Debate Can luteal regression be reversed ?

The corpus luteum is an endocrine gland whose limited lifespan is hormonally programmed. This debate article summarizes findings of our research group that challenge the principle that the end of function of the corpus luteum or luteal regression, once triggered, cannot be reversed. Overturning luteal regression by pharmacological manipulations may be of critical significance in designing strategies to improve fertility efficacy. Background The corpus luteum is a peculiar endocrine gland owing to its limited functional life. How long this gland lives and when it dies is dictated by a synchronized interplay of hormonally regulated events. It undergoes a complex process of formation or luteinization, which is followed by a period of active function that is mostly focused on the production of progesterone. Finally, the gland undergoes a process of regression associated with the decline in progesterone output and the demise of the tissue as a consequence of the programmed death of the luteal cells. A number of excellent review articles have been published in the last 6–7 years compiling the knowledge mastered on the molecular regulation of the formation, function and regression of the corpus luteum [1-13]. Yet, although luteal regression has been intensively studied, many of the regulatory mechanisms involved in loss of function and involution of the luteal structure are not completely understood. One fundamental question that remains without an answer is whether the process of luteal regression, once initiated, can be blocked or even reversed. In other words, can luteal function be rescued when it has already been impaired? Or instead, is luteal regression an irreversible event that cannot be modified when it progresses beyond a particular molecular step? Discussion It is known that a cycling corpus luteum can survive longer if it is rescued by luteotropins. Physiologically this rescue takes place when the gland is fully functioning. For example in humans, chorionic gonadotropin produced by the trophoblast cells targets and rescues the corpus luteum at the mid-luteal phase of the menstrual cycle when the gland is at the maximal steroidogenic output attainable during non-pregnant cycles [8,14]. In the rat, vaginal stimulation during coitus triggers a neuroendocrine reflex that leads to the secretion of pituitary prolactin in a pattern of two daily surges. Prolactin then targets and rescues the corpus luteum in the morning of diestrus day 2 of the estrous cycle, when the capacity of the gland to produce progesterone is also maximal [15]. It is not known, however, whether the corpus luteum can be rescued while it is already in regression, and, consequently, not fully functional. Because luteal regression involves a complex and likely synchronized sequence of molecular events, it is rather difficult to determine when a pharmacological intervention could be made to rescue the corpus luteum making it fully functional again, or, in other words, "bringing it back to life." Published: 30 October 2006 Reproductive Biology and Endocrinology 2006, 4:53 doi:10.1186/1477-7827-4-53 Received: 07 September 2006 Accepted: 30 October 2006 This article is available from: http://www.rbej.com/content/4/1/53 © 2006 Telleria; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.