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Leptin in the canine uterus and placenta: possible implications in pregnancy.

Balogh O, Staub LP, Gram A, Boos A, Kowalewski MP, Reichler IM - Reprod. Biol. Endocrinol. (2015)

Bottom Line: In the Ut/Pl, Lep expression was higher at post-implantation and prepartum luteolysis than at mid-gestation, while in the Ut, Lep mRNA levels did not change during pregnancy.In the Ut, highest LepR mRNA was found at pre- and post-implantation.Aglepristone treatment resulted in a decrease of Lep mRNA levels from 24 to 72 h in the Ut without concomitant changes in the Ut/Pl or in LepR levels.

View Article: PubMed Central - PubMed

ABSTRACT

Background: Leptin (Lep) is known for its involvement in the regulation of reproductive functions. It is important for uterine receptivity, implantation, placental growth and maternal energy homeostasis in several species, but Lep's function in the pregnant dog has not been investigated.

Methods: Pregnant bitches were ovariohysterectomized at pre-implantation, post-implantation, mid-gestation and prepartum luteolysis. Two additional groups were treated with aglepristone in mid-gestation, and ovariohysterectomized 24 or 72 h later. Lep and leptin receptor (LepR) gene expression was detected by semi-quantitative real-time PCR in pre-implantation and inter-placental uterine sections (Ut) and in utero-placental compartments (Ut/Pl). Immunohistochemistry and in situ hybridization (ISH) were performed for Lep and LepR protein and mRNA localization. Parametric one-way ANOVA, paired t-test and Wilcoxon signed-rank test were used for statistical analysis.

Results: In the Ut/Pl, Lep expression was higher at post-implantation and prepartum luteolysis than at mid-gestation, while in the Ut, Lep mRNA levels did not change during pregnancy. LepR expression in the Ut/Pl was up-regulated at prepartum luteolysis compared to the earlier stages. In the Ut, highest LepR mRNA was found at pre- and post-implantation. LepR expression was down-regulated in the Ut/Pl compared to the Ut at post-implantation and at mid-gestation. Aglepristone treatment resulted in a decrease of Lep mRNA levels from 24 to 72 h in the Ut without concomitant changes in the Ut/Pl or in LepR levels. Lep and LepR immunoreactivities were strong in the luminal and glandular epithelium in the Ut with abundant LepR signals in the subepithelial stroma. In the Ut/Pl, fetal trophoblasts stained stronger for Lep and LepR than decidual cells, and signals for both proteins were also detected in the glandular chambers. The myometrium, blood vessel media, and sporadically also the endothelium stained for Lep and LepR. ISH showed similar signal distribution in the Ut and Ut/Pl.

Conclusions: Lep and LepR are differentially expressed in the canine uterus and placenta during pregnancy, and their presence in various cell types indicates paracrine/autocrine roles. The Lep signaling system may be one of the pathways involved in feto-maternal cross-talk, implantation and maintenance of pregnancy, and may have a regulatory role around parturition.

No MeSH data available.


Related in: MedlinePlus

In situhybridization for leptin and leptin receptor in the inter-placental uterus and utero-placental compartments during pregnancy. Localization of leptin (Lep) and leptin receptor (LepR) mRNA by in situ hybridization in inter-placental sections (Ut) at post-implantation (A, B), and in the utero-placental compartments (Ut/Pl) at prepartum luteolysis (C, D). (A) Lep mRNA expression is evident in the surface epithelium (solid arrows) and superficial glandular epithelium (open arrows) with weak sub-epithelial stromal signals (solid arrowheads). Deep uterine glands and the myometrium also stain positively for Lep (inset upper right). A negative control is shown in the lower left inset. (B) LepR mRNA is expressed in the luminal epithelium (solid arrows) and superficial glandular epithelial cells (open arrows). Note the prominent stromal signals (solid arrowheads) close to the lumen. The upper right inset is positive staining for LepR in the deep uterine glands and myometrium, and the lower left inset shows a negative control. (C) Intense Lep expression is noted in the fetal trophoblast cells (open arrowheads) of the placental labyrinth at prepartum luteolysis, in contrast to weak staining in maternal decidual cells (solid arrowheads) and sporadic signals in blood vessel endothelium (thin arrows); the upper right inset shows positive reaction in the myometrium, and the lower left inset is the negative control sense probe for Lep. (D) LepR mRNA expression is strong in the placental labyrinth at prepartum luteolysis within fetal trophoblast cells (open arrowheads), while decidual cells have less intense signals (solid arrowheads) and endothelial cells (thin arrows) stain occasionally; the upper right inset shows LepR mRNA in the myometrium, and the lower left inset presents the negative control sense probe for LepR. DG: Deep uterine glands, MY: Myometrium, MV: maternal vessel.
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Fig6: In situhybridization for leptin and leptin receptor in the inter-placental uterus and utero-placental compartments during pregnancy. Localization of leptin (Lep) and leptin receptor (LepR) mRNA by in situ hybridization in inter-placental sections (Ut) at post-implantation (A, B), and in the utero-placental compartments (Ut/Pl) at prepartum luteolysis (C, D). (A) Lep mRNA expression is evident in the surface epithelium (solid arrows) and superficial glandular epithelium (open arrows) with weak sub-epithelial stromal signals (solid arrowheads). Deep uterine glands and the myometrium also stain positively for Lep (inset upper right). A negative control is shown in the lower left inset. (B) LepR mRNA is expressed in the luminal epithelium (solid arrows) and superficial glandular epithelial cells (open arrows). Note the prominent stromal signals (solid arrowheads) close to the lumen. The upper right inset is positive staining for LepR in the deep uterine glands and myometrium, and the lower left inset shows a negative control. (C) Intense Lep expression is noted in the fetal trophoblast cells (open arrowheads) of the placental labyrinth at prepartum luteolysis, in contrast to weak staining in maternal decidual cells (solid arrowheads) and sporadic signals in blood vessel endothelium (thin arrows); the upper right inset shows positive reaction in the myometrium, and the lower left inset is the negative control sense probe for Lep. (D) LepR mRNA expression is strong in the placental labyrinth at prepartum luteolysis within fetal trophoblast cells (open arrowheads), while decidual cells have less intense signals (solid arrowheads) and endothelial cells (thin arrows) stain occasionally; the upper right inset shows LepR mRNA in the myometrium, and the lower left inset presents the negative control sense probe for LepR. DG: Deep uterine glands, MY: Myometrium, MV: maternal vessel.

Mentions: In the Ut, Lep mRNA was found in the luminal and glandular epithelial cells of the endometrium (Figure 6A). In the Ut/Pl, fetal trophoblasts within the placental labyrinth gave stronger signals than decidual cells (Figure 6C), while the epithelium of the glandular chambers and deep uterine glands stained weakly (not shown). Strong positive signals were also detected in the myometrium (Figure 6A upper right inset and 6C upper right inset), and occasionally in blood vessel endothelium (Figure 6C).Figure 6


Leptin in the canine uterus and placenta: possible implications in pregnancy.

Balogh O, Staub LP, Gram A, Boos A, Kowalewski MP, Reichler IM - Reprod. Biol. Endocrinol. (2015)

In situhybridization for leptin and leptin receptor in the inter-placental uterus and utero-placental compartments during pregnancy. Localization of leptin (Lep) and leptin receptor (LepR) mRNA by in situ hybridization in inter-placental sections (Ut) at post-implantation (A, B), and in the utero-placental compartments (Ut/Pl) at prepartum luteolysis (C, D). (A) Lep mRNA expression is evident in the surface epithelium (solid arrows) and superficial glandular epithelium (open arrows) with weak sub-epithelial stromal signals (solid arrowheads). Deep uterine glands and the myometrium also stain positively for Lep (inset upper right). A negative control is shown in the lower left inset. (B) LepR mRNA is expressed in the luminal epithelium (solid arrows) and superficial glandular epithelial cells (open arrows). Note the prominent stromal signals (solid arrowheads) close to the lumen. The upper right inset is positive staining for LepR in the deep uterine glands and myometrium, and the lower left inset shows a negative control. (C) Intense Lep expression is noted in the fetal trophoblast cells (open arrowheads) of the placental labyrinth at prepartum luteolysis, in contrast to weak staining in maternal decidual cells (solid arrowheads) and sporadic signals in blood vessel endothelium (thin arrows); the upper right inset shows positive reaction in the myometrium, and the lower left inset is the negative control sense probe for Lep. (D) LepR mRNA expression is strong in the placental labyrinth at prepartum luteolysis within fetal trophoblast cells (open arrowheads), while decidual cells have less intense signals (solid arrowheads) and endothelial cells (thin arrows) stain occasionally; the upper right inset shows LepR mRNA in the myometrium, and the lower left inset presents the negative control sense probe for LepR. DG: Deep uterine glands, MY: Myometrium, MV: maternal vessel.
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Fig6: In situhybridization for leptin and leptin receptor in the inter-placental uterus and utero-placental compartments during pregnancy. Localization of leptin (Lep) and leptin receptor (LepR) mRNA by in situ hybridization in inter-placental sections (Ut) at post-implantation (A, B), and in the utero-placental compartments (Ut/Pl) at prepartum luteolysis (C, D). (A) Lep mRNA expression is evident in the surface epithelium (solid arrows) and superficial glandular epithelium (open arrows) with weak sub-epithelial stromal signals (solid arrowheads). Deep uterine glands and the myometrium also stain positively for Lep (inset upper right). A negative control is shown in the lower left inset. (B) LepR mRNA is expressed in the luminal epithelium (solid arrows) and superficial glandular epithelial cells (open arrows). Note the prominent stromal signals (solid arrowheads) close to the lumen. The upper right inset is positive staining for LepR in the deep uterine glands and myometrium, and the lower left inset shows a negative control. (C) Intense Lep expression is noted in the fetal trophoblast cells (open arrowheads) of the placental labyrinth at prepartum luteolysis, in contrast to weak staining in maternal decidual cells (solid arrowheads) and sporadic signals in blood vessel endothelium (thin arrows); the upper right inset shows positive reaction in the myometrium, and the lower left inset is the negative control sense probe for Lep. (D) LepR mRNA expression is strong in the placental labyrinth at prepartum luteolysis within fetal trophoblast cells (open arrowheads), while decidual cells have less intense signals (solid arrowheads) and endothelial cells (thin arrows) stain occasionally; the upper right inset shows LepR mRNA in the myometrium, and the lower left inset presents the negative control sense probe for LepR. DG: Deep uterine glands, MY: Myometrium, MV: maternal vessel.
Mentions: In the Ut, Lep mRNA was found in the luminal and glandular epithelial cells of the endometrium (Figure 6A). In the Ut/Pl, fetal trophoblasts within the placental labyrinth gave stronger signals than decidual cells (Figure 6C), while the epithelium of the glandular chambers and deep uterine glands stained weakly (not shown). Strong positive signals were also detected in the myometrium (Figure 6A upper right inset and 6C upper right inset), and occasionally in blood vessel endothelium (Figure 6C).Figure 6

Bottom Line: In the Ut/Pl, Lep expression was higher at post-implantation and prepartum luteolysis than at mid-gestation, while in the Ut, Lep mRNA levels did not change during pregnancy.In the Ut, highest LepR mRNA was found at pre- and post-implantation.Aglepristone treatment resulted in a decrease of Lep mRNA levels from 24 to 72 h in the Ut without concomitant changes in the Ut/Pl or in LepR levels.

View Article: PubMed Central - PubMed

ABSTRACT

Background: Leptin (Lep) is known for its involvement in the regulation of reproductive functions. It is important for uterine receptivity, implantation, placental growth and maternal energy homeostasis in several species, but Lep's function in the pregnant dog has not been investigated.

Methods: Pregnant bitches were ovariohysterectomized at pre-implantation, post-implantation, mid-gestation and prepartum luteolysis. Two additional groups were treated with aglepristone in mid-gestation, and ovariohysterectomized 24 or 72 h later. Lep and leptin receptor (LepR) gene expression was detected by semi-quantitative real-time PCR in pre-implantation and inter-placental uterine sections (Ut) and in utero-placental compartments (Ut/Pl). Immunohistochemistry and in situ hybridization (ISH) were performed for Lep and LepR protein and mRNA localization. Parametric one-way ANOVA, paired t-test and Wilcoxon signed-rank test were used for statistical analysis.

Results: In the Ut/Pl, Lep expression was higher at post-implantation and prepartum luteolysis than at mid-gestation, while in the Ut, Lep mRNA levels did not change during pregnancy. LepR expression in the Ut/Pl was up-regulated at prepartum luteolysis compared to the earlier stages. In the Ut, highest LepR mRNA was found at pre- and post-implantation. LepR expression was down-regulated in the Ut/Pl compared to the Ut at post-implantation and at mid-gestation. Aglepristone treatment resulted in a decrease of Lep mRNA levels from 24 to 72 h in the Ut without concomitant changes in the Ut/Pl or in LepR levels. Lep and LepR immunoreactivities were strong in the luminal and glandular epithelium in the Ut with abundant LepR signals in the subepithelial stroma. In the Ut/Pl, fetal trophoblasts stained stronger for Lep and LepR than decidual cells, and signals for both proteins were also detected in the glandular chambers. The myometrium, blood vessel media, and sporadically also the endothelium stained for Lep and LepR. ISH showed similar signal distribution in the Ut and Ut/Pl.

Conclusions: Lep and LepR are differentially expressed in the canine uterus and placenta during pregnancy, and their presence in various cell types indicates paracrine/autocrine roles. The Lep signaling system may be one of the pathways involved in feto-maternal cross-talk, implantation and maintenance of pregnancy, and may have a regulatory role around parturition.

No MeSH data available.


Related in: MedlinePlus