PGE2 synthesis and response pathways in cultured corneal endothelial cells: the effects of in vitro aging.
PGE2 synthesis and response pathways in cultured corneal endothelial cells: the effects of in vitro aging.
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培养的角膜内皮细胞中 PGE2 的合成和反应途径：体外衰老的影响。
DOI：
10.1076/ceyr.16.5.428.7048
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发表时间：
1997
影响因子：
2
通讯作者：
Jumblatt,MM
中科院分区：
文献类型：
--
作者：
Jumblatt,MM
目的：建立体外培养的兔角膜内皮细胞衰老模型，并探讨其形态、有丝分裂、前列腺素合成及前列腺素反应途径的增龄变化。方法首次传代的兔角膜内皮细胞传代培养30d。放射免疫法测定PGE2合成。通过测定前列腺素E_2刺激的环磷酸腺苷合成来评价EP_2受体。用流式细胞仪和溴脱氧尿嘧啶核苷(BrdU)掺入法检测细胞周期参数。结果：随着培养时间的延长，角膜内皮细胞密度降低，形态变得不规则，与体内培养的内皮细胞相似。PGE2的合成和反应随培养年限的增加而降低。在年轻和年长的培养中，损伤都会导致PGE2合成增加。在较年轻的培养中，损伤也会导致伤口边缘细胞的有丝分裂，而在较老的培养中，这种反应会大大减弱。结论体外培养的兔角膜内皮细胞的形态和有丝分裂的变化与人和兔的衰老相似。前列腺素合成和反应通路因衰老而改变，可能在伤口修复的自分泌调节中发挥作用，特别是在年轻的细胞中。
PURPOSEThe purpose of these studies is to develop an in vitro model of corneal endothelial aging and to investigate age-related changes in morphology, mitosis, prostaglandin synthesis and prostaglandin response pathways.METHODSFirst-passage rabbit corneal endothelial cells were grown in vitro for up to 30 days after subculture. PGE 2 synthesis was measured by radioimmunoassay. EP 2 receptors were evaluated by determination of PGE 2 stimulated cyclic AMP synthesis. Cell-cycle parameters were evaluated by flow cytometry and by bromodeoxyuridine (BrdU) incorporation in subconfluent, confluent and injured cultures.RESULTSRabbit corneal endothelial cells become less dense and more irregular in shape as they age in culture, thus resembling their in vivo counterparts. PGE 2 synthesis and response decrease with culture age. Injury results in enhanced PGE 2 synthesis in both younger and older cultures. In younger cultures, injury also results in mitosis of cells at the wound margin, and this response is greatly diminished in older cultures.CONCLUSIONSThe morphologic and mitotic changes seen in rabbit corneal endothelial cultures in vitro resemble those seen as a consequence of aging in humans and rabbits. Prostaglandin synthesis and response pathways are modified as a result of aging and may play a role in the autocrine regulation of wound repair, especially in younger cells.