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Gene Expression Profile of Fibrovascular Membranes from Patients with Proliferative Diabetic Retinopathy
  1. Shigeo Yoshida1,*,
  2. Atsushi Ogura2,
  3. Keijiro Ishikawa1,
  4. Ayako Yoshida1,
  5. Richiro Kohno1,
  6. Yoko Yamaji1,
  7. Kazuho Ikeo3,
  8. Takashi Gojobori3,
  9. Toshihiro Kono4,
  10. Tatsuro Ishibashi5
  1. 1 Kyushu University Graduate School of Medical Sciences, Japan;
  2. 2 Ochanomizu University, Japan;
  3. 3 National Institute of Genetics, Mishima, Japan;
  4. 4 Fukuoka University Chikushi Hospital, Japan;
  5. 5 Graduate School of Medical Sciences, Japan
  1. Correspondence to: Shigeo Yoshida, Ophthalmology, Kyushu University, Graduate School of Medicine, 3-1-1 Maidashi, Fukuoka, 812-8582, Japan; yosida{at}med.kyushu-u.ac.jp

Abstract

Background/Aims: The purpose of this study was to generate a profile of genes expressed in preretinal fibrovascular membranes (FVMs) from patients with proliferative diabetic retinopathy.

Methods: A polymerase chain reaction (PCR)-amplified cDNA library was constructed using the RNAs isolated from FVMs obtained during vitrectomy. The sequence from the 5' end was obtained for randomly selected clones and used to generate expressed sequence tags (ESTs). Functional annotation was retrieved from Ensemble database and analyzed by FatiGo. The web-based VisANT software was used to identify the molecular networks within the FVMs.

Results: A total of 2816 ESTs were assembled in 625 nonredundant clusters. Among these, 515 matched the human cDNA database. The 515 clusters were subdivided by functional subsets of genes related to ribosomal activity, oxidative phosphorylation, focal adhesion, cell adhesion, and other functions. Querying against VisANT database yielded 3175 possible physical relationships to other genes/proteins which included an additional 2480 genes that were not detected in the FVM library.

Conclusions: The cDNA library constructed from human FVMs will be a valuable source of information that should facilitate a wide range of studies that can establish the molecular mechanisms underlying the development of FVMs.

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