PLAUR splicing pattern in hereditary angioedema patients' monocytes and macrophages

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Authors

BALLONOVÁ Lucie KULÍŠKOVÁ Petra SLANINA Peter ŠTÍCHOVÁ Julie VLKOVÁ Marcela HAKL Roman LITZMAN Jiří SOUČEK Přemysl FREIBERGER Tomáš

Year of publication 2023
Type Article in Periodical
Magazine / Source Molecular Biology Reports
MU Faculty or unit

Faculty of Medicine

Citation
Web https://link.springer.com/article/10.1007/s11033-023-08391-8
Doi http://dx.doi.org/10.1007/s11033-023-08391-8
Keywords PLAUR; uPAR; HAE; Differentiation; Monocyte; Macrophages
Description BackgroundThe PLAUR gene encodes the urokinase-like plasminogen activator receptor (uPAR) and may undergo alternative splicing. Excluding cassette exons 3, 5 and 6 from the transcript results in truncated protein variants whose precise functions have not been elucidated yet. The PLAUR gene is one of several expressed in myeloid cells, where uPAR participates in different cellular processes, including the contact activation system and kallikrein-kinin system, which play an important role in hereditary angioedema (HAE) pathogenesis. A hypothesis about the PLAUR splicing pattern impact on HAE severity was tested.Methods and resultsThe RT-PCR quantified by capillary electrophoresis was used. Although no significant difference in alternative transcript frequency was observed between healthy volunteers and HAE patients, a significant increase in all cassette exon inclusion variants was revealed during monocyte-to-macrophage differentiation.ConclusionsPLAUR alternative splicing in monocytes and macrophages neither was different between HAE patients and healthy controls, nor reflected disease severity. However, the results showed an PLAUR splicing pattern was changing during monocyte-to-macrophage differentiation, but the significance of these changes is unknown and awaits future clarification.
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