IER3-N-cadherin axis contributes to apoptosis resistance in dermal fibroblasts under profibrotic conditions

IER3 is upregulated in dermal fibroblasts in fibrotic skin lesions and, via N-cadherin (CDH2), suppresses apoptosis in TGF-{beta}1–stimulated cells.

• Why it matters: Persistent fibroblast survival and apoptosis resistance drive pathological skin fibrosis, but IER3’s cutaneous role and downstream survival mechanisms were unclear.
• What they did: Patient skin samples were analyzed for IER3 expression, and primary human dermal fibroblasts were treated with TGF-{beta}1; RNA-seq, siRNA knockdown, qPCR, and flow cytometry mapped an IER3→CDH2 pathway.
• The result: IER3 induction by TGF-{beta}1 was independent of SMAD3 and MEK/ERK, yet CDH2 was linked to IER3 and CDH2 knockdown increased staurosporine-induced apoptosis with a pro-apoptotic gene shift.

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