Objective To investigate the repair and reconstruction mechanism of stromal cell derived factor-1(SDF-1) on rat abdominal aorta grafts.Methods Male Sprague-Darley rats received abdominal aorta grafts from male Wistar abdominal arteries.Immunohistochemical staining(IHC) was performed to detect the SDF-1 expression.The expression of CXCR4,the receptor of SDF-1,was demonstrated by RT-PCR.(Results) SDF-1 was expressed on the endothelium all the time during the course of the abdominal aorta grafts in the bodies of recipients.Furthermore,it was found that there was a significant relationship between the expression of SDF-1 on the endothelia and the thickness of the neointima of the rat abdominal aorta grafts.On the other hand,CXCR4 was detected within the abdominal aorta grafts.Conclusions Stem cells could be mobilized by SDF-1 to the abdominal aorta grafts and differentiated into smooth-muscle like cells.Furthermore,SDF-1 is predictive of grafts arteriosclerosis and the subsequent development of chronic graft dysfunction(CGD).

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling. Here, we focused on the role of Semaphorin 3A (Sema3A), expressed by sensory nerves, in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement (OTM) model. Firstly, bone formation was activated after the 3rd day of OTM, coinciding with a decrease in sensory nerves and an increase in pain threshold. Sema3A, rather than nerve growth factor (NGF), highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM. Moreover, in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells (hPDLCs) within 24 hours. Furthermore, exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload. Mechanistically, Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway, maintaining mitochondrial dynamics as mitochondrial fusion. Therefore, Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation, both as a pain-sensitive analgesic and a positive regulator for bone formation.
Humans ; Bone Remodeling ; Cell Differentiation ; Osteogenesis ; Semaphorin-3A/pharmacology* ; Trigeminal Ganglion/metabolism*