KINETIC-STUDIES ON THE DEVELOPMENT OF THE ADULT-POPULATION OF LEYDIG-CELLS IN TESTES OF THE PUBERTAL RAT
KINETIC-STUDIES ON THE DEVELOPMENT OF THE ADULT-POPULATION OF LEYDIG-CELLS IN TESTES OF THE PUBERTAL RAT
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DOI：
10.1210/endo-124-2-762
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发表时间：
1989-02-01
期刊：
影响因子：
4.8
通讯作者：
EWING, LL
中科院分区：
文献类型：
--
作者：
HARDY, MP;ZIRKIN, BR;EWING, LL
本研究的目的是确定是否出生后大鼠Leydig细胞数量的增加导致分化的前体细胞，分裂现有的Leydig细胞，或两者兼而有之。我们的方法是：1）检查睾丸间质细胞和潜在前体细胞绝对数量的变化（巨噬细胞、周细胞和间充质细胞、内皮细胞和肌样细胞）; 2）检查间充质细胞和间质细胞在产前和产后发育期间分裂的频率;和3）鉴定和检查在产前和产后发育期间间质细胞分裂的后代的命运。体视学方法显示，在产后第-2天，间充质细胞占总间质细胞群的44%，间质细胞占16%，而到产后第56天，这种关系已经逆转;间充质细胞占3%，间质细胞占49%。这些结果表明，间充质和间质细胞之间的相互作用产物的关系，因为没有这样的相互关系间质细胞和巨噬细胞，周细胞，内皮细胞，或肌样细胞之间观察。放射自显影分析[3 H]胸苷掺入间充质和Leydig细胞与此解释是一致的。在一系列脉冲追踪实验中，在产后第2、14、28和56天单次注射[3 H]胸苷后，测量标记的间充质细胞和间质细胞的百分比，此后每隔一定时间（1小时至14天）取样。从第14天开始，注射[3 H]胸苷后立即标记的间质细胞百分比约为1%，注射后6天显著增加至约6%。当大鼠在产后第2、28和56天开始类似注射时，未观察到这种增加。产后第14天至第28天间的间质细胞标记的上升并没有导致标记的间质细胞核上的银颗粒的数量下降，这表明标记细胞的百分比增加不是由间质细胞分裂引起的。这些观察结果使我们得出结论，从第14天到第28天，间质细胞标记的增加是从标记的间充质细胞的隔室募集的结果。相反，我们的分析表明，从产后第28天起，直到Leydig细胞达到成熟数量，Leydig细胞是由形态可识别的Leydig细胞分裂产生的。
The objective of this study was to determine whether postnatal increases in rat Leydig cell number result from differentiation of precursor cells, division of existing Leydig cells, or both. Our approach was 1) to examine changes in the absolute number of Leydig cells and potential precursor cells (macrophages, pericytes, and mesenchymal, endothelial, and myoid cells) per testis on day 19 of gestation (day -2) and days 7, 14, 21, 28, and 56 postpartum; 2) to examine the frequency with which mesenchymal and Leydig cells divide during prenatal and postnatal development; and 3) to identify and examine the fate of the progeny of Leydig and mesenchymal cell divisions during prenatal and postnatal development. Stereological methods were used to show that mesenchymal cells comprised 44% of the total interstitial cell population and Leydig cells 16% on day -2, whereas by day 56 postpartum the relationship had reversed; mesenchymal cells comprised 3% and Leydig cells 49%. These results suggested a precursor-product relationship between mesenchymal and Leydig cells because no such reciprocal relationship was observed between Leydig cells and macrophages, pericytes, endothelial, or myoid cells. Autoradiographic analysis of [3H]thymidine incorporation into mesenchymal and Leydig cells was consistent with this interpretation. In a series of pulse-chase experiments, the percentage of labeled mesenchymal and Leydig cells was measured after a single injection of [3H]thymidine on days 2, 14, 28, and 56 postpartum, each followed by sampling at timed intervals (between 1 h and 14 days) thereafter. Starting on day 14, the percentage of labeled Leydig cells was approximately 1% immediately after injection of [3H]thymidine and increased significantly to approximately 6% by 6 days after injection. No such increase was observed when rats were similarly injected starting on days 2, 28, and 56 postpartum. The rise in Leydig cell labeling between days 14 and 28 postpartum did not result in a decline in the number of silver grains over labeled Leydig cell nuclei, indicating that the increase in the percentage of labeled cells was not caused by Leydig cell division. These observations led us to conclude that the increase in Leydig cell labeling from days 14 to 28 was the result of recruitment from a compartment of labeled mesenchymal cells. In contrast, our analysis indicated that from day 28 postpartum and thereafter until the mature number of Leydig cells is attained, Leydig cells are generated by division of morphologically recognizable Leydig cells.