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Transcriptional profiling of the ductus arteriosus: Comparison of rodent microarrays and human RNA sequencing.
Yarboro MT, Durbin MD, Herington JL, Shelton EL, Zhang T, Ebby CG, Stoller JZ, Clyman RI, Reese J
(2018) Semin Perinatol 42: 212-220
MeSH Terms: Animals, Animals, Newborn, Ductus Arteriosus, Embryo, Mammalian, Gene Expression Profiling, Gene Expression Regulation, Developmental, Genetic Association Studies, Humans, Microarray Analysis, Models, Animal, Rodentia, Sequence Analysis, RNA, Species Specificity, Vascular Patency
Show Abstract · Added November 26, 2018
DA closure is crucial for the transition from fetal to neonatal life. This closure is supported by changes to the DA's signaling and structural properties that distinguish it from neighboring vessels. Examining transcriptional differences between these vessels is key to identifying genes or pathways responsible for DA closure. Several microarray studies have explored the DA transcriptome in animal models but varied experimental designs have led to conflicting results. Thorough transcriptomic analysis of the human DA has yet to be performed. A clear picture of the DA transcriptome is key to guiding future research endeavors, both to allow more targeted treatments in the clinical setting, and to understand the basic biology of DA function. In this review, we use a cross-species cross-platform analysis to consider all available published rodent microarray data and novel human RNAseq data in order to provide high priority candidate genes for consideration in future DA studies.
Copyright © 2018 Elsevier Inc. All rights reserved.
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14 MeSH Terms
Cooperative function of Pdx1 and Oc1 in multipotent pancreatic progenitors impacts postnatal islet maturation and adaptability.
Kropp PA, Dunn JC, Carboneau BA, Stoffers DA, Gannon M
(2018) Am J Physiol Endocrinol Metab 314: E308-E321
MeSH Terms: Adaptation, Physiological, Animals, Animals, Newborn, Cell Differentiation, Cells, Cultured, Diet, High-Fat, Gene Expression Regulation, Developmental, Glucose, Hepatocyte Nuclear Factor 6, Homeodomain Proteins, Insulin-Secreting Cells, Islets of Langerhans, Male, Mice, Mice, Transgenic, Multipotent Stem Cells, Organogenesis, Trans-Activators
Show Abstract · Added April 15, 2019
The transcription factors pancreatic and duodenal homeobox 1 (Pdx1) and onecut1 (Oc1) are coexpressed in multipotent pancreatic progenitors (MPCs), but their expression patterns diverge in hormone-expressing cells, with Oc1 expression being extinguished in the endocrine lineage and Pdx1 being maintained at high levels in β-cells. We previously demonstrated that cooperative function of these two factors in MPCs is necessary for proper specification and differentiation of pancreatic endocrine cells. In those studies, we observed a persistent decrease in expression of the β-cell maturity factor MafA. We therefore hypothesized that Pdx1 and Oc1 cooperativity in MPCs impacts postnatal β-cell maturation and function. Here our model of Pdx1-Oc1 double heterozygosity was used to investigate the impact of haploinsufficiency for both of these factors on postnatal β-cell maturation, function, and adaptability. Examining mice at postnatal day (P) 14, we observed alterations in pancreatic insulin content in both Pdx1 heterozygotes and double heterozygotes. Gene expression analysis at this age revealed significantly decreased expression of many genes important for glucose-stimulated insulin secretion (e.g., Glut2, Pcsk1/2, Abcc8) exclusively in double heterozygotes. Analysis of P14 islets revealed an increase in the number of mixed islets in double heterozygotes. We predicted that double-heterozygous β-cells would have an impaired ability to respond to stress. Indeed, we observed that β-cell proliferation fails to increase in double heterozygotes in response to either high-fat diet or placental lactogen. We thus report here the importance of cooperation between regulatory factors early in development for postnatal islet maturation and adaptability.
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Differential Expression of NF2 in Neuroepithelial Compartments Is Necessary for Mammalian Eye Development.
Moon KH, Kim HT, Lee D, Rao MB, Levine EM, Lim DS, Kim JW
(2018) Dev Cell 44: 13-28.e3
MeSH Terms: Adaptor Proteins, Signal Transducing, Animals, Cell Lineage, Cell Polarity, Cells, Cultured, Cilia, Gene Expression Regulation, Developmental, Humans, Hyperplasia, Mice, Mice, Knockout, Neural Stem Cells, Neurofibromin 2, Organogenesis, Phenotype, Phosphoproteins, Protein-Serine-Threonine Kinases, Retinal Pigment Epithelium, Transcription Factors
Show Abstract · Added February 14, 2018
The optic neuroepithelial continuum of vertebrate eye develops into three differentially growing compartments: the retina, the ciliary margin (CM), and the retinal pigment epithelium (RPE). Neurofibromin 2 (Nf2) is strongly expressed in slowly expanding RPE and CM compartments, and the loss of mouse Nf2 causes hyperplasia in these compartments, replicating the ocular abnormalities seen in human NF2 patients. The hyperplastic ocular phenotypes were largely suppressed by heterozygous deletion of Yap and Taz, key targets of the Nf2-Hippo signaling pathway. We also found that, in addition to feedback transcriptional regulation of Nf2 by Yap/Taz in the CM, activation of Nf2 expression by Mitf in the RPE and suppression by Sox2 in retinal progenitor cells are necessary for the differential growth of the corresponding cell populations. Together, our findings reveal that Nf2 is a key player that orchestrates the differential growth of optic neuroepithelial compartments during vertebrate eye development.
Copyright © 2017 Elsevier Inc. All rights reserved.
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19 MeSH Terms
Loss of mTORC2 signaling in oligodendrocyte precursor cells delays myelination.
Grier MD, West KL, Kelm ND, Fu C, Does MD, Parker B, McBrier E, Lagrange AH, Ess KC, Carson RP
(2017) PLoS One 12: e0188417
MeSH Terms: Animals, Cell Differentiation, Cell Proliferation, Central Nervous System, Gene Expression Regulation, Developmental, Mechanistic Target of Rapamycin Complex 1, Mechanistic Target of Rapamycin Complex 2, Mice, Mice, Knockout, Myelin Sheath, Oligodendrocyte Precursor Cells, Rapamycin-Insensitive Companion of mTOR Protein, Signal Transduction, White Matter
Show Abstract · Added March 14, 2018
Myelin abnormalities are increasingly being recognized as an important component of a number of neurologic developmental disorders. The integration of many signaling pathways and cell types are critical for correct myelinogenesis. The PI3-K and mechanistic target of rapamycin (mTOR) pathways have been found to play key roles. mTOR is found within two distinct complexes, mTORC1 and mTORC2. mTORC1 activity has been shown to play a major role during myelination, while the role of mTORC2 is not yet well understood. To determine the role of mTORC2 signaling in myelinogenesis, we generated a mouse lacking the critical mTORC2 component Rictor in oligodendrocyte precursors (OPCs). Targeted deletion of Rictor in these cells decreases and delays the expression of myelin related proteins and reduces the size of cerebral white matter tracts. This is developmentally manifest as a transient reduction in myelinated axon density and g-ratio. OPC cell number is reduced at birth without detectable change in proliferation with proportional reductions in mature oligodendrocyte number at P15. The total number of oligodendrocytes as well as extent of myelination, does improve over time. Adult conditional knock-out (CKO) animals do not demonstrate a behavioral phenotype likely due in part to preserved axonal conduction velocities. These data support and extend prior studies demonstrating an important but transient contribution of mTORC2 signaling to myelin development.
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RHOA GTPase Controls YAP-Mediated EREG Signaling in Small Intestinal Stem Cell Maintenance.
Liu M, Zhang Z, Sampson L, Zhou X, Nalapareddy K, Feng Y, Akunuru S, Melendez J, Davis AK, Bi F, Geiger H, Xin M, Zheng Y
(2017) Stem Cell Reports 9: 1961-1975
MeSH Terms: Adaptor Proteins, Signal Transducing, Animals, Cell Differentiation, Cell Proliferation, Epiregulin, Epithelium, Gene Expression Regulation, Developmental, Intestine, Small, Mice, Mice, Knockout, Morphogenesis, Phosphoproteins, Stem Cells, Wnt Signaling Pathway, beta Catenin, rho GTP-Binding Proteins
Show Abstract · Added February 7, 2018
RHOA, a founding member of the Rho GTPase family, is critical for actomyosin dynamics, polarity, and morphogenesis in response to developmental cues, mechanical stress, and inflammation. In murine small intestinal epithelium, inducible RHOA deletion causes a loss of epithelial polarity, with disrupted villi and crypt organization. In the intestinal crypts, RHOA deficiency results in reduced cell proliferation, increased apoptosis, and a loss of intestinal stem cells (ISCs) that mimic effects of radiation damage. Mechanistically, RHOA loss reduces YAP signaling of the Hippo pathway and affects YAP effector epiregulin (EREG) expression in the crypts. Expression of an active YAP (S112A) mutant rescues ISC marker expression, ISC regeneration, and ISC-associated Wnt signaling, but not defective epithelial polarity, in RhoA knockout mice, implicating YAP in RHOA-regulated ISC function. EREG treatment or active β-catenin Catnb mutant expression rescues the RhoA KO ISC phenotypes. Thus, RHOA controls YAP-EREG signaling to regulate intestinal homeostasis and ISC regeneration.
Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.
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16 MeSH Terms
Talin regulates integrin β1-dependent and -independent cell functions in ureteric bud development.
Mathew S, Palamuttam RJ, Mernaugh G, Ramalingam H, Lu Z, Zhang MZ, Ishibe S, Critchley DR, Fässler R, Pozzi A, Sanders CR, Carroll TJ, Zent R
(2017) Development 144: 4148-4158
MeSH Terms: Adherens Junctions, Amino Acid Motifs, Animals, Binding Sites, Cell Adhesion, Cell Membrane, Cell Polarity, Gene Expression Regulation, Developmental, Integrin beta1, Kidney Tubules, Collecting, Mice, Inbred C57BL, Morphogenesis, Mutation, Talin, Tight Junction Proteins, Ureter
Show Abstract · Added December 7, 2017
Kidney collecting system development requires integrin-dependent cell-extracellular matrix interactions. Integrins are heterodimeric transmembrane receptors consisting of α and β subunits; crucial integrins in the kidney collecting system express the β1 subunit. The β1 cytoplasmic tail has two NPxY motifs that mediate functions by binding to cytoplasmic signaling and scaffolding molecules. Talins, scaffolding proteins that bind to the membrane proximal NPxY motif, are proposed to activate integrins and to link them to the actin cytoskeleton. We have defined the role of talin binding to the β1 proximal NPxY motif in the developing kidney collecting system in mice that selectively express a Y-to-A mutation in this motif. The mice developed a hypoplastic dysplastic collecting system. Collecting duct cells expressing this mutation had moderate abnormalities in cell adhesion, migration, proliferation and growth factor-dependent signaling. In contrast, mice lacking talins in the developing ureteric bud developed kidney agenesis and collecting duct cells had severe cytoskeletal, adhesion and polarity defects. Thus, talins are essential for kidney collecting duct development through mechanisms that extend beyond those requiring binding to the β1 integrin subunit NPxY motif.
© 2017. Published by The Company of Biologists Ltd.
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16 MeSH Terms
What is a placental mammal anyway?
Abbot P, Capra JA
(2017) Elife 6:
MeSH Terms: Animals, Eutheria, Evolution, Molecular, Female, Gene Expression Regulation, Developmental, Humans, Lactation, Mammals, Mammary Glands, Human, Marsupialia, Placentation, Pregnancy
Show Abstract · Added March 14, 2018
Many developmental functions in marsupials and eutherian mammals are accomplished by different tissues, but similar genes.
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miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development.
Kara N, Wei C, Commanday AC, Patton JG
(2017) Dev Biol 429: 321-334
MeSH Terms: Animal Fins, Animals, Branchial Region, Cartilage, Cell Differentiation, Cell Proliferation, Cell Survival, Chondrogenesis, Embryo, Nonmammalian, Focal Adhesion Protein-Tyrosine Kinases, Gene Expression Regulation, Developmental, Gene Knockdown Techniques, MicroRNAs, Morphogenesis, Neural Crest, Zebrafish
Show Abstract · Added August 4, 2017
Cranial neural crest cells are a multipotent cell population that generate all the elements of the pharyngeal cartilage with differentiation into chondrocytes tightly regulated by temporal intracellular and extracellular cues. Here, we demonstrate a novel role for miR-27, a highly enriched microRNA in the pharyngeal arches, as a positive regulator of chondrogenesis. Knock down of miR-27 led to nearly complete loss of pharyngeal cartilage by attenuating proliferation and blocking differentiation of pre-chondrogenic cells. Focal adhesion kinase (FAK) is a key regulator in integrin-mediated extracellular matrix (ECM) adhesion and has been proposed to function as a negative regulator of chondrogenesis. We show that FAK is downregulated in the pharyngeal arches during chondrogenesis and is a direct target of miR-27. Suppressing the accumulation of FAK in miR-27 morphants partially rescued the severe pharyngeal cartilage defects observed upon knock down of miR-27. These data support a crucial role for miR-27 in promoting chondrogenic differentiation in the pharyngeal arches through regulation of FAK.
Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.
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16 MeSH Terms
Adipocyte Metabolic Pathways Regulated by Diet Control the Female Germline Stem Cell Lineage in .
Matsuoka S, Armstrong AR, Sampson LL, Laws KM, Drummond-Barbosa D
(2017) Genetics 206: 953-971
MeSH Terms: Adipocytes, Animals, Cell Lineage, Diet, Drosophila melanogaster, Fatty Acids, Female, Gene Expression Regulation, Developmental, Germ Cells, Hexokinase, Metabolic Networks and Pathways, Oogonial Stem Cells, Phosphatidylethanolamines, Proteomics, Vitellogenesis
Show Abstract · Added May 2, 2017
Nutrients affect adult stem cells through complex mechanisms involving multiple organs. Adipocytes are highly sensitive to diet and have key metabolic roles, and obesity increases the risk for many cancers. How diet-regulated adipocyte metabolic pathways influence normal stem cell lineages, however, remains unclear. has highly conserved adipocyte metabolism and a well-characterized female germline stem cell (GSC) lineage response to diet. Here, we conducted an isobaric tags for relative and absolute quantification (iTRAQ) proteomic analysis to identify diet-regulated adipocyte metabolic pathways that control the female GSC lineage. On a rich (relative to poor) diet, adipocyte Hexokinase-C and metabolic enzymes involved in pyruvate/acetyl-CoA production are upregulated, promoting a shift of glucose metabolism toward macromolecule biosynthesis. Adipocyte-specific knockdown shows that these enzymes support early GSC progeny survival. Further, enzymes catalyzing fatty acid oxidation and phosphatidylethanolamine synthesis in adipocytes promote GSC maintenance, whereas lipid and iron transport from adipocytes controls vitellogenesis and GSC number, respectively. These results show a functional relationship between specific metabolic pathways in adipocytes and distinct processes in the GSC lineage, suggesting the adipocyte metabolism-stem cell link as an important area of investigation in other stem cell systems.
Copyright © 2017 by the Genetics Society of America.
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15 MeSH Terms
The innate immune response in fetal lung mesenchymal cells targets VEGFR2 expression and activity.
Medal RM, Im AM, Yamamoto Y, Lakhdari O, Blackwell TS, Hoffman HM, Sahoo D, Prince LS
(2017) Am J Physiol Lung Cell Mol Physiol 312: L861-L872
MeSH Terms: Animals, Cell Communication, Cell Movement, Epithelial Cells, Fetus, Gene Expression Regulation, Developmental, Immunity, Innate, Lipopolysaccharides, Lung, Mesoderm, Mice, Inbred C57BL, Signal Transduction, Vascular Endothelial Growth Factor Receptor-2
Show Abstract · Added March 29, 2017
In preterm infants, soluble inflammatory mediators target lung mesenchymal cells, disrupting airway and alveolar morphogenesis. However, how mesenchymal cells respond directly to microbial stimuli remains poorly characterized. Our objective was to measure the genome-wide innate immune response in fetal lung mesenchymal cells exposed to the bacterial endotoxin lipopolysaccharide (LPS). With the use of Affymetrix MoGene 1.0st arrays, we showed that LPS induced expression of unique innate immune transcripts heavily weighted toward CC and CXC family chemokines. The transcriptional response was different between cells from E11, E15, and E18 mouse lungs. In all cells tested, LPS inhibited expression of a small core group of genes including the VEGF receptor Although best characterized in vascular endothelial populations, we demonstrated here that fetal mouse lung mesenchymal cells express and respond to VEGF-A stimulation. In mesenchymal cells, VEGF-A increased cell migration, activated the ERK/AKT pathway, and promoted FOXO3A nuclear exclusion. With the use of an experimental coculture model of epithelial-mesenchymal interactions, we also showed that VEGFR2 inhibition prevented formation of three-dimensional structures. Both LPS and tyrosine kinase inhibition reduced three-dimensional structure formation. Our data suggest a novel mechanism for inflammation-mediated defects in lung development involving reduced VEGF signaling in lung mesenchyme.
Copyright © 2017 the American Physiological Society.
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13 MeSH Terms