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
Scleral hypoxia is considered a trigger in scleral remodeling-induced myopia. Identifying differentially expressed molecules within the sclera is essential for understanding the mechanism of myopia. We developed a scleral fibroblast hypoxia model and conducted RNA sequencing and bioinformatic analysis. RNA interference technology was then applied to knock down targeted genes with upregulated expression, followed by an analysis of COLLAGEN I protein level. Microarray data analysis showed that the expression of Adamts1 and Adamts5 were upregulated in fibroblasts under hypoxia (t-test, p < 0.05). Western blot analysis confirmed increased protein levels of ADAMTS1 and ADAMTS5, and a concurrent decrease in COLLAGEN I in hypoxic fibroblasts. The knockdown of either Adamts1 or Adamts5 in scleral fibroblasts under hypoxia resulted in an upregulation of COLLAGEN I. Moreover, a form-deprivation myopia (FDM) mouse model was established for validation. The sclera tissue from FDM mice exhibited increased levels of ADAMTS1 and ADAMTS5 protein and a decrease in COLLAGEN I, compared to controls. The study suggests that Adamts1 and Adamts5 may be involved in scleral remodeling induced by hypoxia and the development of myopia.
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Source |
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http://dx.doi.org/10.1016/j.exer.2024.110026 | DOI Listing |
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