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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Huang, Chao-Ching Chang, Ying-Chao Hung, Pi-Liang Wang, Feng-Sheng Huang, Hsiu-Mei |
| Description | Country affiliation: Taiwan Author Affiliation: Huang HM ( Department of Ophthalmology Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.); Huang CC ( Department of Pediatrics, National Cheng Kung University Hospital, Tainan City, Taiwan and Department of Pediatrics, Taipei Medical University, College of Medicine, Taipei, Taiwan.); Wang FS ( Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.); Hung PL ( Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.); Chang YC ( Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.) |
| Abstract | PURPOSE: Visual loss associated with hypoxic-ischemic (HI) brain damage is the most common cause of visual impairment in children of developed countries. A neuroprotective role for Wnt/ß-catenin signaling has been demonstrated in several neurodegenerative disorders. The association of Wnt signaling with HI injury in immature retina has not been established. METHODS: On postnatal day 7 (P7), HI was induced by unilateral common carotid artery ligation followed by 8% oxygen hypoxia for 2 hours. The pups received intravitreous injection (i.v.i) of PBS, Dickkopf-1 (DKK-1, the negative modulator of Wnt/ß-catenin pathway) antisense (AS) or sense (S) oligonucleotides at various concentrations for pretreatment (24 and 1 hour before HI) or post treatment (1 and 4 hours after HI). For chronic treatments, animals received repeated intraperitoneal (i.p.) injection of DKK-1-AS, DKK-1-S, lithium chloride (LiCl), or vehicles after HI. The retinal injury was assessed by electroretinography (ERG, P21, and P30) and immunohistochemical staining (P8 or P30). RESULTS: Pretreatment with DKK-1-AS (i.v.i.) attenuated DKK-1 and enhanced ß-catenin expression, but did not protect immature retina against HI injury at both pathological and functional levels. Post treatment with DKK-1-AS (i.v.i. or i.p.) also did not rescue HI retinopathy. Chronic systemic LiCl treatment did not decrease Müller cell activation or neuronal damage in HI retinal injury. CONCLUSIONS: Our data demonstrated that DKK-1 inhibition or chronic lithium treatment did not protect the immature retina from HI injury. It is speculated that the enhanced canonical Wnt/ß-catenin signaling is not sufficient to protect the immature retina from HI injury. |
| ISSN | 01460404 |
| e-ISSN | 15525783 |
| Journal | Investigative Opthalmology & Visual Science |
| Issue Number | 8 |
| Volume Number | 56 |
| Language | English |
| Publisher | Association for Research in Vision and Ophthalmology |
| Publisher Date | 2015-07-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Anoxia Metabolism Retina Wnt Proteins Wnt Signaling Pathway Physiology Beta Catenin Animals Animals, Newborn Blotting, Western Cell Death Disease Models, Animal Electroretinography Pathology Physiopathology Immunohistochemistry In Situ Nick-end Labeling Neurons Rats, Sprague-dawley Signal Transduction Research Support, Non-u.s. Gov't Discipline Ophthalmology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Ophthalmology Sensory Systems Cellular and Molecular Neuroscience |
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