BRIEF COMMUNICATION: Understanding the interaction of prolactin and leukaemia inhibitory factor signalling during the switch from lactation to involution

摘要

The molecular mechanisms involved in involution of the bovine udder, a process which underpins lactation persistency, are poorly understood. During rodent lactation, STATS is activated in response to prolactin (PRL) to stimulate milk protein production (Liu et al., 1997). At the onset of involution, STAT5 is rapidly inactivated (Schmitt-Ney et al., 1992), and STATS is activated by leukaemia inhibitory factor (LIE) to regulate mammary epithelial cell (MEC) apoptosis ,and tissue remodelling (Kritikou et al., 2003). It is unclear how the reciprocal activation of the two STAT pathways is regulated. Recent evidence suggests the LIF-STAT3 pathway may inhibit PRL-STAT5 signalling via suppressor of cytokine signalling 3 (SOCS3) (Dif et al., 2001; Granillo et al., 2007). The aim of this study was to investigate STAT5/3 signalling at the onset of involution in the bovine mammary gland, and construct a mathematical model to determine if LIE suppresses milk synthesis by inhibiting PRL. Ultimately, this may allow the development of novel strategies for improving milk production especially in the later stages of lactation.