한빛사논문
Jee Myung Yang1,2†, Soo Jin Kim1,3,4†, Seongyeol Park5, Wonyung Son6, Anna Kim6 and Junyeop Lee1,3,4*
1Department of Ophthalmology, Asan Medical Center, College of Medicine, University of Ulsan, 88, Olympic-Ro 43-Gil, Songpa-Gu, Seoul 05505, South
Korea.
2Department of Ophthalmology, Dongguk University Ilsan Hospital, Goyang, South Korea.
3Department of Medical Science, Asan Medical Center, AMIST, University of Ulsan College of Medicine, Seoul, South Korea.
4Translational Biomedical Research Group, Asan Institute for Life Science, Asan Medical Center, Seoul, South Korea.
5Genome Insight Technology Inc, Daejeon, South Korea.
6Department of Ophthalmology, Yeungnam University College of Medicine, Daegu, South Korea.
†Jee Myung Yang and Soo Jin Kim contributed equally.
*Correspondence: Junyeop Lee
Abstract
Background: Central serous chorioretinopathy (CSC) is the fourth most prevalent retinal disease leading to age-related macular degeneration (AMD) and retinal atrophy. However, CSC's pathogenesis and therapeutic target need to be better understood.
Results: We investigated exosomal microRNA in the aqueous humor of CSC patients using next-generation sequencing (NGS) to identify potential biomarkers associated with CSC pathogenesis. Bioinformatic evaluations and NGS were performed on exosomal miRNAs obtained from AH samples of 62 eyes (42 CSC and 20 controls). For subgroup analysis, patients were divided into treatment responders (CSC-R, 17 eyes) and non-responders (CSC-NR, 25 eyes). To validate the functions of miRNA in CECs, primary cultured-human choroidal endothelial cells (hCEC) of the donor eyes were utilized for in vitro assays. NGS detected 376 miRNAs. Our results showed that patients with CSC had 12 significantly upregulated and 17 downregulated miRNAs compared to controls. miR-184 was significantly upregulated in CSC-R and CSC-NR patients compared to controls and higher in CSC-NR than CSC-R. In vitro assays using primary cultured-human choroidal endothelial cells (hCEC) demonstrated that miR-184 suppressed the proliferation and migration of hCECs. STC2 was identified as a strong candidate for the posttranscriptional down-regulated target gene of miR-184.
Conclusion: Our findings suggest that exosomal miR-184 may serve as a biomarker reflecting the angiostatic capacity of CEC in patients with CSC.
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