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Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE247184 | GEO | 2024/09/13

REPOSITORIES: GEO

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Isl Identifies the Extraembryonic Mesodermal/Allantois Progenitors and is Required for Placenta Morphogenesis and Vasculature Formation.

Project description:The placenta links feto-maternal circulation for exchanges of nutrients, gases, and metabolic wastes between the fetus and mother, being essential for pregnancy process and maintenance. The allantois and mesodermal components of amnion, chorion, and yolk sac are derived from extraembryonic mesoderm (Ex-Mes), however, the mechanisms contributing to distinct components of the placenta and regulation the interactions between allantois and epithelium during chorioallantoic fusion and labyrinth formation remains unclear. Isl1 is expressed in progenitors of the Ex-Mes and allantois the Isl1 mut mouse line is analyzed to investigate contribution of Isl1+ Ex-Mes / allantoic progenitors to cells of the allantois and placenta. This study shows that Isl1 identifies the Ex-Mes progenitors for endothelial and vascular smooth muscle cells, and most of the mesenchymal cells of the placenta and umbilical cord. Deletion of Isl1 causes defects in allantois growth, chorioallantoic fusion, and placenta vessel morphogenesis. RNA-seq and CUT&Tag analyses revealed that Isl1 promotes allantoic endothelial, inhibits mesenchymal cell differentiation, and allantoic signals regulated by Isl1 mediating the inductive interactions between the allantois and chorion critical for chorionic epithelium differentiation, villous formation, and labyrinth angiogenesis. This study above reveals that Isl1 plays roles in regulating multiple genetic and epigenetic pathways of vascular morphogenesis, provides the insight into the mechanisms for placental formation, highlighting the necessity of Isl1 for placenta formation/pregnant maintenance.

| S-EPMC11348239 | biostudies-literature

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [CUT&Tag]

Project description:To uncover direct targets of ISL1 that could account for its role in allantois, we performed cut tag analysis on wild type allantoic cells using ISL1 antibody at E8.75. Our analyses uncovered 5509 significant binding peaks for ISL1, mainly located at intergenic or intronic regions.

2024-09-13 | GSE247183 | GEO

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [RNA-Seq]

Project description:The transcription factor Isl1 is expressed in the progenitors of the Ex-Mes and allantois, however its role in the placentation remains unclear. Our studies showed that deletion of Isl1 causes defects in allantois growth, chorioallantoic fusion and placenta vessel morphogenesis. RNA-seq analyses have revealed that Isl1 regulates the expression of genes important for Ex-Mes multipotency, differentiation and diversification. Isl1 promotes allantoic endothelial but inhibits mesenchymal cell differentiation. Isl1 plays an important role in regulating multiple genetic and epigenetic pathways of vascular morphogenesis. Allantoic signals regulated by Isl1 in turn mediate the inductive interactions between the allantois and chorion critical for chorionic epithelium differentiation, villous formation, and labyrinth angiogenesis. In conclusion, our study provides an integrated insight into the mechanisms underlying placental lineage differentiation, diversification, and vascular formation, highlighting the necessity of Isl1 for early placenta morphogenesis. Our study suggests the potential utility of Isl1 in regenerative medicine application using the stem cells derived from the placenta, umbilical cord and amnionic membrane.

2024-09-13 | GSE247182 | GEO

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation

Project description:Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation

| PRJNA1036585 | ENA

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [RNA-Seq]

Project description:Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [RNA-Seq]

| PRJNA1036588 | ENA

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [CUT&Tag]

Project description:Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [CUT&Tag]

| PRJNA1036587 | ENA

Cited2 is required for the proper formation of the hyaloid vasculature and for lens morphogenesis.

Project description:Cited2 is a transcriptional modulator with pivotal roles in different biological processes. Cited2-deficient mouse embryos manifested two major defects in the developing eye. An abnormal corneal-lenticular stalk was characteristic of Cited2(-/-) developing eyes, a feature reminiscent of Peters' anomaly, which can be rescued by increased Pax6 gene dosage in Cited2(-/-) embryonic eyes. In addition, the hyaloid vascular system showed hyaloid hypercellularity consisting of aberrant vasculature, which might be correlated with increased VEGF expression in the lens. Deletion of Hif1a (which encodes HIF-1alpha) in Cited2(-/-) lens specifically eliminated the excessive accumulation of cellular mass and aberrant vasculature in the developing vitreous without affecting the corneal-lenticular stalk phenotype. These in vivo data demonstrate for the first time dual functions for Cited2: one upstream of, or together with, Pax6 in lens morphogenesis; and another in the normal formation of the hyaloid vasculature through its negative modulation of HIF-1 signaling. Taken together, our study provides novel mechanistic revelation for lens morphogenesis and hyaloid vasculature formation and hence might offer new insights into the etiology of Peters' anomaly and ocular hypervascularity.

| S-EPMC2654719 | biostudies-literature

Hematopoietic progenitors are required for proper development of coronary vasculature.

Project description:During embryogenesis, hematopoietic cells appear in the myocardium prior to the initiation of coronary formation. However, their role is unknown.Here we investigate whether pre-existing hematopoietic cells are required for the formation of coronary vasculature.As a model of for hematopoietic cell deficient animals, we used Runx1 knockout embryos and Vav1-cre; R26-DTA embryos, latter of which genetically ablates 2/3 of CD45(+) hematopoietic cells. Both Runx1 knockout embryos and Vav1-cre; R26-DTA embryos revealed disorganized, hypoplastic microvasculature of coronary vessels on section and whole-mount stainings. Furthermore, coronary explant experiments showed that the mouse heart explants from Runx1 and Vav1-cre; R26-DTA embryos exhibited impaired coronary formation ex vivo. Interestingly, in both models it appears that epicardial to mesenchymal transition is adversely affected in the absence of hematopoietic progenitors.Hematopoietic cells are not merely passively transported via coronary vessel, but substantially involved in the induction of the coronary growth. Our findings suggest a novel mechanism of coronary growth.

| S-EPMC4558312 | biostudies-literature

Tbx16 and Msgn1 are required to establish directional cell migration of zebrafish mesodermal progenitors.

Project description:The epithelial to mesenchymal transition (EMT) is an essential process that occurs repeatedly during embryogenesis whereby stably adherent cells convert to an actively migrating state. While much is known about the factors and events that initiate the EMT, the steps that cells undergo to become directionally migratory are far less well understood. Zebrafish embryos lacking the transcription factors Tbx16/Spadetail and Mesogenin1 (Msgn1) are a valuable system for investigating the EMT. Mesodermal cells in these embryos are unable to perform the EMT necessary to leave the most posterior end of the body (the tailbud) and join the pre-somitic mesoderm, a process that is conserved in all vertebrates. It has previously been very difficult to study this EMT in vertebrates because of the multiple cell types in the tailbud and the morphogenetic changes the whole embryo undergoes. Here, we describe a novel tissue explant system for imaging the mesodermal cell EMT in vivo that allows us to investigate the requirements for cells to acquire migratory properties during the EMT with high spatio-temporal resolution. This method revealed that, despite the inability of tbx16;msgn1-deficient cells to leave the tailbud, actin-based protrusions form surprisingly normally in these cells and they become highly motile. However, tbx16;msgn1-deficient cells have specific cell-autonomous defects in the persistence and anterior direction of migration because the lamellipodia they form are not productive in driving anteriorward migration. Additionally, we show that mesoderm morphogenesis and differentiation are separable and that there is a migratory cue that directs mesodermal cell migration that is independent of Tbx16 and Msgn1. This work defines changes that cells undergo as they complete the EMT and provides new insight into the mechanisms required in vivo for cells to become mesenchymal.

| S-EPMC4639448 | biostudies-literature

USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta.

Project description:USP22, a component of the SAGA complex, is overexpressed in highly aggressive cancers, but the normal functions of this deubiquitinase are not well defined. We determined that loss of USP22 in mice results in embryonic lethality due to defects in extra-embryonic placental tissues and failure to establish proper vascular interactions with the maternal circulatory system. These phenotypes arise from abnormal gene expression patterns that reflect defective kinase signaling, including TGF? and several receptor tyrosine kinase pathways. USP22 deletion in endothelial cells and pericytes that are induced from embryonic stem cells also hinders these signaling cascades, with detrimental effects on cell survival and differentiation as well as on the ability to form vessels. Our findings provide new insights into the functions of USP22 during development that may offer clues to its role in disease states.

| S-EPMC6398448 | biostudies-literature

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