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Compatibility of Calycosin-Tanshinone IIA improves Ang II-induced renal artery endothelial cell dysfunction through lncRNA-mRNA co-expression network
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Compatibility of Calycosin-Tanshinone IIA improves Ang II-induced renal artery endothelial cell dysfunction through lncRNA-mRNA co-expression network
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Compatibility of Calycosin-Tanshinone IIA improves Ang II-induced renal artery endothelial cell dysfunction through lncRNA-mRNA co-expression network
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Journal Article
Compatibility of Calycosin-Tanshinone IIA improves Ang II-induced renal artery endothelial cell dysfunction through lncRNA-mRNA co-expression network
2025
Overview
This study aimed to investigate the effect of the compatibility of Calycosin and Tanshinone IIA on dysfunction of rat renal artery endothelial cells (RRAECs) induced by angiotensin II (Ang II) and to elucidate the underlying molecular mechanisms. We utilized cell culture to optimize Calycosin and Tanshinone IIA concentrations and assessed autophagy, apoptosis, ATP levels, and cell migration using MDC staining, Annexin V-FITC/PI staining, ATP assay, and Transwell assays, respectively. RNA-seq identified differentially expressed lncRNAs and mRNAs, which were validated by qRT-PCR. The compatibility of Calycosin and Tanshinone IIA significantly enhanced the proliferative capacity of Ang II-induced RRAECs, increased autophagosome formation, reduced cell apoptosis, elevated ATP production, and enhanced cell migration ability. RNA sequencing analysis revealed 146 differentially expressed lncRNAs and 43 differentially expressed mRNAs, and co-expression network analysis identified interactions between 28 lncRNAs and 7 mRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicated that these differentially expressed mRNAs were primarily involved in the regulation of ATPase activity and metabolic processes related to serine family amino acids, triglycerides, arachidonic acid, etc., as well as the MAPK signaling pathway. The compatibility of Calycosin and Tanshinone IIA improved Ang II-induced dysfunction in RRAECs by modulating the lncRNA-mRNA co-expression network, providing new molecular targets and therapeutic strategies for the prevention and treatment of hypertensive renal damage.
Publisher
Society for In Vitro Biology
Subject
/ Angiotensin II - pharmacology
/ Animals
/ Cell Movement - drug effects
/ Cell Proliferation - drug effects
/ Endothelial Cells - drug effects
/ Endothelial Cells - metabolism
/ Endothelial Cells - pathology
/ family
/ Gene Expression Regulation - drug effects
/ Gene Regulatory Networks - drug effects
/ genome
/ mRNA
/ Rats
/ RNA
/ RNA, Long Noncoding - genetics
/ RNA, Long Noncoding - metabolism
/ serine
/ Staining
