Dataset Information

Multipotent fetal-derived Cdx2 cells from placenta regenerate the heart

ABSTRACT: Placental Cdx2 cells can be isolated and utilized for cardiac regeneration in a mouse model of myocardial infarction with evidence of multipotentiality both in vitro and in vivo

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Placenta

SUBMITTER: Niveda Sundararaman

LAB HEAD: Dr. Jennifer Van Eyk

PROVIDER: PXD011783 | Pride | 2019-05-09

REPOSITORIES: Pride

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			Action	DRS
	KR_151210_Elite_cdx2gfp01_Urea_6uL.mzXML	Mzxml
	KR_151210_Elite_cdx2gfp01_Urea_6uL.pep.xml	Pepxml
	KR_151210_Elite_cdx2gfp01_Urea_6uL.raw	Raw
	KR_151210_Elite_cdx2gfp03_Urea_6uL.mzXML	Mzxml
	KR_151210_Elite_cdx2gfp03_Urea_6uL.pep.xml	Pepxml

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Multipotent fetal-derived Cdx2 cells from placenta regenerate the heart.

Vadakke-Madathil Sangeetha S LaRocca Gina G Raedschelders Koen K Yoon Jesse J Parker Sarah J SJ Tripodi Joseph J Najfeld Vesna V Van Eyk Jennifer E JE Chaudhry Hina W HW

Proceedings of the National Academy of Sciences of the United States of America 20190520 24

The extremely limited regenerative potential of adult mammalian hearts has prompted the need for novel cell-based therapies that can restore contractile function in heart disease. We have previously shown the regenerative potential of mixed fetal cells that were naturally found migrating to the injured maternal heart. Exploiting this intrinsic mechanism led to the current hypothesis that Caudal-type homeobox-2 (Cdx2) cells in placenta may represent a novel cell type for cardiac regeneration. Usi ...[more]

PMID: 31109997

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Project description:BackgroundFetal growth restriction (FGR) is associated with increased risks for complications before, during, and after birth, in addition to risk of disease through to adulthood. Although placental insufficiency, failure to supply the fetus with adequate nutrients, underlies most cases of FGR, its causes are diverse and not fully understood. One of the few diagnosable causes of placental insufficiency in ongoing pregnancies is the presence of large chromosomal imbalances such as trisomy confined to the placenta; however, the impact of smaller copy number variants (CNVs) has not yet been adequately addressed. In this study, we confirm the importance of placental aneuploidy, and assess the potential contribution of CNVs to fetal growth.MethodsWe used molecular-cytogenetic approaches to identify aneuploidy in placentas from 101 infants born small-for-gestational age (SGA), typically used as a surrogate for FGR, and from 173 non-SGA controls from uncomplicated pregnancies. We confirmed aneuploidies and assessed mosaicism by microsatellite genotyping. We then profiled CNVs using high-resolution microarrays in a subset of 53 SGA and 61 control euploid placentas, and compared the load, impact, gene enrichment and clinical relevance of CNVs between groups. Candidate CNVs were confirmed using quantitative PCR.ResultsAneuploidy was over tenfold more frequent in SGA-associated placentas compared to controls (11.9% vs. 1.1%; p = 0.0002, OR = 11.4, 95% CI 2.5-107.4), was confined to the placenta, and typically involved autosomes, whereas only sex chromosome abnormalities were observed in controls. We found no significant difference in CNV load or number of placental-expressed or imprinted genes in CNVs between SGA and controls, however, a rare and likely clinically-relevant germline CNV was identified in 5.7% of SGA cases. These CNVs involved candidate genes INHBB, HSD11B2, CTCF, and CSMD3.ConclusionsWe conclude that placental genomic imbalances at the cytogenetic and submicroscopic level may underlie up to ~ 18% of SGA cases in our population. This work contributes to the understanding of the underlying causes of placental insufficiency and FGR, which is important for counselling and prediction of long term outcomes for affected cases.