Pastor L M, Zuasti A, Ferrer C, Bernal-Mañas C M, Morales E, Beltrán-Frutos E, Seco-Rovira V
Department of Cellular Biology and Histology, Aging Institute, Medical School, University of Murcia, Murcia, Spain.
Reprod Domest Anim. 2011 Feb;46(1):155-64. doi: 10.1111/j.1439-0531.2009.01573.x.
Imbalances in the proliferation and apoptosis processes are involved in numerous epithelial alterations. In the seminiferous epithelium, normal spermatogenesis is regulated by spermatogonia proliferation and germ cell apoptosis, and both processes are involved in diverse pathological alterations of the seminiferous epithelium. Other physiological phenomena including aging and short photoperiod, in which apoptosis and proliferation seem to play important roles, cause testicular changes. Aging is accompanied by diminished proliferation and increased apoptosis, the latter occurring in specific states of the seminiferous cycle and considered the cause of epithelium involution. However, there is no clear evidence concerning whether proliferation decreases in the spermatogonia themselves or is due to an alteration in the cell microenvironment that surrounds them. As regards the factors that regulate the process, the data are scant, but it is considered that the diminution of c-kit expression in the spermatagonia, together with the diminution in antiapoptotic factors (Bcl-x(L))) of the intrinsic molecular pathway of apoptosis play a part in epithelial regression. A short photoperiod, especially in rodents, produces a gradual involution of the seminiferous epithelium, which is related with increased apoptosis during the regression phase and a diminution of apoptosis during recrudescence. Proliferative activity varies, especially during the total regression phase, when it usually increases in the undifferentiated spermatogonia. In other species showing seasonal reproduction, however, decreased proliferation is considered the main factor in the regression of the seminiferous epithelium. Little is known about how both phenomena are regulated, although data in rodents suggest that both the intrinsic and extrinsic pathways of apoptosis contribute to the increase in this process. In conclusion, regression of the seminiferous epithelium in physiological situations, as in many pathological situations, is a result of alterations in equilibrium between the proliferation and apoptosis of germinal cell types. However, both physiological phenomena showed important differences as regard proliferation/apoptosis and their regulation pathways, probably as a result of their irreversible or reversible character.
增殖和凋亡过程的失衡与众多上皮细胞改变有关。在生精上皮中，正常的精子发生受精原细胞增殖和生殖细胞凋亡调控，这两个过程均参与生精上皮的多种病理改变。包括衰老和短光照周期在内的其他生理现象也会导致睾丸变化，其中凋亡和增殖似乎起着重要作用。衰老伴随着增殖减少和凋亡增加，后者发生在生精周期的特定阶段，被认为是上皮退化的原因。然而，关于增殖减少是发生在精原细胞自身，还是由于其周围细胞微环境的改变，尚无明确证据。关于调节这一过程的因素，数据很少，但人们认为精原细胞中c-kit表达的减少，以及凋亡内在分子途径中抗凋亡因子（Bcl-x(L)）的减少，在生精上皮退化中起作用。短光照周期，尤其是在啮齿动物中，会导致生精上皮逐渐退化，这与退化期凋亡增加和再生期凋亡减少有关。增殖活性会发生变化，尤其是在完全退化期，此时未分化的精原细胞增殖通常会增加。然而，在其他表现出季节性繁殖的物种中，增殖减少被认为是生精上皮退化的主要因素。尽管啮齿动物的数据表明凋亡的内在和外在途径都促成了这一过程的增加，但对于这两种现象如何被调节知之甚少。总之，与许多病理情况一样，生理情况下生精上皮的退化是生殖细胞类型增殖和凋亡平衡改变的结果。然而，这两种生理现象在增殖/凋亡及其调节途径方面表现出重要差异，这可能是由于它们不可逆或可逆的特性所致。
