Nijsure Madhura P, Tobin Brendan, Jones Dakota L, Lang Annemarie, Hallström Grey, Baitner Miriam, Tanner Gabrielle I, Moharrer Yasaman, Panebianco Christopher J, Seidl Elizabeth G, Dyment Nathaniel A, Szeto Gregory L, Wood Levi, Boerckel Joel D
Department of Bioengineering, University of Pennsylvania, Philadelphia, PA, USA.
Department of Orthopedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
bioRxiv. 2024 Dec 23:2024.12.23.630086. doi: 10.1101/2024.12.23.630086.
Bone fracture repair initiates by periosteal expansion. The periosteum is typically quiescent, but upon fracture, periosteal cells proliferate and contribute to bone fracture repair. The expansion of the periosteum is regulated by gene transcription; however, the molecular mechanisms behind periosteal expansion are unclear. Here, we show that Yes-Associated Protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) mediate periosteal expansion and periosteal cell proliferation. Bone fracture increases the number of YAP-expressing periosteal cells, and deletion of YAP and TAZ from Osterix (Osx) expressing cells impairs early periosteal expansion. Mechanistically, YAP regulates both 'cell-intrinsic' and 'cell-extrinsic' factors that allow for periosteal expansion. Specifically, we identified Bone Morphogenetic Protein 4 (BMP4) as a cell extrinsic factor regulated by YAP, that rescues the impairment of periosteal expansion upon YAP/TAZ deletion. Together, these data establish YAP mediated transcriptional mechanisms that induce periosteal expansion in the early stages of fracture repair and provide new putative targets for therapeutic interventions.
骨折修复通过骨膜扩张启动。骨膜通常处于静止状态,但骨折后,骨膜细胞增殖并促进骨折修复。骨膜的扩张受基因转录调控;然而,骨膜扩张背后的分子机制尚不清楚。在这里,我们表明Yes相关蛋白(YAP)和具有PDZ结合基序的转录共激活因子(TAZ)介导骨膜扩张和骨膜细胞增殖。骨折增加了表达YAP的骨膜细胞数量,从表达osterix(Osx)的细胞中删除YAP和TAZ会损害早期骨膜扩张。从机制上讲,YAP调节允许骨膜扩张的“细胞内在”和“细胞外在”因子。具体而言,我们确定骨形态发生蛋白4(BMP4)是一种受YAP调节的细胞外因子,它可挽救YAP/TAZ缺失后骨膜扩张的损伤。总之,这些数据建立了YAP介导的转录机制,该机制在骨折修复的早期阶段诱导骨膜扩张,并为治疗干预提供了新的假定靶点。