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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

Immunohistochemical detection of leptin and leptin receptor in the utero-placental compartments during pregnancy. Immunohistochemical localization of leptin (Lep; A, C, E) and leptin receptor (LepR; B, D, F) in the utero-placental compartments (Ut/Pl) during pregnancy. (A) Lep signals are strong in fetal trophoblast cells (open arrowheads) of the placental labyrinth at mid-gestation, while maternal decidual cells (solid arrowheads) stain more weakly and blood vessel endothelial cells (thin arrows) show sporadic signals. (B) LepR positive trophoblasts (open arrowheads) are present in the placental labyrinth at mid-gestation. LepR immunoreactivity is less intense in decidual cells (solid arrowheads) and in blood vessel endothelium (thin arrows). (C) Strong Lep immunoreactivity is evident in fetal trophoblast cells (open arrowheads) of the placental labyrinth at prepartum luteolysis with weaker signals in decidual cells (solid arrowheads) and occasional staining in the endothelium (thin arrows). Intense signals are detected in trophoblasts at the base of the labyrinth invading large maternal vessels (inset). (D) LepR positive trophoblast cells (open arrowheads) are shown in the placental labyrinth at prepartum luteolysis with less intense staining in maternal decidual cells (solid arrowheads) and blood vessel endothelium (thin arrows). The inset shows positive reaction in fetal trophoblast cells invading large maternal vessels at the base of the labyrinth. (E) Lep staining is present in the epithelial cells of the glandular chambers (solid arrows) and sporadic signals are also visible in the stroma (solid arrowheads). Positive staining in the myometrium is shown in the inset. (F) In the glandular chambers, epithelial cells stain positive for LepR (solid arrows) and stromal signals (solid arrowheads) are also present. Positive immunoreactivity in the myometrium is presented in the inset. MV: maternal vessel, MY: myometrium.
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Fig5: Immunohistochemical detection of leptin and leptin receptor in the utero-placental compartments during pregnancy. Immunohistochemical localization of leptin (Lep; A, C, E) and leptin receptor (LepR; B, D, F) in the utero-placental compartments (Ut/Pl) during pregnancy. (A) Lep signals are strong in fetal trophoblast cells (open arrowheads) of the placental labyrinth at mid-gestation, while maternal decidual cells (solid arrowheads) stain more weakly and blood vessel endothelial cells (thin arrows) show sporadic signals. (B) LepR positive trophoblasts (open arrowheads) are present in the placental labyrinth at mid-gestation. LepR immunoreactivity is less intense in decidual cells (solid arrowheads) and in blood vessel endothelium (thin arrows). (C) Strong Lep immunoreactivity is evident in fetal trophoblast cells (open arrowheads) of the placental labyrinth at prepartum luteolysis with weaker signals in decidual cells (solid arrowheads) and occasional staining in the endothelium (thin arrows). Intense signals are detected in trophoblasts at the base of the labyrinth invading large maternal vessels (inset). (D) LepR positive trophoblast cells (open arrowheads) are shown in the placental labyrinth at prepartum luteolysis with less intense staining in maternal decidual cells (solid arrowheads) and blood vessel endothelium (thin arrows). The inset shows positive reaction in fetal trophoblast cells invading large maternal vessels at the base of the labyrinth. (E) Lep staining is present in the epithelial cells of the glandular chambers (solid arrows) and sporadic signals are also visible in the stroma (solid arrowheads). Positive staining in the myometrium is shown in the inset. (F) In the glandular chambers, epithelial cells stain positive for LepR (solid arrows) and stromal signals (solid arrowheads) are also present. Positive immunoreactivity in the myometrium is presented in the inset. MV: maternal vessel, MY: myometrium.

Mentions: In the Ut/Pl, fetal trophoblasts of the placental labyrinth stained positively for Lep, and maternal decidual cells had weaker signals at all pregnancy stages (Figure 5A,C). Invading trophoblast cells surrounding large maternal vessels at the base of the placental labyrinth showed intense immunoreactivity (Figure 5C inset). Epithelial cells of the glandular chambers stained weakly with signals present also in the stroma (Figure 5E).Figure 5


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)

Immunohistochemical detection of leptin and leptin receptor in the utero-placental compartments during pregnancy. Immunohistochemical localization of leptin (Lep; A, C, E) and leptin receptor (LepR; B, D, F) in the utero-placental compartments (Ut/Pl) during pregnancy. (A) Lep signals are strong in fetal trophoblast cells (open arrowheads) of the placental labyrinth at mid-gestation, while maternal decidual cells (solid arrowheads) stain more weakly and blood vessel endothelial cells (thin arrows) show sporadic signals. (B) LepR positive trophoblasts (open arrowheads) are present in the placental labyrinth at mid-gestation. LepR immunoreactivity is less intense in decidual cells (solid arrowheads) and in blood vessel endothelium (thin arrows). (C) Strong Lep immunoreactivity is evident in fetal trophoblast cells (open arrowheads) of the placental labyrinth at prepartum luteolysis with weaker signals in decidual cells (solid arrowheads) and occasional staining in the endothelium (thin arrows). Intense signals are detected in trophoblasts at the base of the labyrinth invading large maternal vessels (inset). (D) LepR positive trophoblast cells (open arrowheads) are shown in the placental labyrinth at prepartum luteolysis with less intense staining in maternal decidual cells (solid arrowheads) and blood vessel endothelium (thin arrows). The inset shows positive reaction in fetal trophoblast cells invading large maternal vessels at the base of the labyrinth. (E) Lep staining is present in the epithelial cells of the glandular chambers (solid arrows) and sporadic signals are also visible in the stroma (solid arrowheads). Positive staining in the myometrium is shown in the inset. (F) In the glandular chambers, epithelial cells stain positive for LepR (solid arrows) and stromal signals (solid arrowheads) are also present. Positive immunoreactivity in the myometrium is presented in the inset. MV: maternal vessel, MY: myometrium.
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Related In: Results  -  Collection

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Fig5: Immunohistochemical detection of leptin and leptin receptor in the utero-placental compartments during pregnancy. Immunohistochemical localization of leptin (Lep; A, C, E) and leptin receptor (LepR; B, D, F) in the utero-placental compartments (Ut/Pl) during pregnancy. (A) Lep signals are strong in fetal trophoblast cells (open arrowheads) of the placental labyrinth at mid-gestation, while maternal decidual cells (solid arrowheads) stain more weakly and blood vessel endothelial cells (thin arrows) show sporadic signals. (B) LepR positive trophoblasts (open arrowheads) are present in the placental labyrinth at mid-gestation. LepR immunoreactivity is less intense in decidual cells (solid arrowheads) and in blood vessel endothelium (thin arrows). (C) Strong Lep immunoreactivity is evident in fetal trophoblast cells (open arrowheads) of the placental labyrinth at prepartum luteolysis with weaker signals in decidual cells (solid arrowheads) and occasional staining in the endothelium (thin arrows). Intense signals are detected in trophoblasts at the base of the labyrinth invading large maternal vessels (inset). (D) LepR positive trophoblast cells (open arrowheads) are shown in the placental labyrinth at prepartum luteolysis with less intense staining in maternal decidual cells (solid arrowheads) and blood vessel endothelium (thin arrows). The inset shows positive reaction in fetal trophoblast cells invading large maternal vessels at the base of the labyrinth. (E) Lep staining is present in the epithelial cells of the glandular chambers (solid arrows) and sporadic signals are also visible in the stroma (solid arrowheads). Positive staining in the myometrium is shown in the inset. (F) In the glandular chambers, epithelial cells stain positive for LepR (solid arrows) and stromal signals (solid arrowheads) are also present. Positive immunoreactivity in the myometrium is presented in the inset. MV: maternal vessel, MY: myometrium.
Mentions: In the Ut/Pl, fetal trophoblasts of the placental labyrinth stained positively for Lep, and maternal decidual cells had weaker signals at all pregnancy stages (Figure 5A,C). Invading trophoblast cells surrounding large maternal vessels at the base of the placental labyrinth showed intense immunoreactivity (Figure 5C inset). Epithelial cells of the glandular chambers stained weakly with signals present also in the stroma (Figure 5E).Figure 5

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