Effects of transforming growth factor-β deficiency on bone development:: A Fourier transform-infrared imaging analysis
Effects of transforming growth factor-β deficiency on bone development:: A Fourier transform-infrared imaging analysis
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DOI：
10.1016/s8756-3282(02)00905-5
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发表时间：
2002-12-01
期刊：
影响因子：
4.1
通讯作者：
Boskey, AL
中科院分区：
文献类型：
--
作者：
Atti, E;Gomez, S;Boskey, AL
转化生长因子 -β1（TGF -β1）是TGF -β超家族的一种细胞因子成员，参与多种细胞类型的增殖和分化控制。TGF -β1在骨形成和吸收中起重要作用。为了确定TGF -β1缺乏对骨矿物质和基质的影响，对TGF -β1表达被消除的小鼠（TGF -β1基因敲除）的胫骨进行了分析，并通过傅里叶变换红外成像（FTIRI）和组织化学与背景和年龄匹配的野生型（WT）对照动物进行比较。FTIRI能够在超微结构水平上对未脱矿的薄组织切片进行表征，空间分辨率约为7微米。计算的光谱参数包括：矿物质与基质的比率（先前已表明与灰分重量相对应）；矿物质结晶度（与晶体学确定的磷灰石c轴方向的微晶尺寸和完整性有关）；以及胶原蛋白成熟度（与吡啶啉：脱氧 - DHLNL胶原蛋白交联的比率有关）。从次级骨化中心到远端骨干，在同一标本中选择了几个区域来代表骨发育的不同阶段。根据年龄和基因型对解剖学上等效的区域进行了比较。光谱结果以彩色编码图像以及所监测的每个参数的像素群体分布来表示。基于组织化学和FTIRI的比较，存在明显的年龄和基因型差异。在所有检测的年龄中，TGF -β1基因敲除小鼠的生长板中，碱性磷酸酶（ALP）活性和胶原蛋白成熟度降低，但未观察到对矿物质含量或结晶度的影响。在TGF -β1基因敲除小鼠的干骺端，小梁持续存在，但矿物质含量或结晶度无显著变化。相比之下，TGF -β1基因敲除小鼠的次级骨化中心和皮质骨中的矿物质含量、矿物质结晶度和胶原蛋白成熟度降低。这些结果与TGF -β1基因敲除小鼠骨成熟受损的机制一致，可能与TGF -β1缺乏直接相关，并与TGF -β1基因敲除小鼠中炎性细胞因子表达增加间接相关。（C）2002年，爱思唯尔科学公司版权所有。
Transforming growth factor-beta 1 (TGF-beta1) is a cytokine member of the TGF-beta superfamily involved in the control of proliferation and differentiation of various cell types. TGF-beta1 plays an important role in bone formation and resorption. To determine the effect of TGF-beta1 deficiency on bone mineral and matrix, tibias from mice in which TGF-beta1 expression had been ablated (TGF-beta1 null) were analyzed and compared with background- and age-matched wild-type (WT) control animals by Fourier transform-infrared imaging (FTIRI) and histochemistry. FTIRI allows the characterization of nondemineralized thin tissue sections at the ultrastructural level with a spatial resolution of similar to7 pm. The spectroscopic parameters calculated were: mineral-to-matrix ratio (previously shown to correspond to ash weight); mineral crystallinity (related to the crystallographically determined crystallite size and perfection in the apatite c-axis direction); and collagen maturity (related to the ratio of pyridinoline:delf-DHLNL collagen cross-links). Several fields were selected to represent different stages of bone development within the same specimen from the secondary ossification center to the distal diaphysis. Anatomically equivalent areas were compared as a function of age and genotype. The spectroscopic results were expressed both as color-coded images and as pixel population distributions for each of the thread parameters monitored. Based on comparisons of histochemistry and FTIRI, there were distinctive age and genotype variations. At all ages examined, in the TGF-beta1 null mice growth plates, alkaline phosphatase (ALP) activity and collagen maturity were reduced, but no effect on mineral content or crystallinity was noted. In the TGF-beta1 null mice metaphyses, there was a persistence of trabeculae, but no significant alterations in mineral content or crystallinity. In contrast, mineral content, mineral crystallinity, and collagen maturity were reduced in the secondary ossification center and cortical bone of the TGF-beta1 null mice. These results, consistent with a, mechanism of impaired bone maturation in the TGF-beta1 null mice, may be directly related to TGF-beta1 deficiency and indirectly to increased expression of inflammatory cytokines in the TGFbeta1 null mice. (C) 2002 by Elsevier Science Inc. All rights reserved.