TY - JOUR A1 - , T1 - Auto-paracrine regulation of the proliferation of pituitary ACTH-producing cells demonstrated by immunoblockade of IL-1? JO - Eur. J. Anat. SN - 1136-4890 Y1 - 2006 VL - 10 SP - 7 EP - 13 UR - http://www.eurjanat.com/web/paper.php?id=06010007 KW - corticotropin KW - cycline KW - interleukin 1beta KW - animal cell KW - animal experiment KW - animal tissue KW - apoptosis KW - article KW - cell culture KW - cell proliferation KW - cell size KW - controlled study KW - corticotropin release KW - hormone release KW - hypophysis KW - hypophysis cell KW - immunohistochemistry KW - in vitro study KW - male KW - nonhuman KW - paracrine signaling KW - rat N2 - IL-1? is an interleukin synthesised in the pituitary gland and is involved in the stimulation of ACTH secretion. However, to date it has not been determined whether IL-1? is able to regulate the proliferation of pituitary ACTH-producing cells, like other regulatory factors involved in the regulation of ACTH such as vasopressin or CRH. The aim of the present study was to address whether IL-1? is involved in regulating the proliferation and apoptosis of pituitary ACTH-secreting cells. Thus, we performed an in vitro study on monolayer cultures of rat pituitary cells, neutralising the possible paracrine effect of IL-1? by immunoblockade of the interleukin and later determining the degree of proliferation or apoptosis of ACTH-secreting cells. The effects of immunoblockade were validated by determining the modifications in the patterns of the immunohistochemical reaction to ACTH-positive cells. Immunoblockade of IL-1? decreased the percentage and proliferation of ACTH-positive cells at all time-points analysed, mainly between 6 and 12 h (p < 0.01). Moreover, immunoblockade decreased the sizes of the cellular and nuclear areas at all time-points studied, with significant decreases (p < 0.01) after 3, 6 and 12 hours. The results obtained suggest that -in the same way as it regulates the secretion of the hormone- IL-1? could be involved in regulating the proliferation of ACTH cells. ER -