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ADAMTS1 and Versican: Partners in Ovulation and Fertilization

Ovulation is a dynamic, orchestrated process set in motion by the midcycle surge of luteinizing hormone (LH) and culminates in the breakdown of the follicular wall and extrusion of the oocyte. This pre-ovulatory surge of LH initiates and synchro-nizes a series of biochemical events that result in the transformation of granulosa cells to luteal cells, changes in the steroidogenic potential of the transforming granulosa-luteal cells, expansion of the cumulus cells surrounding the oocyte, and changes in the extracellular matrix (ECM) at the apex of the follicle. Proteinases have been proposed to act to bring about changes in the ECM to allow expansion of the cells of the cumulus oocyte complex (COC) and degradation of the apical follicular wall. Indeed, there is a body of literature that supports a role for various proteinases such as the plasminogen activators, matrix metalloproteinases, cathepsins, and the ADAMTS (A Disintegrin And Metalloproteinase with ThromboSpondin-like motifs) in COC expansion and ovulation. These proteinases are induced after the LH surge, and administration of exogenous inhibitors for these proteinases results in a block of COC expansion and/or inhibition of oocyte release [1]. Despite this evidence, data from studies employing mice lacking specific proteinases (i.e., knockout models) have yielded little insight into the key players in the ovulatory process, potentially due to redundancy and overlapping functions of these proteolytic pathways. To date, the only proteinase that has been convincingly shown, using knockout mice, to play a role in ovulation