Skeletal development of mice lacking bone sialoprotein (BSP)--impairment of long bone growth and progressive establishment of high trabecular bone mass.
Skeletal development of mice lacking bone sialoprotein (BSP)--impairment of long bone growth and progressive establishment of high trabecular bone mass.
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DOI：
10.1371/journal.pone.0095144
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Malaval L
中科院分区：
文献类型：
--
作者：
Bouleftour W;Boudiffa M;Wade-Gueye NM;Bouët G;Cardelli M;Laroche N;Vanden-Bossche A;Thomas M;Bonnelye E;Aubin JE;Vico L;Lafage-Proust MH;Malaval L
与野生型相比，成年Ibsp基因敲除小鼠（BSP−/−）显示出更短的身材、更低的骨转换和更高的骨小梁质量，后者是由于骨吸收受损所致。出乎意料的是，BSP基因敲除也会影响生殖行为，因为雌性小鼠不能为后代建造一个合适的“巢”。尽管如此，多个杂交实验表明，BSP−/−小鼠从出生到整个生命周期的较矮身材和较低体重，以及较短的股骨和胫骨与母亲的基因型无关，因此反映了遗传。在BSP−/−新生儿中，µCT分析显示膜性初级骨化延迟，颅缝较宽，股骨皮质骨较薄，组织矿物质密度较低，反映在骨形成标记物的表达较低。然而，长骨的骨小梁体积和破骨细胞参数在基因型之间没有差异。出生后3周，突变体破骨细胞数量和表面下降，伴随着骨小梁的积累。新生儿的生长板呈现较薄的肥大区，6天大的BSP−/−小鼠的IGF-1全骨表达较低，IHH较高。在3周时，BSP-/-小鼠的增殖区较薄，肥大区较厚，比任何性别的BSP+/+小鼠，可能反映了较低的软骨细胞增殖和受损的软骨吸收的组合。6日龄的BSP−/−小鼠表现出较低的成骨细胞标志物表达，但较高的MEPE和较高的骨桥蛋白（Opn）/Runx 2比值。血清Opn在第6天在突变体中和在成人中较高。因此，缺乏BSP改变了长骨生长和膜/皮质初级骨形成和矿化。然而，在突变小鼠中软骨内骨发育是正常的，并且在成年小鼠中观察到的骨小梁的积累在出生后的几周内进行性发展。补偿性高Opn可能允许BSP−/−小鼠正常的软骨内发育，同时损害初级矿化。
Adult Ibsp-knockout mice (BSP−/−) display shorter stature, lower bone turnover and higher trabecular bone mass than wild type, the latter resulting from impaired bone resorption. Unexpectedly, BSP knockout also affects reproductive behavior, as female mice do not construct a proper "nest" for their offsprings. Multiple crossing experiments nonetheless indicated that the shorter stature and lower weight of BSP−/− mice, since birth and throughout life, as well as their shorter femur and tibia bones are independent of the genotype of the mothers, and thus reflect genetic inheritance. In BSP−/− newborns, µCT analysis revealed a delay in membranous primary ossification, with wider cranial sutures, as well as thinner femoral cortical bone and lower tissue mineral density, reflected in lower expression of bone formation markers. However, trabecular bone volume and osteoclast parameters of long bones do not differ between genotypes. Three weeks after birth, osteoclast number and surface drop in the mutants, concomitant with trabecular bone accumulation. The growth plates present a thinner hypertrophic zone in newborns with lower whole bone expression of IGF-1 and higher IHH in 6 days old BSP−/− mice. At 3 weeks the proliferating zone is thinner and the hypertrophic zone thicker in BSP−/− than in BSP+/+ mice of either sex, maybe reflecting a combination of lower chondrocyte proliferation and impaired cartilage resorption. Six days old BSP−/− mice display lower osteoblast marker expression but higher MEPE and higher osteopontin(Opn)/Runx2 ratio. Serum Opn is higher in mutants at day 6 and in adults. Thus, lack of BSP alters long bone growth and membranous/cortical primary bone formation and mineralization. Endochondral development is however normal in mutant mice and the accumulation of trabecular bone observed in adults develops progressively in the weeks following birth. Compensatory high Opn may allow normal endochondral development in BSP−/− mice, while impairing primary mineralization.
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影响因子：
15.9
作者：
Yakar, S;Rosen, CJ;LeRoith, D
通讯作者：
LeRoith, D
影响因子：
2.9
作者：
Fisher, LW;Fedarko, NS
通讯作者：
Fedarko, NS
影响因子：
6.2
作者：
Yakar, Shoshana;Courtland, Hayden-William;Clemmons, David
通讯作者：
Clemmons, David
影响因子：
4.1
作者：
HUNTER, GK;GOLDBERG, HA
通讯作者：
GOLDBERG, HA
DOI：
10.1093/jmicro/51.6.413
发表时间：
2002-01-01
期刊：
JOURNAL OF ELECTRON MICROSCOPY
影响因子：
--
作者：
Sawae, Y;Sahara, T;Sasaki, T
通讯作者：
Sasaki, T