The objective of this study was to determine the ability of prostaglandin E2 (PGE2) to induce ovulation and expression of PGE2 receptor (EP2 and EP4) and COX genes (COX-1 and COX-2) in the ovary and pituitary of prepubertal mice. The positive control consisted of the application of 5 μg of gonadotropin-releasing hormone (GnRH, n = 29); the negative control applied 0.5 mL of phosphate buffered saline (PBS, n=31); the treatment tested the application of 250 μg of PGE2 (n = 29), making a total of 89 prepubertal mice (BALB/c). Mice were euthanized 14 to 15 h after treatments to detect ovulation and tissue collection. A Chi-square test was used to compare the proportion of animals ovulating. Gene expressions and number of ovulation were analyzed by one-way ANOVA and Tukey’s test was used to compare means among groups. A greater proportion of mice (P < 0.001) ovulated after receiving GnRH (89.7%, 26/29) compared to PGE2 group (58.6%, 17/29). However, the proportion was higher compared to those treated with PBS (0%, 0/31). Ep2 gene expression in the pituitary was > two-fold higher (P < 0.05) in the PGE2 group compared to the PBS and GnRH groups. Further, PGE2 stimulated Cox1 (2.7 fold, P < 0.05) while GnRH stimulated Cox2 expression (6.5 fold, P < 0.05) in the pituitary when compared to the PBS group. In conclusion, our results support the hypothesis that PGE2 can induce ovulation in prepubertal mice with a concomitant increase in Ep2 and Cox1 gene expression in the pituitary gland.

Erythrocyte insulin receptor binding measurements were evaluated in 8 dogs with spontaneous hyperadrenocorticism. These dogs had normal serum glucose concentration, with normal to high serum insulin concentration (range, 45 to 1,400 pmol/L; normal, 40 to 170 pmol/L). Dogs with hyperadrenocorticism had significant (P < 0.01) decrease in mean +/- SEM percentage of maximal binding for erythrocyte insulin receptors (2.25 +/- 0.21%), compared with results in 11 clinically normal pet dogs (4.29 +/- 0.42%). The decrease in erythrocyte receptor binding was attributed to significant (P < 0.01) decrease inhigh-affinity receptor sites in dogs with hyperadrenocorticism (14.5 +/- 2.8), compared with clinically normal dogs (31.2 +/- 4.3). Significant differences in receptor affinity were not apparent between the 2 groups. Percentage of maximal binding for erythrocyte insulin receptors for dogs with hyperadrenocorticism was inversely correlated with serum insulin concentration (r = - 0.85, P < 0.01). Results indicate that the observed decrease in erythrocyte insulin receptor binding could contribute to insulin resistance and hyperinsulinemia associated with hyperadrenocorticism. Alternatively, decreased binding of insulin receptors in animals with hyperadrenocorticism may result from down-regulation secondary to hyperinsulinemia itself caused by insulin resistance at a postreceptor site (decreasedresponsiveness).

Interleukin-1 Receptor 8 (IL-1R8) is a transmembrane protein of the IL-1 receptor family and represents an important regulator of the balance of innate and inflammatory responses. Depending on the immunological insult, IL1-R8 protects from the immunopathology or impairs the protective immune response against the insult. The expression pattern of IL-1R8 in dog tissues is unknown. Given the relevance of inflammatory diseases in dog, the aims of this study were to identify the sequence, analyze the phylogenesis and investigate the differential expression and distribution of IL-1R8 in a wide panel of non-pathologic tissues and organs by means of quantitative Real-Time PCR and uncover species-specific peculiarities. In Canis lupus familiaris, the IL1-R8 gene maps on chromosome 18, and includes ten exons. We first compared the coding sequence of dog IL-1R8 with sequences of other carnivors. Phylogenetic analysis revealed that IL-1R8 shares significantly high sequence homology with IL-1R8 of other canids particularly fox, sharing a common progenitor. Our study demonstrated that IL-1R8 is highly expressed in pancreas, considerably expressed in kidney, heart, liver, skeletal muscle, thymus, salivary gland, lymph node and lung. Interestingly, the expression pattern disclosed a unique profile for canine tissues when compared to tissues from other animal’s species. Imbalance of pro-inflammatory response leads to a vicious loop whither pro-inflammatory signaling and injury sustain each other and booster the disease. Therefore, it is crucial to investigate key regulator molecules such as IL-1R8, which functions both in homeostasis and disease and has potential to be a valid diagnostic, prognostic and therapeutic biomarker.