rhPDGF-BB via ERK pathway osteogenesis and adipogenesis balancing in ADSCs for critical-sized calvarial defect repair.

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)

Adipose-derived stem cells (ADSCs) with the capacity of differentiating into osteo-like cells have been widely investigated for bone tissue engineering as a novel seed cell source. Recombinant human platelet-derived growth factor (rhPDGF-BB) is a clinically proven growth factor with the potential of promoting cell proliferation and osteogenic differentiation during the bone regeneration process. In this study, we investigated the effects of rhPDGF-BB on the proliferation and osteogenic and adipogenic differentiation of rat ADSCs and explored whether the extracellular signal-related kinase (ERK) signaling pathway might be involved. We found that rhPDGF-BB significantly enhanced ADSCs proliferation and osteogenic differentiation, as detected by MTT, real-time polymerase chain reaction (PCR), ALP activity assays, and calcium deposition in vitro, in concert with ERK pathway activation. In contrast, the adipogenesis of ADSCs, as detected by real-time PCR and Oil Red O staining, was suppressed in the presence of rhPDGF-BB. Furthermore, with the supplement of the ERK inhibitor PD98059, cell proliferation and osteogenesis were reduced; as expected, adipogenesis was enhanced. Subsequently, for the first time, we evaluated the effect of ADSCs associated with rhPDGF-BB on bone regeneration in a critical-sized rat calvarial defect model with silk scaffold as a carrier. Micro-computed tomog

Evidence level

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

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