Dataset Information

Bone marrow-derived cells or C-X-C motif chemokine 12 (CXCL12) treatment improve thin endometrium in a mouse model.

ABSTRACT: Successful implantation and pregnancy is dependent on sufficient endometrial growth during each reproductive cycle. Here, we report the therapeutic effect of either bone marrow-derived cells (BMDCs) or the stem cell chemo-attractant C-X-C motif chemokine 12 (CXCL12) on endometrial receptivity in a murine ethanol induced thin endometrium model. Endometrial epithelial area was significantly increased in mice treated with BMDCs, CXCL12, or by co-treatment with both compared with PBS-treated controls. Ki-67 and CD31 immunoreactivity was significantly higher in mice treated with either BMDCs, CXCL12, or both. The mRNA expression levels of endometrial receptivity markers leukemia inhibitory factor, interleukin-1?, and integrin beta-3 were increased in mice treated with either BMDCs, CXCL12, or both. The mRNA levels of matrix metalloproteinase-2 and -9 were significantly decreased by BMDCs but not by CXCL12. Pregnancy rates and litter size were increased after either treatment. Both BMDCs and CXCL12 displayed a comparable efficacy on endometrial regeneration in mice with thin endometrium. Our findings indicate the potential therapeutic effects of BMDCs and CXCL12 on infertility related to thin endometrium. Bone marrow-derived cells and CXCL12 displayed a comparable efficacy on endometrial regeneration in mice with thin endometrium.

SUBMITTER: Yi KW

PROVIDER: S-EPMC6335209 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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Bone marrow-derived cells or C-X-C motif chemokine 12 (CXCL12) treatment improve thin endometrium in a mouse model.

Yi Kyong Wook KW Mamillapalli Ramanaiah R Sahin Cagdas C Song Jaeyen J Tal Reshef R Taylor Hugh S HS

Biology of reproduction 20190101 1

Successful implantation and pregnancy is dependent on sufficient endometrial growth during each reproductive cycle. Here, we report the therapeutic effect of either bone marrow-derived cells (BMDCs) or the stem cell chemo-attractant C-X-C motif chemokine 12 (CXCL12) on endometrial receptivity in a murine ethanol induced thin endometrium model. Endometrial epithelial area was significantly increased in mice treated with BMDCs, CXCL12, or by co-treatment with both compared with PBS-treated control ...[more]

PMID: 30084961

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Project description:The placenta, a unique organ that only develops during pregnancy, is essential for nutrient, oxygen, and waste exchange between offspring and mother. Yet, despite its importance, the placenta remains one of the least understood organs and knowledge of early placental formation is particularly limited. Abnormalities in placental development result in placental dysfunction or insufficiency whereby normal placental physiology is impaired. Placental dysfunction is a frequent source of pregnancy loss in livestock, inflicting serious economic impact to producers. Though the underlying causes of placental dysfunction are not well-characterized, initiation of disease is thought to occur during establishment of functional fetal and placental circulation. A comprehensive understanding of the mechanisms controlling placental growth and vascularization is necessary to improve reproductive success in livestock. We propose chemokine C-X-C motif ligand 12 (CXCL12) signaling through its receptor CXCR4 functions as a chief coordinator of vascularization through direct actions on fetal trophoblast and maternal endometrial and immune cells. To investigate CXCL12-CXCR4 signaling on uteroplacental vascular remodeling at the fetal-maternal interface, we utilized a CXCR4 antagonist (AMD3100). On day 12 post-breeding in sheep, osmotic pumps were surgically installed and delivered either AMD3100 or saline into the uterine lumen ipsilateral to the corpus luteum for 14 days. On day 35 of ovine pregnancy, fetal/placental and endometrial tissues were collected, snap-frozen in liquid nitrogen, and uterine horn cross sections were preserved for immunofluorescent analysis. Suppressing CXCL12-CXCR4 at the fetal-maternal interface during initial placental vascularization resulted in diminished abundance of select angiogenic factors in fetal and maternal placenta on day 35. Compared to control, less vascular endothelial growth factor (VEGF) and VEFG receptor 2 (KDR) were observed in endometrium when CXCL12-CXCR4 was diminished. Less VEGF was also evident in fetal placenta (cotyledons) in ewes receiving AMD3100 infusion compared to control. Suppressing CXCL12-CXCR4 at the fetal-maternal interface also resulted in greater autophagy induction in fetal and maternal placenta compared to control, suggestive of CXCL12-CXCR4 impacting cell survival. CXCL12-CXCR4 signaling may govern placental homeostasis by serving as a critical upstream mediator of vascularization and cell viability, thereby ensuring appropriate placental development.

Dataset Information

Bone marrow-derived cells or C-X-C motif chemokine 12 (CXCL12) treatment improve thin endometrium in a mouse model.

Publications

Bone marrow-derived cells or C-X-C motif chemokine 12 (CXCL12) treatment improve thin endometrium in a mouse model.

Similar Datasets

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