Department of Biologic and Materials Sciences & Prosthodontics, School of Dentistry, University of Michigan, Ann Arbor, Michigan, USA.
Section of Pediatric Dentistry, Department of Oral Growth and Development, Fukuoka Dental College, Fukuoka, Japan.
Genesis. 2021 Oct;59(10):e23450. doi: 10.1002/dvg.23450. Epub 2021 Sep 6.
Podoplanin, PDPN, is a mucin-type transmembrane glycoprotein widely expressed in many tissues, including lung, kidney, lymph nodes, and mineralized tissues. Its function is critical for lymphatic formation, differentiation of type I alveolar epithelial lung cells, and for bone response to biomechanical loading. It has previously been shown that Pdpn null mice die at birth due to respiratory failure emphasizing the importance of Pdpn in alveolar lung development. During the course of generation of Pdpn mutant mice, we found that most Pdpn null mice in the 129S6 and C57BL6/J mixed genetic background die at the perinatal stage, similar to previously published studies with Pdpn null mice, while all Pdpn null mice bred with Swiss outbred mice survived. Surviving mutant mice in the 129S6 and C57BL6/J mixed genetic background showed alterations in the osteocyte lacunocanalicular network, especially reduced osteocyte canaliculi in the tibial cortex with increased tibial trabecular bone. However, adult Pdpn null mice in the Swiss outbred background showed no overt differences in their osteocyte lacunocnalicular network, bone density, and no overt differences when challenged with exercise. Together, these data suggest that genetic variations present in the Swiss outbred mice compensate for the loss of function of PDPN in lung, kidney, and bone.
Podoplanin(PDPN)是一种广泛表达于多种组织(包括肺、肾、淋巴结和矿化组织)的粘蛋白型跨膜糖蛋白。其功能对于淋巴管形成、I 型肺泡上皮细胞的分化以及骨骼对生物力学负荷的反应至关重要。先前的研究表明,Pdpn 敲除小鼠由于呼吸衰竭而在出生时死亡,这强调了 Pdpn 在肺泡肺发育中的重要性。在生成 Pdpn 突变小鼠的过程中,我们发现,129S6 和 C57BL6/J 混合遗传背景下的大多数 Pdpn 敲除小鼠在围产期死亡,这与先前发表的 Pdpn 敲除小鼠研究相似,而与瑞士近交系小鼠繁殖的所有 Pdpn 敲除小鼠均存活。在 129S6 和 C57BL6/J 混合遗传背景下存活的突变小鼠表现出骨细胞陷窝管腔网络的改变,尤其是胫骨皮质中的骨细胞管腔减少,胫骨小梁骨增多。然而,瑞士近交系背景下的成年 Pdpn 敲除小鼠在其骨细胞陷窝管腔网络、骨密度以及运动挑战方面没有明显差异。总之,这些数据表明,瑞士近交系小鼠中存在的遗传变异补偿了 PDPN 在肺、肾和骨骼中的功能丧失。