Cell death in avian tibial dyschondroplasia
Cell death in avian tibial dyschondroplasia
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DOI：
10.2307/1592578
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发表时间：
1998-01-01
期刊：
影响因子：
1.4
通讯作者：
Balog, JM
中科院分区：
文献类型：
--
作者：
Rath, NC;Huff, WE;Balog, JM
胫骨软骨发育不良(TD)是快速生长家禽生长板的一种局部缺陷，移行区软骨不能吸收，并持续存在，阻止软骨内骨形成。我们比较了正常和TD影响的生长板的软骨的差异，使用MTS的减少来评估软骨的活性。分离软骨细胞和生长板切片，采用DNA片段化、原位末端标记法和荧光素-dUTP原位标记法检测软骨细胞的凋亡率。受TD影响的软骨表现出明显较低的MTS还原水平和三氯乙酸(TCA)可沉淀DNA含量的降低。琼脂糖凝胶电泳法显示，TD软骨DNA片段率较高。从TD影响的软骨中分离出的软骨细胞数量显著增加，形态致密，核缩小，胞质较少，荧光素-dUTP掺入核内证实为TUNEL阳性。体内实验结果类似地显示，生长板切片的原位TUNEL染色显示，移行区有大量软骨细胞凝聚和凋亡。正常生长板，在相似的条件下，肥大和软骨化区的软骨细胞没有明显的凋亡。凝集和凋亡细胞死亡可能是生长板活性降低、DNA含量减少和DNA片段化增加的原因。虽然TD的发病机制尚不清楚，但生长板肥大区软骨细胞的异常死亡可能是导致软骨堆积和软骨内骨形成受阻的原因。
Tibial dyschondroplasia (TD) is a local defect of growth plates in fastgrowing poultry where the transitional zone cartilage fails to resorb and persists as an avascular plug that prevents endochondral bone formation. We compared the differences in the cartilages from normal and TD-affected growth plates using the reduction of MTS to assess cartilage viability. Chondrocyte apoptosis was determined using biochemical measurement of DNA fragmentation, and in situ labeling of nuclei with fluorescein-dUTP using terminal deoxynucleotide transferase (TdT)-mediated nick end labeling (TUNEL) of isolated chondrocytes and growth plate sections. The TD-affected cartilage showed a significantly lower level of MTS reduction and a decrease in trichloroacetic acid (TCA)-precipitable DNA content. The TD cartilages had a higher percentage of fragmented DNA, which was also evident with agarose gel electrophoresis. A significantly higher number of chondrocytes isolated from TD-affected cartilages had condensed morphology, shrunken nuclei with little cytoplasm, and were TUNEL positive as identified by the incorporation of fluorescein-dUTP into the nuclei. In vivo results similarly showed a significant population of chondrocytes in transition zones undergoing condensation and apoptosis as determined by in situ TUNEL staining of growth plate sections. Normal growth plates, under similar conditions, showed no significant apoptosis of chondrocytes from hypertrophic and chondrolyzing zones. The condensation and apoptotic cell death may be responsible for the reduction of growth plate viability as well as the reduction in DNA content and increased DNA fragmentation. While the cause of the pathogenesis of TD is unknown, it appears that the aberrant death of chondrocytes in hypertrophic regions of growth plates may be responsible for the accumulation of cartilage and the arrest of endochondral bone formation.