Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Purpose: sFlt-1, a soluble secreted variant of the vascular endothelial growth factor (VEGF) receptor-1 that possesses only its extracellular domain, is a specific endogenous inhibitor of VEGF, which is involved in retinal vasculogenesis. Our objective was to determine the effects of various sFlt-1 gene fragments on retinal neovascularization in vivo using a murine oxygen-induced ischemic retinopathy (OIR) model.
Methods: Lentiviral expression plasmids carrying the sFlt-1 gene fragments containing Ig-like domains 2nd-3rd and 2nd-4th were constructed. Retinal neovascularization was induced by exposing neonatal mice to hyperoxia (75% O(2)) on post-natal day 7 (P7) and then returning them to normoxia (21% O(2)) on P12. After sFlt-1 gene fragment transfer, retinal neovascularization was examined via fluorescein angiography and hematoxylin-eosin staining. In addition, changes in the expression of VEGF and its functional receptor KDR/Flk-1 were examined via Western blotting and immunohistochemistry.
Results: Lenti.sFlt-1(2-3) and lenti.sFlt-1(2-4) both significantly inhibited neovascularization in OIR mice. Retinas from mice treated with lenti.sFlt-1(2-3) demonstrated a more marked reduction in neovascular cell nuclei compared with mice treated with lenti.sFlt-1(2-4), and these results were confirmed by fluorescence angiography. Gene transfer showed a very weak effect on VEGF protein expression, whereas KDR/Flk-1 protein expression was strongly inhibited, particularly in mice treated with lenti.sFlt-1(2-3).
Conclusions: Lentivirus-mediated sFlt-1 gene transfer significantly inhibits retinal neovascularization in OIR. Thus, sFlt-1 gene transfer may represent a potential therapeutic strategy for preventing retinal neovascularization.
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Source |
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http://dx.doi.org/10.1080/02713680902862971 | DOI Listing |
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