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Corpus luteum growth and endocrine function are closely dependent on the formation of new capillaries. The objectives of this study were to evaluate (i) tissue growth and microvascular development in the equine cyclic luteal structures; (ii) in vitro angiogenic activity of luteal tissues in response to luteotrophic (LH, PGE 2 ) and luteolytic (PGF 2␣ ) hormones and (iii) to relate data to luteal endocrinological function. Our results show that microvascular density was increased in the early and mid luteal phase, followed by a fall in the late luteal phase and a further decrease in the corpus albicans. Hyperplasia of luteal tissue increased until the mid luteal phase and it was followed by tissue regression. Luteal explants were cultured with no hormone added, or with PGF 2␣ , LH, PGE 2 , LH + PGE 2 or LH + PGF 2␣ . Media conditioned by equine luteal tissue from different stages of the luteal phase were able to stimulate mitogenesis of bovine aortic endothelial cells (BAEC), suggesting the presence of angiogenic activity. No difference was observed among luteal structures on their mitogenic capacity, for any treatment used. Nevertheless, Late-CL conditioned-media with PGF 2␣ showed a significant decrease in BAEC proliferation (p < 0.05) and LH + PGF 2␣ a tendency to reduce mitogenesis. Thus, prostaglandin F 2␣ may play a role on vascular regression of the CL during the late luteal phase in the * Corresponding author. Tel.: +351 213652859; fax: +351 213652889. -mail address: gmlfdias@fmv.utl.pt (G. Ferreira-Dias Ferreira-Dias et al. / Domestic Animal Endocrinology 30 (2006) [247][248][249][250][251][252][253][254][255][256][257][258][259] mare. These data suggest that luteal angiogenesis and vascular regression in the mare are coordinated with the development of non-vascular tissue and might be regulated by many different factors. E

Contents We have shown that bacteria induce neutrophil extracellular traps (NETs) in mare endometrium. Besides killing pathogens, NETs may contribute for endometrosis (chronic endometrium fibrosis). Since elastase (ELA) is a NETs component that regulates fibrosis and prostaglandin (PG) output, the aim was to evaluate if inhibition of ELA would affect collagen 1 (COL1) transcription and PGs secretion by endometrium explants, in different estrous cycle phases. Follicular‐FP (n = 8) and mid luteal–MLP (n = 7) phases explants were cultured for 24–48 hr with medium alone (Control), ELA (0.5 μg/ml,1 μg/ml), sivelestat ‐ ELA inhibitor (INH,10 μg/ml), or ELA (0.5 μg/ml,1 μg/ml) + INH (10 μg/ml). COL1 gene transcription was done by qRT‐PCR and PGE2 and PGF2α determination in culture medium by EIA. In FP, at 24 hr, ELA0.5 increased COL1 transcription (p < 0.001) but its inhibition (ELA0.5 + INH10) decreased COL1 transcription (p < 0.01) and PGF2α production (p < 0.05). Also, ELA0.5 + INH10 or ELA1 + INH10 raised PGE2 production (p < 0.01). At 48 hr, ELA1 increased COL1 transcription (p < 0.01) and PGF2α production (p < 0.001), but its inhibition (ELA1 + INH10) decreased these actions (p < 0.01; p < 0.05, respectively). Besides, ELA1 + INH10 incubation increased PGE2 (p < 0.05). PGF2α also augmented with ELA0.5 (p < 0.001), but lowered with ELA0.5 + INH10 (p < 0.01). In MLP, ELA0.5 up‐regulated COL1 transcription (24 hr, p < 0.01; 48 hr, p < 0.001), but ELA0.5 + INH10 decreased it (24 hr, p < 0.05; 48 hr, p < 0.001). At 48 hr, incubation with ELA1 also increased COL1 transcription and PGF2α production (p < 0.05), but PGF2α production decreased with ELA1 + INH10 incubation (p < 0.05). PGE2 production was higher in ELA1 + INH10 incubation (p < 0.05). Therefore, ELA inhibition may reduce the establishment of mare endometrial fibrosis by stimulating the production of anti‐fibrotic PGE2 and inhibiting pro‐fibrotic PGF2α.