Mesenchymal stem cells undergoing apoptosis recover cyclophosphamide-induced cleft palate through modulation of NLR signaling mediated pyroptosis.

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)

Background Cleft palate is a common developmental disorder in craniofacial region, which cause the severe postnatal oral dysfunction. Mesenchymal stem cell (MSC) therapy has been revealed as a promising therapeutic approach in fetal developmental defects. However, since placental barrier blocks the transfer of cells from maternal circulation, how the MSC exert therapeutic effects and biological function to repair developmental injuries and maintain tissue homeostasis remains elusive. Methods Cyclophosphamide (CP)-induced cleft palate mice were used with replenishment of adipose-derived MSC (ADSC) or apoptotic vesicles (apoVs) derived from MSC, which of cleft palate were characterized by morphological analysis. PKH26 labeling and TUNEL assay were used in tracing of MSC or MSC-derived apoVs. Mechanistical studies were assessed by combinations of RNA-seq analysis, proteomic re-analysis and immunoassay. Results Exogenous MSC recovered the CP-induced cleft palate in E14.5 and E16.5 fetuses. Intriguingly, we unexpectedly found that MSC decreased rapidly and underwent apoptosis in maternal placenta. Accordingly, we assumed MSC-derived apoVs were the mediator of MSC exerting therapeutic effects. MSC-derived apoVs were injected into the pregnant mice and remarkedly improved CP-induced cleft palate, which were traced in fetal multiple organs, particularly in palatine shelves. Mechanistic

Evidence level

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

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