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Therefore, an upstream signal may be required to induce the granulosa cells to generate threshold KITL levels before follicle activation can proceed. This signal may be a reduction in inhibitors, an increase in activators, or a combination of both. KITL has been reported to be a survival factor for a number of different cell types, including hematopoietic stem cells, spermatogonia, and primordial germ cells. However, recombinant mouse KITL did not enhance the survival of oocytes in cultured neonatal mouse ovaries or rabbit ovarian cortical explants. Similarly, the addition of KITL-neutralizing antibody did not increase the proportion of atretic follicles in these tissues. Definitive evidence in support of an antiapoptotic role for KITL during folliculogenesis is currently lacking, and the published data are contradictory. Yoshida et al. reported that follicle survival was not affected in mice injected with the KIT-blocking antibody ACK2. In contrast, inhibition of the KITL/KIT interaction with ACK2 has been shown to decrease the survival of preantral mouse oocytes maintained in vitro. Recently, KITL has been shown to promote primordial follicle survival in cultured mouse ovaries.