Mechansm study of structural functonal dual bommetc composte bone scaffold for repar of mandbular defects n rabbts

Abstract

The present study amsto explore the potental mechansms of bonetssue-engneered trply perodc mnmal surfaces (TPMS) scaffolds contanng njectable plateletrch fibrn and stromal cell-derved factor-1 (n short, SIT scaffolds) n promotng angogeness n mandbular defects. Surface structures wth a 70% porosty were created usng the Matlab R2020a program. SIT scaffolds were fabrcated usng dgtal laser processng. Hstologcal structures on SIT scaffolds noculated wth rabbt bone marrow mesenchymal stem cells (BMSCs) were observed usng alkalne phosphatase (ALP) mmunohstochemcal stanng, Alcan blue stanng, and Masson-Goldner stanng. ouble-end sequencng n PE150 mode was performed usng the Illumna NovaSeq™ 6000. Analyses such as Gene Ontology (GO), Kyoto Encyclopeda of Genes and Genomes (KEGG), proten-proten nteractons, and gene set enrchment analyss (GSEA) were conducted to delneate the gene functons. RT-qPCR was performed to confirm the expresson of genes of nterest. Fnally, cells on dfferent samples were examned by confocal laser scannng mcroscopy to observe c-Jun expresson. Confocal magng and quanttatve analyss showed that BMSCs supported by the SIT scaffold had a greater tendency to dfferentate nto osteoblasts than those supported by the TPMS scaffold or the control group. The SIT group exhbted the most ntense ALP stanng. The expresson of angogeness-related factors VEGFA was sgnficantly upregulated n T and SIT groups. Expresson of osteogenc gene RUNX2 and c-Fos/c-Jun pathway genes FOS/JUN was sgnficantly upregulated n the SIT group. GSEA revealed that the WNT sgnalng pathway and MAPK sgnalng pathway were more actve n the SIT group. Immunofluorescence showed that the c-Jun s hghly expressed n newly formed capllares n the SIT group. In concluson, both TPMS and SIT scaffolds promote angogeness n mandbular defects.