Recombinant human parathyroid hormone 1-34 (Shanghai United Cell Biotech)

Polylactide (PLA) is one of the most promising polymers that has been widely used for the repair of damaged tissues due to its biocompatibility and biodegradability. PLA composites with multiple properties, such as mechanical properties and osteogenesis, have been widely investigated. Herein, PLA/graphene oxide (GO)/parathyroid hormone (rhPTH(1-34)) nanofiber membranes were prepared using a solution electrospinning method. The tensile strength of the PLA/GO/rhPTH(1-34) membranes was 2.64 MPa, nearly 110% higher than that of a pure PLA sample (1.26 MPa). The biocompatibility and osteogenic differentiation test demonstrated that the addition of GO did not markedly affect the biocompatibility of PLA, and the alkaline phosphatase activity of PLA/GO/rhPTH(1-34) membranes was about 2.3-times that of PLA. These results imply that the PLA/GO/rhPTH(1-34) composite membrane may be a candidate material for bone tissue engineering.

Teriparatide, recombinant parathyroid hormone (PTH[1‐34]), and abaloparatide, an analogue of PTH related‐peptide (PTHrP[1‐34]), are both anabolic medications for osteoporosis that target the PTH receptor PTH1R. PTH1R is a G protein–coupled receptor, and the stimulatory Gs protein is an important mediator of the anabolic actions of PTH1R activation in bone. We have published that mice lacking the α subunit of Gs in osteoprogenitors do not increase bone mass in response to PTH(1‐34). Unexpectedly, however, PTH(1‐34) still increases osteoblast numbers and bone formation rate in male mice, suggesting that PTH1R may have both Gs‐dependent and ‐independent actions in bone. Here we examine the role of Gs signaling in the anabolic actions of abaloparatide. We find that abaloparatide increases bone formation in male mice with postnatal deletion of Gsα in Osx‐expressing osteoprogenitors (P‐GsαOsxKO mice) but not in female P‐GsαOsxKO mice. Therefore, abaloparatide has anabolic effects on bone in male but not female mice that appear to be independent of Gs‐mediated signaling. © 2022 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.