Heparin, But Not N-Desulfated Heparin, Enhances Cumulus Expansion of Mouse and Cow Oocytes in Serum-Free Medium
Glycosaminoglycans (GAGs) are follicular constituents that have been implicated as regulators of several cellular processes in ovarian follicles. In a dose-dependent manner, commercially available GAGs inhibited cumulus mass expansion in the presence of FSH and serum (6) and inhibited gonadotropin binding to granulosa cells (1,2). In the same manner, follicular GAGs inhibited LDL degradation and progesterone production (3) and zona pellucida hardening in vitro (4). Heparin, one type of GAG, inhibits those cellular processes and is the most “potent” inhibitor of the chemical classes of GAGs tested (1–4). Heparin has O- and N-substituted sulfate groups and is the most highly sulfated of the GAGs (5). The ability of GAGs to affect FSH-induced expansion of cumulus cells is related to degree of GAG sulfation (6). GAGs containing less sulfate, such as the chondroitin sulfates and hyaluronic acid, were less effective at inhibiting FSH-induced cumulus mass expansion (6). This suggested importance of sulfation in the ability of GAGs to inhibit FSH-induced cumulus cell expansion, but there are also other structural differences between those classes of GAGs (1). It is not known if GAGs affect cumulus mass expansion in cultures lacking FSH. Desulfation of heparin affects its interactions with many cells. For example, desulfation of heparin reduced its ability to inhibit LDL degradation and progesterone production by granulosa cells (3).
KeywordsHyaluronic Acid Granulosa Cell Follicular Fluid Zona Pellucida Cumulus Cell
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