Podoplanin is dispensable for mineralized tissue formation and maintenance in the Swiss outbred mouse background.
Podoplanin is dispensable for mineralized tissue formation and maintenance in the Swiss outbred mouse background.
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DOI：
10.1002/dvg.23450
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发表时间：
2021-10
期刊：
影响因子：
--
通讯作者：
Mishina Y
中科院分区：
文献类型：
--
作者：
Toda Nakamura M;Zhang H;Guo D;Ueharu H;Pan H;Scott G;Harris M;Ray M;Feng JQ;Harris SE;Bonewald LF;Mishina Y
Podoplanin，PDPN，是一种粘蛋白型跨膜糖蛋白，广泛表达于肺、肾、淋巴结和矿化组织等多种组织中。其功能对于淋巴管形成、I型肺泡上皮肺细胞的分化以及骨对生物力学负荷的反应至关重要。先前已经显示，Pdpn敲除小鼠在出生时由于呼吸衰竭而死亡，强调了Pdpn在肺泡肺发育中的重要性。在产生Pdpn突变小鼠的过程中，我们发现，大多数Pdpn null小鼠在129 S6和C57 BL 6/J混合遗传背景中的围产期死亡，类似于先前发表的研究与Pdpn null小鼠，而所有的Pdpn null小鼠与瑞士远交小鼠繁殖存活。在129 S6和C57 BL 6/J混合遗传背景中存活的突变小鼠表现出骨细胞腔隙-小管网络的改变，特别是胫骨皮质中骨细胞小管减少，胫骨小梁骨增加。然而，在瑞士远交系背景的成年Pdpn基因敲除小鼠在骨细胞腔隙性网络、骨密度方面没有明显差异，在运动挑战时也没有明显差异。总之，这些数据表明，瑞士远交小鼠中存在的遗传变异弥补了肺、肾和骨中PDPN功能的丧失。
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.
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影响因子：
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