The morphology of the intestine has been studied in a species of warm water fish, Tilapia spp., a hybrid teleost of notable economic importance. Light and electron microscope results show that the intestine is a relatively undifferentiated muscular tube lined with a simple columnar epithelium interspersed with goblet cells. The proximal region has a greater surface area, manifested by elongated mucosal ridges. The enterocytes are covered apically with uniform microvilli and exhibit the typical ultrastructural features of pinocytosis, namely extensive invaginations of the luminal plasma membrane and massive accumulation of vesicles in the apical cytoplasm. The distal intestine mucosa is thinner and less elaborately folded and consists of columnar cells with shorter and sparser microvilli. Their supranuclear cytoplasm contains abundant clear vacuoles. Numerous endocrine cells can also be seen. Regional cellular ultrastructural features are correlated with digestive functions.
The objective of the present study was to investigate in rabbit corpora lutea (CL), at both the cellular and molecular level, intraluteal cyclooxygenase (COX)-1, COX-2 and prostaglandin (PG) E2-9-ketoreductase (PGE2-9-K) enzymatic activities as well as in vitro PGE2 and PGF2a synthesis following PGF2a treatment at either early-(day-4) or mid-luteal (day-9) stage of pseudopregnancy. By immunohistochemistry, positive staining for COX-2 was localized in luteal and endothelial cells of stromal arteries at both the stages. In CL of both stages, basal COX-2 mRNA levels were poorly expressed, but rose (P!0.01) 4-to 10-fold 1.5-6 h after treatment and then gradually decreased within 24 h. Compared to mid-stage, day-4 CL had lower (P!0.01) COX-2 and PGE2-9-K basal activities, and PGF2a synthesis rate, but higher (P!0.01) PGE2 production. Independent of luteal stage, PGF2a treatment did not affect COX-1 activity. In day-4 CL, PGF2a induced an increase (P!0.01) in both COX-2 activity and PGF2a synthesis, whereas that of PGE2 remained unchanged. In day-9 CL, PGF2a up-regulated (P!0.01) both COX-2 and PGE-9-K activities, and PGF2a production, but decreased (P!0.01) PGE2 synthesis. All changes in gene expression and enzymatic activities occurred within 1.5 h after PGF2a challenge and were more marked in day-9 CL. Our data suggest that PGF2a directs intraluteal PG biosynthesis in mature CL, by affecting the CL biosynthetic machinery to increase the PGF2a synthesis in an autoamplifying manner, with the activation of COX-2 and PGE-9-K; this may partly explain their differentially, age-dependent, luteolytic capacity to exogenous PGF2a in rabbits.
The aim of this study was to better understand the role of the endothelin-1 (ET-1) system in the process of controlling the corpora lutea (CL) life span in rabbits. ET-1 (10 microg iv) administration at d 9 and 12 of pseudopregnancy induced a functional luteolysis within 24 h of injection, but it was ineffective at both d 4 and 6. Pretreatments with Bosentan, a dual ET(A)/ET(B) receptor antagonist, or cyclooxygenase (COX) inhibitor blocked the luteolytic action of ET-1 but not that induced by prostaglandin F2alpha (PGF2alpha). In CL cultured in vitro, ET-1 increased (P = 0.01) both PGF(2alpha) production and luteal nitric oxide synthase activity but decreased (P < or = 0.01) progesterone release. Addition of ET(A) receptor antagonist BQ123 or COX inhibitor blocked the ET-1 luteolytic effects. Positive staining for ET-1 receptors was localized in ovarian blood vessels, granulosa cells of large follicles, and luteal cells. Immunoblot analysis of ET-1 receptor protein revealed a strong band of approximately 48 kDa in d-9 CL. Up to d 6 of pseudopregnancy, ET-1 mRNA abundance in CL was poorly expressed but then increased (P < or = 0.01) at d 9 and 13. ET(A)-receptor transcript increased (P < or = 0.01) at d 6, remained at the same level up to d 13, and then declined to the lowest (P < or = 0.01) levels at d 22. ET(B)-receptor mRNA increased (P < or = 0.01) throughout the late-luteal stage from d 13 up to d 18. Our data suggest that the luteolytic action of ET-1 may be a result of PGF2alpha synthesis from both luteal and accessory cells, via the COX pathways.
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