Tailored modulation of S100A1 and RASSF8 expression by butanediamide augments healing of rotator cuff tears

Abstract

Objectives This investigation sought to elucidate promising treatment modalities for rotator cuff tears (RCTs) by delving into the molecular machinations instigating the affliction. The focus was on differentially expressed genes (DEGs) linked to RCTs, and the exploration of their roles and operative pathways. Methods DEGs were discerned from GEO datasets, followed by the establishment of a protein-protein interaction (PPI) network. Subsequently, the network’s core genes were determined employing a Venn diagram. Enrichment analysis facilitated the unveiling of the biological roles and signal transduction pathways of these pivotal genes, thus shedding light on molecular strategies for RCT-targeted treatment. The Discovery Studio 2019 software was employed to sift through FDA-sanctioned drugs targeting these essential proteins. Moreover, the efficaciousness of these FDA-endorsed drugs vis-à-vis RCTs was corroborated by the construction of an in vivo animal model of the injury and the in vitro cultivation of tendon-derived stem cells. Results Bioinformatics outcomes revealed a significant overexpression of S100A1 and RASSF8 in RCT patients. The FDA drug repository indicated that Butanediamide has a selective affinity for S100A1 and RASSF8. Subsequent in vivo and in vitro experimentation demonstrated that Butanediamide could suppress S100A1 expression and bolster TDSC proliferation, thereby facilitating RCT healing. Conclusions S100A1 and RASSF8 are pivotal genes implicated in RCTs, and their roles have been elucidated. The FDA-approved compound, Butanediamide, may represent a prospective therapeutic agent for RCTs by targeting S100A1 and RASSF8, respectively.

Keywords

• Rotator cuff tear (rct)
• S100A1
• RASSF8
• Zinc compound
• TDSC