ИСТИНА

Background/Objectives: Previously published data and the results of our own research suggest the significant role of T-cadherin in endothelial function under normal conditions and in pathology (https://doi.org/10.1016/j.ejcb.2021.151183). Methods: We first utilized the GSE164829 series for bioinformatic analysis. Data analysis was conducted using Seurat. Cell type annotation was performed using the automatic cell type identification tool - SingleR. To identify cellular targets and signaling partners of T-cadherin cascades, we utilized STRING. Total RNA was reverse-transcribed to generate cDNA, followed by real-time polymerase chain reaction (PCR). Primer design was carried out using NCBI Primer-BLAST. Results: Bioinformatic analysis yielded 6 cell clusters expressing CDH13 (T-cadherin). Co-expression of CDH13, CDH5, and CTNNB1 genes was detected in all clusters. Construction of protein-protein interaction maps using the STRING.ORG web platform revealed potential protein partners of T-cadherin, including CTNNB1, CDH5, CDH2, CAV1, BRCA1, DNMT1, SRFP1, and ADIPOR1. The bioinformatic findings were validated through RT-PCR analysis. Total RNA was extracted from the human endothelial cells Eahy926 (cells overexpressing T-cadherin or control cells). RT-PCR confirmed the expression of target genes identified by bioinformatics. Endothelial cells overexpressing T-cadherin exhibited reduced mRNA levels of β-catenin, VE-cadherin, N-cadherin, CAV1, BRCA1, SRFP1, and AdipoR2. Grant References: The study was supported by the Russian Science Foundation, grant No. 19-75-30007, and under the State Assignment # 03р- 23/110-03 of Lomonosov MSU.