摘要
Bone-specific H vessels, together with their vascular pericytes, play a key role in regulating osteogenesis and maintaining homeostasis. Parathyroid hormone (PTH) is a commonly used drug for the treatment of osteoporosis. Previous studies found PTH can promote the formation of H-type blood vessels and vascular pericytes in long bone and further promote osteogenesis. However, the specific mechanism and whether there is a similar phenomenon in alveolar bone need to be further explored. 20 8-week-old C57BL6/J male mice were randomly divided into PTH injection group and control group. PTH (20 μ g / kg/day) or normal saline was injected twice a day. 14 days later, bilateral leg and mandible tissues were fixed and decalcified to make paraffin sections or preserved in liquid nitrogen to extract RNA and total protein. HE staining, TRAP staining and immunohistochemical staining (ALP, endomucin, α SMA, HIF α, VEGF, KDR, PTHR1, c-kit, LepR) and real-timePCR (endomucin, α SMA, HIF α, VEGF, KDR, PTHR1, c-kit, LepR, VE-codherin, VASH1) were performed. MS1 endothelial cells were cultured in vitro. Scratch test, migration test and tube formation test were carried out under the condition of PTH stimulation. Total RNA and mi-RNA were extracted and real-timePCR was used to detect vascular related genes. There are also H-type blood vessels in alveolar bone. PTH stimulation can increase the number of H-type blood vessels and enlarge the lumen diameter and may promote osteogenesis through HIF1 α / MALAT1/VEGFA signal axis. PTH regulates H-type blood vessels and vascular pericytes to promote bone defect healing.