Zinc Silicate/Nano-Hydroxyapatite/Collagen Scaffolds Promote Angiogenesis and Bone Regeneration via the p38 MAPK Pathway in Activated Monocytes.
Yue SongHao WuYi GaoJunqin LiKaifeng LinBin LiuXing LeiPengzhen ChengShuaishuai ZhangYixiao WangJinbo SunLong BiGuo-Xian PeiPublished in: ACS applied materials & interfaces (2020)
Recent studies show that biomaterials are capable of regulating immune responses to induce a favorable osteogenic microenvironment and promote osteogenesis and angiogenesis. In this study, we investigated the effects of zinc silicate/nanohydroxyapatite/collagen (ZS/HA/Col) scaffolds on bone regeneration and angiogenesis and explored the related mechanism. We demonstrate that 10ZS/HA/Col scaffolds significantly enhanced bone regeneration and angiogenesis in vivo compared with HA/Col scaffolds. ZS/HA/Col scaffolds increased tartrate-resistant acid phosphatase (TRAP)-positive cells, nestin-positive bone marrow stromal cells (BMSCs) and CD31-positive neovessels, and expression of osteogenesis (Bmp-2 and Osterix) and angiogenesis-related (Vegf-α and Cd31) genes increased in nascent bone. ZS/HA/Col scaffolds with 10 wt % ZS activated the p38 signaling pathway in monocytes. The monocytes subsequently differentiated into TRAP+ cells and expressed higher levels of the cytokines SDF-1, TGF-β1, VEGF-α, and PDGF-BB, which recruited BMSCs and endothelial cells (ECs) to the defect areas. Blocking the p38 pathway in monocytes reduced TRAP+ differentiation and cytokine secretion and resulted in a decrease in BMSC and EC homing and angiogenesis. Overall, these findings demonstrate that 10ZS/HA/Col scaffolds modulate monocytes and, thereby, create a favorable osteogenic microenvironment that promotes BMSC migration and differentiation and vessel formation by activating the p38 signaling pathway.
Keyphrases
- bone regeneration
- endothelial cells
- tissue engineering
- vascular endothelial growth factor
- signaling pathway
- induced apoptosis
- bone marrow
- wound healing
- dendritic cells
- mesenchymal stem cells
- high glucose
- immune response
- peripheral blood
- cell cycle arrest
- stem cells
- pi k akt
- poor prognosis
- endoplasmic reticulum stress
- epithelial mesenchymal transition
- transforming growth factor
- nk cells
- oxidative stress
- angiotensin ii
- cell death
- dna methylation
- binding protein
- atomic force microscopy
- body composition