PGE2: a mediator of corneal endothelial wound repair in vitro.
PGE2: a mediator of corneal endothelial wound repair in vitro.
复制标题
PGE2：体外角膜内皮伤口修复的介质。
DOI：
10.1152/ajpcell.1994.266.1.c269
复制
发表时间：
1994
期刊：
影响因子：
--
通讯作者：
B. Meklir
中科院分区：
文献类型：
--
作者：
N. Joyce;B. Meklir
维持角膜内皮细胞单层的完整性对角膜透明性至关重要。衰老、创伤、炎症和疾病（如糖尿病）可损害单层完整性，导致角膜水肿和视力丧失。在成年人中，单层的修复主要通过两种形式的细胞移动发生：“迁移”，其中单个细胞从伤口边缘移动以重新填充缺损，和“扩散”，其中细胞扩大并变平，导致单层作为片材移动以覆盖缺损。这个实验室以前的研究表明，这两种运动形式可以被很好地分开。在当前的研究中，使用已建立的组织培养模型来确定前列腺素E2（PGE 2）和腺苷3 '，5'-环一磷酸（cAMP）途径的介质对单个细胞迁移的影响。吲哚美辛，前列腺素合成的抑制剂，显着降低个别细胞迁移时，伤口暴露于培养基单独获得的水平以下。PGE 2，而不是PGF 2 α，以剂量依赖性方式恢复这种反应。在吲哚美辛，毛喉素，直接腺苷酸环化酶激活剂的存在下，刺激个别细胞迁移。腺苷酸环化酶抑制剂2 '，5'-二脱氧腺苷可逆转毛喉素和PGE 2的刺激作用。二丁酰cAMP（DBcAMP）也刺激个别细胞迁移的存在下，吲哚美辛，而H89，蛋白激酶A抑制剂，逆转DBcAMP和PGE 2诱导的效果。这些结果提供的证据表明，cAMP途径的刺激增强了个体细胞迁移，并且通过该途径起作用的PGE 2可能是角膜内皮伤口修复期间该反应的内源性刺激物。
Maintenance of the integrity of the corneal endothelial monolayer is essential for corneal clarity. Aging, trauma, inflammation, and diseases, such as diabetes, can compromise monolayer integrity, resulting in corneal edema and loss of visual acuity. In adult humans, repair of the monolayer occurs mainly by two forms of cell movement: "migration," in which individual cells move from the wound edge to repopulate the defect, and "spreading," in which cells enlarge and flatten, causing movement of the monolayer as a sheet to cover the defect. Previous studies from this laboratory have shown that these two forms of movement can be pharmacologically separated. In the current studies, an established tissue culture model was used to determine the effect of prostaglandin E2 (PGE2) and of mediators of the adenosine 3',5'-cyclic monophosphate (cAMP) pathway on individual cell migration. Indomethacin, an inhibitor of prostaglandin synthesis, significantly decreased individual cell migration below levels obtained when wounds were exposed to culture medium alone. PGE2, but not PGF2 alpha, restored this response in a dose-dependent manner. In the presence of indomethacin, forskolin, a direct adenylate cyclase activator, stimulated individual cell migration. 2',5'-Dideoxyadenosine, an adenylate cyclase inhibitor, reversed the stimulatory effects of both forskolin and PGE2. Dibutyryl cAMP (DBcAMP) also stimulated individual cell migration in the presence of indomethacin, whereas, H89, a protein kinase A inhibitor, reversed both the DBcAMP and PGE2-induced effects. These results provide evidence that stimulation of the cAMP pathway enhances individual cell migration and that PGE2, acting via this pathway, may be an endogenous stimulator of this response during corneal endothelial wound repair.
登录
查看更多内容
DOI：
10.1001/archopht.1985.01050090099041
发表时间：
1985
期刊：
Archives of ophthalmology (Chicago, Ill. : 1960)
影响因子：
--
作者：
Glasser,DB;Matsuda,M;Gager,WE;Edelhauser,HF
通讯作者：
Edelhauser,HF
角膜内皮β-肾上腺素能受体脱敏。
DOI：
10.1089/jop.1985.1.263
发表时间：
1985
期刊：
Journal of ocular pharmacology
影响因子：
--
作者：
Chao,WT;Walkenbach,RJ
通讯作者：
Walkenbach,RJ
从肾上腺素到环AMP。
DOI：
10.1126/science.2841758
发表时间：
1988
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Levitzki,A
通讯作者：
Levitzki,A
影响因子：
4.2
作者：
SCHULTZ, RO;MATSUDA, M;SCHULTZ, KJ
通讯作者：
SCHULTZ, KJ