# YBX1 Modulates Intimal Hyperplasia by Regulating Expression and Alternative Splicing of Cell Cycle Associated Genes in RASMCs

## TL;DR

This study shows that YBX1 influences intimal hyperplasia by affecting cell cycle genes and splicing in aortic smooth muscle cells.

## Contribution

The novel contribution is identifying YBX1's role in regulating cell cycle genes and alternative splicing in RASMCs related to intimal hyperplasia.

## Key findings

- YBX1 knockdown reduces RASMC proliferation, migration, and induces apoptosis.
- Transcriptome analysis reveals 1598 differentially expressed genes and 629 alternative splicing events linked to cell cycle and migration pathways.
- Key genes like CCNB1 and TPM1 are highlighted as crucial for vascular cell behavior.

## Abstract

YBX1, a DNA‐/RNA‐binding protein, is implicated in various diseases, yet its role in intimal hyperplasia (IH) remains unclear. This study investigates YBX1's function in rat aortic smooth muscle cells (RASMCs) through knockdown experiments. Results show that YBX1 knockdown reduces cell proliferation and migration while inducing apoptosis. ELISA and western blot analyses revealed increased levels of the anti‐inflammatory factor IL10 and markers for phenotypic transformation, Calponin and Myocardin. Transcriptome sequencing identified 1598 differentially expressed genes (DEGs), with 347 upregulated and 1251 downregulated. Upregulated DEGs were linked to pathways like ECM–receptor interaction and Wnt signalling, while downregulated genes involved cell cycle and p53 signalling. Additionally, 629 significant alternative splicing events were noted, primarily affecting pathways related to cell division and migration. Integrated analysis of YBX1‐bound RNAs and RNA‐seq data highlighted key DEGs, such as CCNB1 and TPM1, which are crucial for vascular cell behaviour. This study underscores YBX1's vital role in RASMCs and suggests potential therapeutic targets for IH treatment.