title: Retinoic acid suppresses the adhesion and migration of human retinal pigment epithelial cells.
abstract: The study was designed to better understand how retinoic acid (RA) influenced the migration and invasion abilities of retinal pigment epithelial cells (RPE) in vitro and how the related genes of the extracellular matrix (ECM) were expressed. The inhibition effects of RA on proliferative vitreoretinopathy (PVR) formation induced by RPE cells were studied in rabbits. Wound healing and Boyden chamber assays were used to show the abilities of migration and invasion of RPE. Microarray, real-time quantitative PCR (qPCR) and Western blotting showed how RA regulated the ECM genes. RA (10(-5) M) significantly (P < 0.05) inhibited PVR membrane and traction retinal detachment formation (80%). Moreover, RA treatment significantly inhibited the migration (80%) and invasion (65%) behaviors of human RPE cells (P < 0.05) by wound healing and Boyden chamber assays, respectively. Microarray and q PCR analysis showed RA treatment did inhibit the motility of human RPE cells by inhibition of metalloproteinases (MMP) 1, 2, 9, fibronectin-1, transforming growth factor beta, thrombospondin-1, tenascin C, most collagen, integrin, laminin molecules and along enhancing E-cadherin and MMP3 genes expression. And Western blotting indicated the coincident results on protein level of MMP1, 2, 3, 9, 14; fibronectin-1; integrinαM, β2 and E-cadherin. In conclusions, RA is a vital drug to inhibit the abilities of migration and invasion of RPE and to hamper the PVR formation by regulating some genes expression of ECM.
authors: Department of Ophthalmology, The Second Hospital of HeBei Medical University, ShiJiaZhuang 050000, China.
authors: Ying-Hua
authors: YH
authors: Du
authors: Kazuyuki
authors: K
authors: Hirooka
authors: Osamu
authors: O
authors: Miyamoto
authors: Yong-Qin
authors: YQ
authors: Bao
authors: Bin
authors: B
authors: Zhang
authors: Jian-Bin
authors: JB
authors: An
authors: Jing-Xue
authors: JX
authors: Ma
mesh_terms: D000328:Adult; D000818:Animals; D000970:Antineoplastic Agents / Q000378:metabolism / Q000494:pharmacology; D002448:Cell Adhesion / Q000187:drug effects* / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D002465:Cell Movement / Q000187:drug effects* / Q000502:physiology; D002478:Cells, Cultured; D003599:Cytoskeleton / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000187:drug effects / Q000502:physiology; D016326:Extracellular Matrix Proteins / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects / Q000502:physiology; D006801:Humans; D020411:Oligonucleotide Array Sequence Analysis; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D055213:Retinal Pigment Epithelium / Q000166:cytology* / Q000187:drug effects* / Q000502:physiology; D014212:Tretinoin / Q000378:metabolism / Q000494:pharmacology*; D018630:Vitreoretinopathy, Proliferative / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D014945:Wound Healing / Q000187:drug effects / Q000502:physiology
chemical_list: D000970:Antineoplastic Agents; D015815:Cell Adhesion Molecules; D016326:Extracellular Matrix Proteins; D012333:RNA, Messenger; D014212:Tretinoin