, as measured by calcein fluorescence quenching, was AQP1-dependent in cultured keratocytes, as was keratocyte migration following a scratch wound. Keratocyte migration in vivo was compared in wildtype and AQP1 knockout mice by histology and immunofluorescence of corneal sections at different times after partial-thickness corneal stromal debridement. AQP1 expression in keratocytes was increased by 24 h after corneal debridement. Wound healing and keratocyte appearance near the wound margin were significantly reduced in AQP1 knockout mice, and the number of neutrophils was increased. These results implicate AQP1 water permeability as a new determinant of keratocyte migration in cornea.     

骨形成蛋白-7在大鼠角膜损伤愈合的表达及作用

目的:通过观察大鼠角膜损伤愈合过程中骨形成蛋白-7(bone morphogenetic protein 7,BMP-7)的表达规律来探讨其在大鼠角膜损伤愈合过程中可能发挥的作用。方法:雄性Wistar大鼠42只,随机分为7组,每组6只,其中一组为正常对照组,动物模型组均取右眼制造角膜针刺损伤模型。于损伤后各时间点(6h;1,3,5,7,14d)取角膜标本,HE染色行组织病理学检查,免疫组织化学染色观察BMP-7的表达与分布,计算机图像分析系统对结果进行分析。结果:鼠角膜上皮BMP-7的表达于损伤后1,3d逐渐升高(P<0.05);损伤后5d时表达逐渐降低,至损伤后14d时表达恢复正常。角膜基质层及角膜内皮层中BMP-7的表达未见明显变化。结论:BMP-7在大鼠角膜上皮层均有表达,可能作为负性的生长因子参与角膜损伤愈合过程。