Division of Anatomy, Meikai University School of Dentistry, 1-1 Keyakidai, Sakado, Saitama, 3500283, Japan.
Department of Anatomy (Macro), School of Medicine, Dokkyo Medical University, 880 Kitakobayashi, Mibu, Tochigi, 3210293, Japan.
Histochem Cell Biol. 2021 Apr;155(4):439-449. doi: 10.1007/s00418-020-01953-y. Epub 2021 Jan 4.
In our previous study, fatty acid-binding protein 5 (FABP5) was expressed in septoclasts with long processes which are considered to resorb uncalcified matrix of the growth plate (GP) cartilage, and no apparent abnormalities were detected in the histo-architecture of the GP of FABP5-deficient (FABP5) mice. Those finding lead us to hypothesize that another FABP can compensate the deletion of FABP5 in septoclasts of its gene-mutant mice. Based on the hypothesis, the present study examined the expression levels of several other FABPs in septoclasts and their morphology in FABP5 mouse tibiae. Processes of FABP5 septoclasts tend to be shorter than wild septoclasts. FABP4-positive septoclasts in FABP5 mice were more numerous than those cells in wild mice.Peroxisome proliferator-activated receptor (PPAR) γ was expressed in FABP4-positive septoclasts of FABP5 mice as well as mice administered with GW1929, a PPARγ agonist, suggesting that the occurrence of PPARγ induces an increase of FABP4-positive septoclasts. The present finding suggests that the functional exertion of FABP5 in septoclasts is supplemented by FABP4 in normal and FABP5 mice, and that the expression of FABP4 is up-regulated in accompany with PPARγ in FABP5 for maintenance of resorptive activity in the GP.
在我们之前的研究中，脂肪酸结合蛋白 5（FABP5）在具有长突起的破骨细胞中表达，这些突起被认为可以吸收生长板（GP）软骨中未钙化的基质，而在 FABP5 缺陷（FABP5）小鼠的 GP 组织形态中没有检测到明显的异常。这些发现使我们假设另一种 FABP 可以在其基因突变小鼠的破骨细胞中补偿 FABP5 的缺失。基于该假设，本研究检查了几种其他 FABP 在 FABP5 小鼠破骨细胞中的表达水平及其在 FABP5 小鼠胫骨中的形态。FABP5 破骨细胞的突起往往比野生型破骨细胞短。FABP5 小鼠中的 FABP4 阳性破骨细胞比野生型小鼠中的细胞多。过氧化物酶体增殖物激活受体（PPAR）γ在 FABP5 小鼠和给予 PPARγ 激动剂 GW1929 的小鼠的 FABP4 阳性破骨细胞中表达，表明 PPARγ 的发生诱导了 FABP4 阳性破骨细胞的增加。本研究结果表明，FABP5 在破骨细胞中的功能发挥可被 FABP4 在正常和 FABP5 小鼠中补充，并且 FABP4 的表达在 FABP5 中与 PPARγ 一起上调，以维持 GP 中的吸收活性。
