title: [Alterations of retinal tissue induced by amyloid β(1- 42) subretinal injection in mice].
abstract: OBJECTIVE
  To investigate the alterations of retinal tissue induced by OAβ(1-42) subretinal injection in normal C57BL/6N mice.
  
  
  METHODS
  Experimental study. One hundred and twenty C57BL/6N mice aged 8 weeks participated in this study. Among them, 60 eyes received subretinal injection of OAβ(1-42); another 60 received double distilled water as control. The concentration of OAβ(1-42) was 0.312 5 mmol/L. We took fundus photograph and autofluorescence, electroretinogram(ERG), haematoxylineosin staining of retinal paraffin sections, β-galactosidase staining of neural retinal flatmounts, immunofluorescence of senescence marker P16INK4a of RPE/choroidal flatmounts, Western blot and RT-PCR of senescence relative cytokines IL-6, TGF-β1 before and after the injection. The data were analyzed by independent sample t-test.
  
  
  RESULTS
  Comparing with controls, 1 week post injection, the experimental group eyes had atrophied area with high autofluorescence site, and showed evident decrease in amplitudes of a wave (39.94±7.75)µV comparing with the controls (225.27±28.94)µV(t=12.45, P<0.001) in scotopia ERG, so did the amplitude of b wave (185.55±4.62)µV comparing with the controls (873.78±43.80)µV(t=27.06, P<0.001), retinal structures appeared significant loss of retinal thickness (t=75.13, P<0.001) along with hypo- or hyperpigmentation; the experimental eyes had high frequency of blue-green deposits in retinal β-gal staining; the green fluorescence sites of RPE/choroidal flatmounts were clear and bright, indicating higher expression of P16INK4a in the nucleus; these results were the same till 8 weeks post operation. Western blot and RT-PCR vertified conspicuous increases in expression of TGF-β1, IL-6 in retinas of experimental eyes compared with the control ones 1 week post injection.
  
  
  CONCLUSIONS
  OAβ(1-42) subretinal injection could induce visual function deficiency and retinal tissue senescence. All the manifestations were AMD-like retinopathy, which implied that Aβ(1-42) might be an essential clue in human AMD pathology.
authors: Department of Ophthalmology, Tenth People's Hospital of Tongji University, Shanghai 200072, China.
authors: Chaoqi
authors: C
authors: Liu
authors: Department of Ophthalmology, Tenth People's Hospital of Tongji University, Shanghai 200072, China.
authors: Zhe
authors: Z
authors: Sun
authors: Department of Ophthalmology, Tenth People's Hospital of Tongji University, Shanghai 200072, China.
authors: Lining
authors: L
authors: Cao
authors: Department of Ophthalmology, Tenth People's Hospital of Tongji University, Shanghai 200072, China; Email: dreyemilwang_122@163.com.
authors: Fang
authors: F
authors: Wang
mesh_terms: D016229:Amyloid beta-Peptides / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D002829:Choroid / Q000737:chemistry; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000032:analysis*; D004596:Electroretinography; D006801:Humans; D015850:Interleukin-6 / Q000032:analysis; D051379:Mice; D008810:Mice, Inbred C57BL; D010446:Peptide Fragments / Q000008:administration & dosage / Q000494:pharmacology*; D012160:Retina / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D012164:Retinal Diseases / Q000209:etiology; D053773:Transforming Growth Factor beta1 / Q000032:analysis*; D014785:Vision, Ocular
chemical_list: D016229:Amyloid beta-Peptides; C417743:Cdkn2a protein, mouse; D019941:Cyclin-Dependent Kinase Inhibitor p16; D015850:Interleukin-6; D010446:Peptide Fragments; D053773:Transforming Growth Factor beta1; C075222:amyloid beta-protein (1-42)