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Author Zhou, Rong-Mei ♦ Wang, Xiao-Qun ♦ Yao, Jin ♦ Shen, Yi ♦ Chen, Sai-Nan ♦ Yang, Hong ♦ Jiang, Qin ♦ Yan, Biao
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ BLOOD ♦ CELL PROLIFERATION ♦ DIAGNOSIS ♦ DISEASES ♦ GENE THERAPY ♦ IN VITRO ♦ INDICATORS ♦ MEMBRANES ♦ PATHOLOGY ♦ PATIENTS ♦ RNA ♦ SURGERY ♦ VISION
Abstract Proliferative vitreoretinopathy (PVR) is a serious complication of retinal detachment and vitreoretinal surgery, which can lead to severe vision reduction. Long non-coding RNAs (lncRNAs) play critical roles in many biological processes and disease development. We attempted to determine the role of lncRNAs in the setting of PVR. Microarray analysis revealed that 78 lncRNAs were abnormally expressed in the epiretinal membranes (ERMs) of PVR patients, including 48 up-regulated and 30 down-regulated lncRNA transcripts. We subsequently focus on one lncRNA, MALAT1, and investigated its expression pattern in the biofluid of PVR patients. MALAT1 was significantly up-regulated in the cellular and plasma fraction of peripheral blood in PVR patients. MALAT1 expression was obviously reduced after PVR operation. In vitro experiments revealed the role of MALAT1 in regulating RPE proliferation and migration, which is critical for ERMs formation. This study suggests that lncRNAs are the potential regulators of PVR pathology. MALAT1 is a potential prognostic indicator and a target for the diagnosis and gene therapy for PVR diseases. - Highlights: • 78 lncRNAs are differentially expressed between PVR-ERMs and secondary ERMs. • MALAT1 level is elevated in the ERMs of PVR patients. • Circulating MALAT1 level is up-regulated in PVR patients. • MALAT1 knockdown regulates RPE proliferation and migration.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2015-09-25
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 465
Issue Number 3


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