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RIPK3 and RIPK1 gene expression in pterygium: unveiling molecular insights into pathogenesis.

Authors :
Divandari M
Javadifar A
Moghadam AB
Janatabadi AA
Source :
Molecular biology reports [Mol Biol Rep] 2024 Apr 17; Vol. 51 (1), pp. 524. Date of Electronic Publication: 2024 Apr 17.
Publication Year :
2024

Abstract

Background: Pterygium, characterized by the abnormal proliferation of epithelial cells, matrix remodeling, vascularization, and lesion migration, is a prevalent ocular surface disease involving the growth of fibrovascular tissue on the cornea. Despite the unclear underlying causes of pterygium, numerous investigations have indicated the involvement of cell death pathways in the regulation of cell cycle dynamics. Consequently, the objective of this study was to assess the expression levels of necroptosis markers in individuals diagnosed with pterygium, aiming to shed light on the potential role of necroptosis in the pathogenesis of this condition.<br />Methods: This study aimed to investigate the expression patterns of receptor-interacting serine/threonine kinase 3 (RIPK3) and receptor-interacting serine/threonine kinase 1 (RIPK1) genes in pterygium tissues. 41 patients undergoing pterygium excision surgery were recruited. Resected pterygium samples and normal conjunctival tissues were collected, and RIPK3 and RIPK1 mRNA levels were measured using quantitative real-time PCR.<br />Results: Our findings reveal that the expression of RIPK3 is significantly increased in samples obtained from individuals with pterygium. However, no significant alterations were observed in the expression of RIPK1 in these samples. Results showed significantly higher RIPK3 expression in pterygium tissues compared to controls. Moreover, increased RIPK3 levels correlated negatively with pterygium recurrence rates.<br />Conclusions: These findings suggest RIPK3 may play a protective role against pterygium recurrence through necroptosis.<br /> (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

Details

Language :
English
ISSN :
1573-4978
Volume :
51
Issue :
1
Database :
MEDLINE
Journal :
Molecular biology reports
Publication Type :
Academic Journal
Accession number :
38630344
Full Text :
https://doi.org/10.1007/s11033-024-09368-x