In previous in vitro studies we found that contact between mouse primordial germ cells and other cell types (neighbouring somatic cells or established TM4 or STO cell lines) is crucial for supporting primordial germ cell survival and proliferation and for activating their motility. We have studied primordial germ cell adhesion to different cell monolayers (STO, TM4, COS and F9 cells) as an in vitro model for interactions between primordial germ cells and cellular substrates. The results suggest that these cell interactions are mediated by multiple mechanisms involving Steel factor and its receptor encoded by c-kit, carbohydrates and possibly other unknown factors. We find that Steel factor and leukaemia inhibitory factor are survival rather than proliferation factors for primordial germ cells. Both molecules prevent primordial germ cell death in culture by suppressing apoptosis. Morphological and molecular features of primordial germ cell apoptosis in vitro are reported. Activation of protein kinase C does not promote primordial germ cell proliferation, but compounds known to enhance intracellular levels of cAMP (i.e. dibutyryl cAMP and forskolin) markedly stimulate primordial germ cells to proliferate in culture. We have preliminary results indicating that neuropeptides PACAP-27 and PACAP-28 are possible physiological activators of adenylate cyclase in primordial germ cells.
|Number of pages||11|
|Journal||Ciba Foundation symposium|
|Publication status||Published - 1994|
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