PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Embryonic Development”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,297 records · Page 72Linked to original sources
PubMed2007

Changes in regulation of sodium/calcium exchanger of avian ventricular heart cells during embryonic development.

It has been suggested that the sodium/calcium exchanger NCX1 may have a more important physiological role in embryonic and neonatal hearts than in adult hearts. However, in chick heart sarcolemmal vesicles, sodium-dependent calcium transport is reported to be small and, moreover, to be 3-12 times smaller in hearts at embryonic day (ED) 4-5 than at ED18, the opposite of what would be expected of a transporter that is more important in early development. To better assess the role of NCX1 in calcium regulation in the chick embryonic heart, we measured the activity of NCX1 in chick embryonic hearts as extracellular calcium-activated exchanger current (I(NCX)) under controlled ionic conditions. With intracellular calcium concentration ([Ca(2+)](i)) = 47 nM, I(NCX) density increased from 1.34 +/- 0.28 pA/pF at ED2 to 3.22 +/- 0.55 pA/pF at ED11 (P = 0.006); however, with [Ca(2+)](i) = 481 nM, the increase was small and statistically insignificant, from 4.54 +/- 0.77 to 5.88 +/- 0.73 pA/pF (P = 0.20, membrane potential = 0 mV, extracellular calcium concentration = 2 mM). Plots of I(NCX) density against [Ca(2+)](i) were well fitted by the Michaelis-Menton equation and extrapolated to identical maximal currents for ED2 and ED11 cells (extracellular calcium concentration = 1, 2, or 4 mM). Thus the increase in I(NCX) at low [Ca(2+)](i) appeared to reflect a developmental change in allosteric regulation of the exchanger by intracellular calcium rather than an increase in the membrane density of NCX1. Supporting this conclusion, RT-PCR demonstrated little change in the amount of mRNA encoding NCX1 expression from ED2 through ED18.

Allosteric Regulation↗
PubMed1997

Png-1, a nervous system-specific zinc finger gene, identifies regions containing postmitotic neurons during mammalian embryonic development.

To identify genes associated with early postmitotic cortical neurons, gene fragments were examined for expression in postmitotic, but not proliferative, zones of the embryonic murine cortex. Through this approach, a novel member of the zinc finger gene family, containing 6 C2HC fingers, was isolated and named postmitotic neural gene-1, or png-1. Embryonic png-1 expression was: 1) nervous system-specific; 2) restricted to zones containing postmitotic neurons; and 3) detected in all developing neural structures examined. In the cortex, png-1 expression was first observed on embryonic day 11, correlating temporally and spatially with the known generation of the first cortical neurons. Gradients of png-1 expression throughout the embryonic central nervous system further correlated temporally and spatially with known gradients of neuron production. With development, expression remained restricted to postmitotic zones, including those containing newly-postmitotic neurons. Png-1 was also detected within two days of neural retinoic acid induction in P19 cells, and expression increased with further neuronal differentiation. These data implicate png-1 as one of the earliest molecular markers for postmitotic neuronal regions and suggest a function as a panneural transcription factor associated with neuronal differentiation.

Amino Acid Sequence↗
PubMed1993

The expression of GAP-43 mRNA in developing embryonic striatal tissue grafts.

We have studied by quantitative in situ hybridization histochemistry the mRNA expression of the growth associated phosphoprotein (GAP-43) in grafts of foetal striatal neurones implanted into the ibotenic acid lesioned adult rat neostriatum. Animals were studied at 7, 15, 30 and 90 days after implantation. Using a 35S-labelled specific oligonucleotide probe we observed the highest levels of GAP-43 mRNA in 15-day-old grafts; levels were significantly reduced at 30 days and in 3-month-old grafts GAP-43 mRNA expression was not significantly different from the very low levels in the normal rat striatum. The data indicate that GAP-43 mRNA is highly expressed in developing but not mature neurones and suggest that embryonic striatal grafts may develop a relatively adult phenotype within the host brain by about 4 weeks; by which time most of the synaptic connections are established.

Animals↗
PubMed2000

Role of HIF-1 as a transcription factor involved in embryonic development, cancer progression and apoptosis (review).

Hypoxia-inducible factor-1 (HIF-1) is a transcription factor first identified as being activated by hypoxia but also in normoxic conditions by insulin and IGF-2. It is able to induce the expression of glycolytic genes and hence the ATP production, it also regulates the expression of the angiogenic factor VEGF and stimulates erythropoiesis via EPO production. HIF-1 is a protein necessary for the normal embryonic and cardiovascular system development, but seems to be also involved in cancer progression and apoptosis. Thus, it appears that HIF-1 plays a central role in normal cellular functions and in tissue metabolism but it is also involved in pathological evolutions raising its interest as a therapeutic target. In this review, we summarize the dual role of HIF-1 as a major component of the embryo development, as well as an element of tumor progression and of anoxia-induced apoptosis.

Animals↗
PubMed2005

Differential teratogenic effect of alcohol on embryonic development between C57BL/6 and DBA/2 mice: a new view.

BACKGROUND: Alcohol exposure during the fetal stage generates variable severity in different organs, as seen in fetal alcohol syndrome and fetal alcohol effect. Whether genetic factors or conditions of alcohol exposure influence the susceptibility to alcohol-related developmental impairment remains a question. METHODS: To investigate the contribution of genotype to the susceptibility to alcohol-induced toxicity during development beyond confounding maternal factors and variables of alcohol exposures, the authors tested the effect of alcohol exposure under definitive concentration using a whole embryonic culture of two inbred strains previously known to be vulnerable (C57BL/6 [C6]) or resistant (DBA/2 [D2]) to alcohol. On gestational day 8, embryos from each group bearing three to six somites were collected and then cultured for 44 hr in a medium added with 400 mg/dl of ethanol. The viability and morphological malformations, as well as developmental staging of the embryos, were all scored at the end of the culture. RESULTS: The authors found, in contrast to previous reports, that alcohol treatment retarded embryonic growth and induced abnormalities, including the neural tube opening and the hypoplasia of the optic vesicle in both strains. However, alcohol specifically compromised the heart and caudal neural tube in C6, whereas it specifically decreased the number of somites and the development of branchial bars among others in D2. CONCLUSIONS: These results demonstrated that both strains of embryos are vulnerable to the same amount and pattern of alcohol exposures at the same developmental stage, but each with unique vulnerability in specific organs, with alcohol having greater teratogenic effects in D2 than in C6. These differential vulnerabilities are results of greater genetic influence, rather than the maternal influence or conditions of alcohol.

Abnormalities, Drug-Induced↗
PubMed2005

The forkhead box m1 transcription factor is essential for embryonic development of pulmonary vasculature.

Transgenic and gene knock-out studies demonstrated that the mouse Forkhead Box m1 (Foxm1 or Foxm1b) transcription factor (previously called HFH-11B, Trident, Win, or MPP2) is essential for hepatocyte entry into mitosis during liver development, regeneration, and liver cancer. Targeted deletion of Foxm1 gene in mice produces an embryonic lethal phenotype due to severe abnormalities in the development of liver and heart. In this study, we show for the first time that Foxm1(-/-) lungs exhibit severe hypertrophy of arteriolar smooth muscle cells and defects in the formation of peripheral pulmonary capillaries as evidenced by significant reduction in platelet endothelial cell adhesion molecule 1 staining of the distal lung. Consistent with these findings, significant reduction in proliferation of the embryonic Foxm1(-/-) lung mesenchyme was found, yet proliferation levels were normal in the Foxm1-deficient epithelial cells. Severe abnormalities of the lung vasculature in Foxm1(-/-) embryos were associated with diminished expression of the transforming growth factor beta receptor II, a disintegrin and metalloprotease domain 17 (ADAM-17), vascular endothelial growth factor receptors, Polo-like kinase 1, Aurora B kinase, laminin alpha4 (Lama4), and the Forkhead Box f1 transcription factor. Cotransfection studies demonstrated that Foxm1 stimulates transcription of the Lama4 promoter, and this stimulation requires the Foxm1 binding sites located between -1174 and -1145 bp of the mouse Lama4 promoter. In summary, development of mouse lungs depends on the Foxm1 transcription factor, which regulates expression of genes essential for mesenchyme proliferation, extracellular matrix remodeling, and vasculogenesis.

ADAM Proteins↗
PubMed1989

Transcriptional pattern of 21-hydroxylase gene (P-450C21) during embryonic development, before, and after birth in mice as determined by in situ hybridization.

21-Hydroxylase is a member of the P-450 superfamily of genes involved in the biosynthesis of cortisol and aldosterone in the adrenal cortex. Congenital adrenal hyperplasia, a well-characterized disease, originates from a lack of this enzyme. We present in this report an in situ hybridization study aimed at detecting 21-hydroxylase activity during murine development, from mid gestation to adulthood. Our results demonstrate that even during the embryonic period the adrenal cortex is the only major site of transcription of this enzyme, which is detectable beginning at embryonic day 14. In addition, a peculiar topographical pattern of transcriptional activity, characteristic of the stage of differentiation of the gland, could be drawn. Using a computer-assisted method, we were able to quantitate the relative transcription level at each stage of development. A steady increase in the level of transcription was demonstrated throughout embryonic life to birth, with a drop during the prepubertal period and a final rise at adult age. The possible physiological significance of our findings is discussed.

Adrenal Cortex↗
PubMed1997

Selective expression of dopamine D3 receptor mRNA in proliferative zones during embryonic development of the rat brain.

We studied by in situ hybridization histochemistry the expression of D3 receptor (D3R) mRNA at various stages of rat brain development. The first expression of D3R mRNA was detected at embryonic day 14 (E14) in the striatal and rhinencephalic neuroepithelia and throughout the tectal neuroepithelium. From E16 to E19 D3R mRNA expression extended along a rostrocaudal axis to additional proliferative ventricular zones of the basal forebrain, including the neuroepithelia of the olfactory bulb, nucleus accumbens, septum, and amygdala, whereas D1 and D2 receptor (D1R and D2R) mRNAs were expressed predominantly by migrating neuroblasts and/or differentiating striatal neurons. Only a few neuroblasts, migrating in the lateral cortical stream or developing as cerebellar Purkinje cells, expressed D3R mRNA from E18. At birth D3R expression mRNA appeared in differentiating neuronal fields of the nucleus accumbens and medial mamillary body primordia and on P5 reached a distribution similar to that found in adult. In addition, a transient upregulation was detected on P5 in the medial mamillary bodies, parietofrontal cortex, and olfactory tubercle. In the adult brain D3R gene expression continued in the striatal proliferative subventricular zone. The late expression D3R mRNA in neurons, after achievement of dopamine innervation, supports the existence of a regulating factor released from dopamine neurons, as suggested by denervation studies in the adult. The sustained and abundant D3R gene expression, predominantly in germinative neuroepithelial zones actively involved in neurogenesis of most basal forebrain structures, supports the hypothesis of a neurogenetic but minor morphogenetic modulatory role for the D3R during CNS development.

Animals↗
PubMed1999

Mice lacking the folic acid-binding protein Folbp1 are defective in early embryonic development.

Periconceptional folic acid supplementation reduces the occurrence of several human congenital malformations, including craniofacial, heart and neural tube defects. Although the underlying mechanism is unknown, there may be a maternal-to-fetal folate-transport defect or an inherent fetal biochemical disorder that is neutralized by supplementation. Previous experiments have identified a folate-binding protein (Folbp1) that functions as a membrane receptor to mediate the high-affinity internalization and delivery of folate to the cytoplasm of the cell. In vitro, this receptor facilitates the accumulation of cellular folate a thousand-fold relative to the media, suggesting that it may be essential in cytoplasmic folate delivery in vivo. The importance of an adequate intracellular folate pool for normal embryogenesis has long been recognized in humans and experimental animals. To determine whether Folbp1 is involved in maternal-to-fetal folate transport, we inactivated Folbp1 in mice. We also produced mice lacking Folbp2, another member of the folate receptor family that is GPI anchored but binds folate poorly. Folbp2-/- embryos developed normally, but Folbp1-/- embryos had severe morphogenetic abnormalities and died in utero by embryonic day (E) 10. Supplementing pregnant Folbp1+/- dams with folinic acid reversed this phenotype in nullizygous pups. Our results suggest that Folbp1 has a critical role in folate homeostasis during development, and that functional defects in the human homologue (FOLR1) of Folbp1 may contribute to similar defects in humans.

Animals↗