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Ontogeny of expression of transforming growth factor-beta and its receptors and their possible relationship with scarless healing in human fetal skin.

Fetal cutaneous wounds that occur in early gestation heal without scar formation. Although much work has been done to characterize the role of transforming growth factor-beta (TGF-beta) isoforms and their receptors in the wound healing process, their roles in scarless wound repair observed in early gestation and their functions in human fetal skin development, and structural and functional maintenance are still not well understood. In this study, we explore the expression and distribution characteristics of three TGF-beta isoforms and their receptors, TGF-betaRI (TBRI) and TGF-betaRII (TBRII), in fetal and postnatal skins to understand the relevance of these five proteins to skin development and elucidate the mechanism(s) underlying the phenotypic transition from scarless to scar-forming healing observed during fetal gestation. Fetal skin biopsies of human embryo were obtained from spontaneous abortions at different gestational ages from 13 to 32 weeks and postnatal skin specimens were collected from patients undergoing plastic surgery. Gene expression and positive immunohistochemical signals of TGF-beta(1), TGF-beta(2), TGF-beta(3), TBRI, and TBRII could all be detected in fetal and postnatal skins. In early gestation, gene expression of TGF-beta(1), TBRI, and TBRII was weaker and protein contents were less compared with postnatal skins (p < 0.05). In contrast, more TGF-beta(2) mRNA transcript was found in early gestation than in late gestation and in postnatal skins, whereas protein content of this growth factor increased during gestation. Lastly, mRNA transcript and protein contents of TGF-beta(3) were apparently higher in early gestation compared to postnatal skin (p < 0.05). In postnatal skin, granules containing the three TGF-beta isoforms were mainly distributed in the cytoplasm and extracellular matrix of epidermal cells, interfollicular keratinocytes, and some fibroblasts. TBRI and TBRII were chiefly located in the cellular membrane of epidermal keratinocytes and some fibroblasts. The endogenous three TGF-beta isoforms and their receptors may be involved in the development of embryonic skin and in the maintenance of cutaneous structure and function, and also in postnatal wound healing. The differential levels of TGF-beta isoforms may provide either a predominantly antiscarring or profibrotic signal upon wounding depending on the gestational period. Lower expression of their receptors in early gestational skins may be a reason for the reduced ability to perceive ligands, ultimately leading to scar-free healing.

Cicatrix↗
PubMed1982

Comparative studies of rat liver and sea urchin embryo nuclear matrices: partial fractionation and protein kinase activity distribution.

Rat liver and sea urchin embryo nuclear matrices were found to differ in composition and in the strength of the association of their structural elements. Apart from the qualitative differences in composition, the embryonic matrices retained greater amounts of nuclear proteins and DNA, and were less susceptible to ultrasonic treatment than those of rat liver. They were essentially resistant to mild sonication, by which the rat liver matrix structure was resolved into two distinct fractions, referred to by Berezney (1980) as matricin and ribonucleoprotein (RNP). Both sub-fractions exhibited a protein kinase activity; the phosphorylating capacity of the RNP-associated protein kinases was found to be higher than that of the matricin-bound enzyme. The preferred substrate was among the secondary matrix proteins. In sea urchin embryos, sonication introduced no change in the type and lesion of the matrix proteins phosphorylated by the associated enzyme.

Animals↗
PubMed2004

Determination of electrical properties of ES cell-derived cardiomyocytes using MEAs.

Pluripotent embryonic stem cells (ES cells) provide a novel tool to study cardiomyogenesis under in vitro conditions. This overview article focuses on the technical properties of extracellular recordings of ES cell-derived cardiomyocytes using Microelectrode Arrays (MEAs). It reviews recent experimental observations, in an effort to describe basic characteristics of field potentials (FPs) in the ES cell model of developing myocardium. ES cells kept in permanent culture are differentiated within aggregates ("embryoid bodies", EBs) in which among other cell types cardiomyocytes appear 3-4 days after plating. These form spontaneously beating clusters mostly consisting of expanded regions of cardiac cells connected with narrow tissue strands. To record the electrical activity of these contracting areas substrate-integrated MEAs consisting of 60 substrate-integrated electrodes can be used. We previously investigated the influence of Na+-, K+- and Ca2+ channel blockers on the electrical signal generation and propagation as well as on the shape of FPs. We also used ES cell-derived cardiac myocytes as a multicellular in vitro model for cardiac development. Long-term recordings with a MEA enabled the examination of electrophysiological properties during the ongoing differentiation process. During time in culture the beating aggregate of cardiac myocytes differentiating from ES cells increased in size (7-fold). This change was accompanied by an increase of the beating frequency from 1 to 5 Hz and a decrease of the FP duration. Furthermore a shortening of the FP upstroke velocity could be observed concomitant with a functional segregation of slow upstroke velocities in the area of the pacemaker. Our data indicate a functional differentiation and segregation of the cells into pacemaker and myocard-like regions. This in vitro development of a three-dimensional heart like structure closely follows the development known from mouse embryonic heart. The preparation thus forms an ideal model to monitor the development of electrical activity in embryonic cardiac myocytes for wild type and genetically modified ES cells, thereby taking into account the functional differentiation of the tissue. Our data suggest that EBs plated on MEAs provide a suitable tool for pre-screening of cardioactive substances.

Animals↗
PubMed1995

Tail bud determination in the vertebrate embryo.

BACKGROUND: Although as humans we lose our tails in the second month of embryonic development, a persistent tail is a prominent structural feature of most adult vertebrates. Indeed, the post-anal tail is part of the definition of a chordate. The internal organization of the developing tail--with neural tube, notochord and paired somites--is the same as that of the main body axis, so it can be expected that the mechanism of tail formation has a close relationship to that of the vertebrate body plan as a whole. Despite this, almost nothing is known about how tails arise. RESULTS: We present evidence to show that the tail bud of Xenopus laevis arises as the result of interactions between distinct zones of tissue at the posterior of the embryo at the neurula stage. These tissue interactions were demonstrated by manipulations of exogastrulae, which normally form no tail, and by transplantation experiments performed on the neural plate of stage 13 neurulae, whereby embryos with supernumary tails were produced. CONCLUSIONS: We propose a new model of tail bud determination, termed the NMC model, to explain the results we have obtained. In this model, the tail bud is initiated by an interaction between two territories in the neural plate and a posterior mesodermal territory.

Animals↗
PubMed2002

Cis elements of the villin gene control expression in restricted domains of the vertical (crypt) and horizontal (duodenum, cecum) axes of the intestine.

Villin, an actin bundling protein found in the apical brush border of absorptive tissues, is one of the first structural genes to be transcriptionally activated in the embryonic intestinal endoderm. In the adult, villin is broadly expressed in every cell of the intestinal epithelium on both the vertical axis (crypt to villus tip) and the horizontal axis (duodenum through colon) of the intestine. Here, we document that a 12.4-kilobase region of the mouse villin gene drives high level expression of two different reporter genes (LacZ and Cre recombinase) within the entire intestinal epithelium of transgenic mice. Deletion of a portion of this transgene results in reduction of beta-galactosidase activity in restricted domains of the small intestine (duodenum) and large intestine (cecum). In addition, expression is reduced in the crypt compartment throughout the intestine. Thus, the global expression pattern of villin in the intestine is apparently the consequence of an amalgam of distinct and individual domain-specific control processes. That is, expression of villin in the duodenum and cecum requires different regulatory sequences than the rest of the intestine, and the expression of villin in crypts is regulated by different circuitry than expression of villin on villus tips.

Animals↗
PubMed1990

Embryonal remnants in inguinal hernia sacs.

Inguinal herniorrhaphy is the most common general surgical procedure performed on the neonate or young pediatric patient. The vas deferens and epididymis are vulnerable to damage, including transection during inguinal exploration or hernia repair. Occasionally the surgical pathologist encounters glandular or tubular epithelial-lined structures in hernia sac tissue. Significant medicolegal implications arise when embryonal remnants are mistakenly identified as true vas deferens or epididymis. This study evaluates the incidence and morphology of these embryonal remnants in hernia sacs from patients of The Children's Hospital, Denver, CO. Embryonal remnants were found in 1.5% of 599 hernia sacs from 427 consecutively operated males aged 37 weeks gestation to 19 years. True vas deferens and epididymis were each identified once for an incidence of 0.33%. The remnants resemble either vas deferens or epididymis. The average remnant diameter is 0.17 mm, and did not change significantly with age. Remnants are surrounded by varying amounts of condensed mesenchyme, trichrome-negative for muscle. The testes and vasa differentia from 32 autopsy cases, ranging in age from 26 weeks gestation to 7 years of age, were used to evaluate normal development and morphology of the vas deferens, epididymis and embryonal remnants. The vas deferens is well developed by 26 weeks gestation. The surrounding smooth-muscle coat does not stain with trichrome until 32 weeks gestation. The vas deferens increases in diameter in a linear fashion during gestation, and continues to increase in diameter in the postnatal period. The vas deferens at 4 months of age is 1.2 to 1.4 mm in diameter; this is also the age of highest incidence of bilateral herniorrhaphies and presence of remnants.

Adolescent↗
PubMed2000

Activin betaC and betaE genes are not essential for mouse liver growth, differentiation, and regeneration.

The liver is an essential organ that produces several serum proteins, stores vital nutrients, and detoxifies many carcinogenic and xenobiotic compounds. Various growth factors positively regulate liver growth, but only a few negative regulators are known. Among the latter are the transforming growth factor beta (TGF-beta) superfamily members TGF-beta1 and activin A. To study the function of novel activin family members, we have cloned and generated mice deficient in the activin betaC and betaE genes. Expression analyses demonstrated that these novel genes are liver specific in adult mice. Here, we show by RNase protection that activin betaC transcripts are present in the liver beginning at embryonic day 11.5 (E11.5) whereas activin betaE expression is detected starting from E17.5. Gene targeting in embryonic stem cells was used to generate mice with null mutations in either the individual activin betaC and betaE genes or both genes. In contrast to the structurally related activin betaA and betaB subunits, which are necessary for embryonic development and pituitary follicle-stimulating hormone homeostasis, mice deficient in activin betaC and betaE were viable, survived to adulthood, and demonstrated no reproductive abnormalities. Although activin betaC and betaE mRNAs are abundantly expressed in the liver of wild-type mice, the single and double mutants did not show any defects in liver development and function. Furthermore, in the homozygous mutant mice, liver regeneration after >70% partial hepatectomy was comparable to that in wild-type mice. Our results suggest that activin betaC and betaE are not essential for either embryonic development or liver function.

Activins↗
PubMed2000

Crystal structure of the Xrcc4 DNA repair protein and implications for end joining.

XRCC4 is essential for carrying out non-homologous DNA end joining (NHEJ) in all eukaryotes and, in particular, V(D)J recombination in vertebrates. Xrcc4 protein forms a complex with DNA ligase IV that rejoins two DNA ends in the last step of V(D)J recombination and NHEJ to repair double strand breaks. XRCC4-defective cells are extremely sensitive to ionizing radiation, and disruption of the XRCC4 gene results in embryonic lethality in mice. Here we report the crystal structure of a functional fragment of Xrcc4 at 2.7 A resolution. Xrcc4 protein forms a strikingly elongated dumb-bell-like tetramer. Each of the N-terminal globular head domains consists of a beta-sandwich and a potentially DNA-binding helix- turn-helix motif. The C-terminal stalk comprising a single alpha-helix >120 A in length is partly incorporated into a four-helix bundle in the Xrcc4 tetramer and partly involved in interacting with ligase IV. The Xrcc4 structure suggests a possible mode of coupling ligase IV association with DNA binding for effective ligation of DNA ends.

Amino Acid Sequence↗
PubMed2003

A novel double-stranded RNA-binding protein, disco interacting protein 1 (DIP1), contributes to cell fate decisions during Drosophila development.

We report the identification of the Disco Interacting Protein 1 (DIP1) gene isolated in a yeast interaction trap screen using the zinc finger protein disconnected (disco) as a bait. DIP1 encodes a protein containing two double-stranded RNA binding domains (dsRBD). Consistent with the presence of dsRBD, DIP1 binds dsRNA or structured RNAs in Northwestern assays. DIP1 is found in nuclear subdomains resembling speckles known to accumulate transcription and splicing factors. In early embryos, nuclear localization of DIP1 protein coincides with the onset of zygotic gene expression. Later in development DIP1 expression is decreased in dividing cells in different tissues. Overexpression of DIP1 in the eye-antennal imaginal disc, early in embryonic and larval development, causes the formation of supernumerary structures in the head capsule. A role for DIP1 in epigenetic mechanisms that lead to the establishment and/or maintenance of cell fate specification is discussed.

Amino Acid Sequence↗
PubMed1994

The role of cell fusion in erythropoiesis--Part 2.

In a prior study, cell fusion was found to play an important part in erythropoiesis in both the chicken and frog. Erythropoiesis in both organisms could be traced back to groups of embryonic cells which first fused to form an aggregate structure consisting of multiple nuclei enclosed by a common cytoplasm. The cytoplasm of the fused aggregate underwent dissolution to give rise to a set of denuded nuclei which, by manufacturing a haemoglobinized cytoplasm, were transformed into erythroblasts. Following these findings, the question of cell fusion in erythropoiesis in the human was investigated, and the results are reported here. Leishman stained smears of marrow aspirate were used, and care taken to prevent the immature cells coming into contact with plasma. The reason for this was that plasma was found to alter the normal structure of the immature haemopoietic cells, particularly the megakaryocyte series. Free from plasma contact, the nucleus of the megakaryocyte was found to be not multilobulated, but composed of a compact set of small nuclei. The mode of development of the megakaryocyte and its fate could be deciphered in the smears. The megakaryocytes arose as a result of fusion of small basophilic embryonic-like cells. After the megakaryocyte had attained a certain size, fusion ceased and the cytoplasm of the megakaryocyte underwent dissolution and was shed in the form of platelets, thus denuding the nuclei. The latter, bared of cytoplasm, were transformed directly into erythroblasts. The fate of the denuded nuclei in this manner goes against the accepted view that the denuded nucleus is phagocytosed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Serotonin in the developing stomatogastric system of the lobster, Homarus americanus.

We studied the development of the serotonergic modulation of the stomatogastric nervous system of the lobster, Homarus americanus. Although the stomatogastric ganglion (STG) is present early in embryonic development, serotonin immunoreactivity is not visible in the STG until the second larval stage. However, incubation of the STG with exogenous serotonin showed that a serotonin transporter is present in embryonic and early larval stages. Serotonin uptake was blocked by paroxetine and 0% Na(+) saline. The presence of a serotonin transporter in the embryonic STG suggests that hormonally liberated serotonin could be taken up by the STG, and potentially released as a "borrowed transmitter". Consistent with a potential hormonal role, serotonin is found in the pericardial organs, a major neurosecretory structure, by midembryonic development. The rhythmic motor patterns produced by embryonic and larval STGs were decreased in frequency by serotonin. Lateral Pyloric (LP) neuron-evoked excitatory junctional potentials (EJPs) in the embryos and the first larval stage (LI) were larger, slower, and more variable than those in the adult. The amplitude of adult LP neuron-evoked EJPs was increased more than twofold in serotonin, but in embryos and LI preparations this effect was negligible. In embryos and LI preparations, serotonin increased the occurrence of muscle fiber action potentials and altered the EJP wave-form. These data demonstrate that serotonin receptors are present in the stomatogastric nervous system early in development, and suggest that the role of serotonin changes from modulation of muscle fiber excitability early in development to enhancement of neurally evoked EJPs in the adult.

Age Factors↗
PubMed1993

Ryanodine receptor expression in embryonic avian cardiac muscle.

The cardiac ryanodine receptor serves as a sarcoplasmic reticulum calcium release channel and contributes to the rise in cytosolic calcium necessary for contraction of the heart. We have investigated the presence and oligomeric form of the ryanodine receptor during embryonic development of the avian heart. A single isoform of the ryanodine receptor was identified both in adult and in embryonic cardiac tissue from Days 4 to 20 of development, using anti-receptor monoclonal antibodies in conjunction with [3H]ryanodine binding. The results of sucrose density gradient sedimentation analysis and [3H]ryanodine binding indicated that the cardiac ryanodine receptor is present in a tetrameric form in both the adult and embryos at Day 6 of development. The observation of specific [3H]ryanodine binding in hearts from Days 4 and 5 of embryonic development also indicates the presence of a tetrameric receptor protein. Although the heart begins to beat at approximately 33-38 hr (Day 1.5) of embryonic development, we were unable to detect the cardiac ryanodine receptor, using biochemical or immunological techniques, prior to Embryonic Day 4. Ryanodine was found to alter the chronotropic state of intact hearts as early as Hamburger and Hamilton stages 15-19 (Embryonic Day 3) suggesting that receptor protein may be present in a limited subset of cells involved in pacemaker activity in the very early embryo. After Embryonic Day 4, ryanodine also exerted a negative inotropic effect on embryonic hearts. Our results suggest that a single isoform of the ryanodine receptor is present from Day 4 to Day 20 of embryonic development in avian cardiac muscle and that the ryanodine receptor assumes a tetrameric structure capable of forming a functional calcium release channel that participates excitation-contraction coupling as early as Embryonic Day 4. In addition, a ryanodine receptor-related function may serve as a determinant of chronotropic effects in the very early embryonic heart.

Animals↗
PubMed1990

Localized calcium influx orients axon formation in embryonic hippocampal pyramidal neurons.

A fundamental property of neurons is their polarization into distinct axonal and dendritic compartments which have characteristic structural and functional properties. The mechanisms regulating the formation of neuronal polarity are unknown. We used cultured embryonic rat hippocampal pyramidal neurons to test the hypothesis that a localized calcium influx can orient axon formation, and thereby direct the establishment of neuronal polarity. Transection of an initial axon, or focal application of A23187 or K+ to the initial axon, caused a new axon to form at a site distant from the initial axon. Fura-2 measurements of intracellular calcium revealed a localized calcium influx at the site of axon transection or focal application of A23187 or K+, and a calcium gradient spreading into the soma. New axon formation was inhibited when axons were transected in medium lacking calcium or containing calcium-elevating agents (conditions which prevented the formation of a calcium gradient). When calcium ionophore A23187 was applied focally to neurons which had not yet established an axon, the axon always formed at a site distant from the site of ionophore application; bath exposure to A23187 prevented axon formation. Taken together, these data demonstrate that a localized influx of calcium can suppress axon formation at the site of influx, and can thereby influence where the axon forms. These data suggest that gradients of intracellular calcium may be involved in orienting neuronal polarity.

Animals↗
PubMed2000

Small GTPase Rac1: structure, localization, and expression of the human gene.

Rac1 is a member of the Rho family of small GTPases involved in signal transduction pathways that control proliferation, adhesion, and migration of cells during embryonic development and invasiveness of tumor cells. Here we present the complete structure of the human RAC1 gene and characterize its expression. The gene comprises 7 exons over a length of 29 kb and is localized to chromosome 7p22. The GC-rich gene promoter shows characteristics of a housekeeping gene and Northern blot studies revealed ubiquitous expression of two rac1 transcripts, 1.2 and 2.5 kb in size. The two transcripts are expressed in tissue-specific ratios, reflecting competition between two alternative polyadenylation sites. The RAC1 but not RAC2 gene contains an additional exon 3b that is included by alternative splicing into the variant Rac1b, a constitutively active mutant which induces the formation of lamellipodia in fibroblasts. These data indicate that the RAC1 gene encodes two signaling GTPases. The gene structure reported here will enable studies on the regulation of RAC1 expression during tumorigenesis and development.

5' Untranslated Regions↗
PubMed2001

Infant methylenetetrahydrofolate reductase 677TT genotype is a risk factor for congenital heart disease.

OBJECTIVE: Recently, an association between the homozygous C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene in infants with congenital neural tube defects or congenital oral clefts has been shown. However, no data are available so far with respect to the MTHFR 677TT genotype in children with underlying structural congenital heart disease (CHD). METHODS: We investigated the MTHFR genotype in 114 Caucasian CHD patients aged newborn to 16 years (median 0.6 years; 53% male) and in 228 age- and sex-matched healthy controls. RESULTS: In childhood patients with CHD the homozygous MTHFR 677TT genotype was found in 21 out of 114 subjects (18.4%) compared with 21 out of 228 controls (9.2%; odds ratio (OR) 2.2, 95%-confidence interval (CI) 1.2-4.3; P=0.027). In patients with pulmonary valve stenosis, hypoplastic left heart syndrome, coarctation of the aorta, aortic valve stenosis or subaortic stenosis the frequency of the TT genotype varied between 38 and 67% with corresponding ORs from 6.1 (CI, 1.4-27.5; P=0.034) to 20.4 (CI, 1.8-235.0; P=0.025), whereas in other structural CHD the frequency of this genotype was not significantly different from the controls. CONCLUSIONS: With the present study we can show for the first time that the embryonal MTHFR 677TT genotype is significantly associated with the development of structural congenital heart malformations during early pregnancy. It remains to be clarified, whether this genotype is at least a risk marker or a risk factor for structural congenital heart malformations.

Adolescent↗
PubMed2005

Arp2/3 complex-deficient mouse fibroblasts are viable and have normal leading-edge actin structure and function.

RNA interference silencing of up to 90% of Arp3 protein expression, a major subunit of the Arp2/3 complex, proportionately decreases the intracellular motility of Listeria monocytogenes and actin nucleation activity ascribable to the Arp2/3 complex in mouse embryonic fibroblasts. However, the Arp2/3-deficient cells exhibit unimpaired lamellipodial actin network structure, translational locomotion, spreading, actin assembly, and ruffling responses. In addition, Arp3-silenced cells expressing neural Wiskott-Aldrich syndrome protein-derived peptides that inhibit Arp2/3 complex function in wild-type cells retained normal PDGF-induced ruffling. The Arp2/3 complex can be dispensable for leading-edge actin remodeling.

Actin-Related Protein 2-3 Complex↗
PubMed2000

[New approaches in developmental genetics and gene therapy: xenotransplantation of Drosophila embryonic nerve cells into the brain of vertebrate animals].

The author's studies dealing with xenotransplantations of the embryonic nervous tissue into the brain of amphibian and mammals are reviewed. Drosophila nerve cells have been shown to survive inside the brain, differentiate, form ganglion-resembling structure, and come into synaptic contact with the host tissue. The embryonic nerve cells of transgenic Delta mutants of Drosophila melanogaster carrying a gene of bacterial galactosidase (lacZ) were also transplanted into the brain of adult rats and then identified histologically by X-gal staining of brain sections for the lacZ-gene product. The xenografts were shown to survive in the host brain for at least 2-3 weeks, after which they were attacked by macrophages. No glial scar tissue formed around the site of the xenograft. Cotransplantation of Drosophila embryonic nerve cells and the homologous embryonic nerve tissue was favorable for homograft survival and development, because formation of the glial scar was blocked, whereas homograft vascularization and differentiation of its nerve cells were stimulated. The results obtained are of interest with regard to neurosurgery, because they may be used to prevent formation of glial scar, an important factor in successful neurotransplantation.

Amphibians↗
PubMed1986

Acquisition of developmental autonomy in the equatorial region of the Xenopus embryo.

This paper describes a continuing effort to define the location and mode of action of morphogenetic determinants which direct the development of dorsal body axis structures in embryos of the frog Xenopus laevis. Earlier results demonstrated that presumptive endodermal cells in one vegetal quadrant of the 64-cell embryo can, under certain experimental conditions, induce partial or complete body axis formation by progeny of adjacent equatorial cells. (R.L. Gimlich and J.C. Gerhart, 1984, Dev. Biol. 104, 117-130). I have now assessed the importance of other blastomeres for embryonic axis formation in a series of transplantation experiments using cells from the equatorial level of the 32-cell embryo. The transplant recipients were embryos which had been irradiated with ultraviolet light before first cleavage. Without transplantation, embryos failed to develop the dorsal structures of the embryonic body axis. However, cells of these recipients were competent to respond to inductive signals from transplanted tissue and to participate in normal embryogenesis. Dorsal equatorial cells, but not their lateral or ventral counterparts, often caused partial or complete body axis development in irradiated recipients, and themselves formed much of the notochord and some prechordal and somitic mesoderm. These are the same structures that they would have formed in the normal donor. Thus, the dorsal equatorial blastomeres were often at least partially autonomous in developing according to their prospective fates. In addition, they induced progeny of neighboring host cells to contribute to the axial mesoderm and to form most of the central nervous system. The frequency with which such transplants caused complete axis formation in irradiated hosts increased when they were made at later and later cleavage stages. In contrast, the inductive activity of vegetal cells remained the same or declined during the cleavage period. These and other results suggest that the egg cytoplasmic region containing "axial determinants" is distributed to both endodermal and mesodermal precursors in the dorsal-most quadrant of the early blastula.

Animals↗