Epiregulin promotes the migration and chemotaxis ability of adipose-derived mesenchymal stem cells via mitogen-activated protein kinase signaling pathways.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

To investigate the function of epiregulin (EREG) in the migration and chemotaxis ability of mesenchymal stem cells. Adipose-derived stem cells (ADSCs) were used in this investigation. Lentiviral EREG short hairpin RNA was applied to silence EREG expression in ADSCs. Human recombinant EREG protein (rhEREG) was used to perform a gain-of-function study. Scratch-simulated wound migration and transwell chemotaxis assays were used to examine the migration and chemotaxis capacity of ADSCs in vitro. Using a Western blot assay, the expressions of p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase (JNK), extracellular signal-regulated protein kinases 1 and 2 (Erk1/2), and protein kinase B were detected. Depletion of EREG caused by specific short hairpin RNA restrained the migration and chemotaxis ability of ADSCs and inhibited the expressions of phosphorylated p38 MAPK, JNK, and Erk1/2. rhEREG improved ADSCs migration and chemotaxis capacity, which was repressed by knockdown of EREG and rescued the expressions of phosphorylated p38 MAPK, JNK, and Erk1/2 impaired by silencing EREG. Furthermore, rhEREG-improved migration and chemotaxis ability in EREG-depleted-ADSCs was restricted by a specific inhibitor, SB203580, for blocking p38 MAPK signaling, PD98059 for blocking Erk1/2 signaling, or SP600125 for blocking JNK signaling in ADSCs separately. EREG promotes migration

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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