Panoply™ Human ERBB4 Knockdown Stable Cell Line

Here, researchers explored the role of Erb-B2 receptor tyrosine kinase 4 (ERBB4) in the pathogenesis of aortic dissection (AD) and its value as a potential therapeutic target for cell therapy. Results showed that ERBB4 knockdown significantly inhibited cell viability, migration, proliferation, and angiogenesis. In vivo experiments demonstrated that ERBB4 knockdown reduced inflammatory cell infiltration and enhanced collagen fiber contractility (confirmed by Masson staining). Mechanistic studies revealed that ERBB4 silencing suppressed the expression of integrin-binding proteins (CD151, ITGAE, ITGB5) and inhibited the NF-κB signaling pathway (p-IκBα, p-NF-κB-65). These findings suggest that ERBB4 plays a crucial role in AD progression, and that ERBB4 knockdown can alleviate pathological changes in human aortic smooth muscle cells (HASMCs), reduce inflammatory responses, and restore collagen fiber contractility. ERBB4 holds promise as a potential target for cell therapy to repair vascular integrity and function, providing new treatment strategies for AD patients.

CCK-8 results showed that ERBB4 knockdown cells exhibited inhibited cell viability compared to control cells (Figure 1A). Colony formation assays indicated that ERBB4 knockdown cells showed inhibited cell proliferation compared to control cells (Figure 1B). Cell cycle analysis revealed a reduced number of cells in S phase in ERBB4 knockdown cells, with cell cycle arrest occurring at either the G1/S or G2/M phase. These results suggest that ERBB4 knockdown inhibits cell proliferation (Figure 1C).

Figure 1. ERBB4 knockdown suppressed HASMCs proliferation. (Shi Y, et al., 2025)