bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression patterns of Wnts, Frizzleds, sFRPs, and misexpression in transgenic mice suggesting a role for Wnts in pancreas and foregut pattern formation
Authors: Heller R. Scott , Dichmann Darwin S. , Jensen Jan , Miller Chris , Wong Gordon , Madsen Ole D. , Serup Palle 
Published: November 2002

AbstractIt is well established that gut and pancreas development depend on epithelial‐mesenchymal interactions. We show here that several Wnt, Frizzled, and secreted frizzled‐related protein (sFRP) encoding mRNAs are present during mouse pancreatic morphogenesis. Wnt5a and 7b mRNA is broadly expressed in foregut mesenchyme starting around embryonic day 10 in mice. Other members expressed are Wnt2b, Wnt5b, and Wnt11. In addition, genes for the Wnt receptors, Frizzled2, 3, 4, 5, 6, 7, 8, and 9 are expressed. To understand potential Wnt functions in pancreas and foregut development in vivo, we analyzed transgenic F0 mouse fetuses expressing Wnt1 and 5a cDNAs under control of the PDX‐1 gene promoter. In PDX‐Wnt1 fetuses, the foregut region normally comprising the proximal duodenum instead resembles a posterior extension of the stomach, often associated with complete pancreatic and splenic agenesis. Furthermore, the boundary between expression domains of gastric and duodenal markers is shifted in a posterior direction. In PDX‐Wnt5a fetuses, several structures derived from the proximal foregut are reduced in size, including the pancreas, spleen, and stomach, without any apparent shift in the stomach to duodenum transition. In these fetuses, overall pancreatic morphology is changed and the pancreatic epithelium is dense and compact, consistent with Wnt5A effects on cell movements and/or attachment. Taken together, these results suggest that Wnt genes participate in epithelial‐mesenchymal signaling and may specify region identity in the anterior foregut. © 2002 Wiley‐Liss, Inc.
Role of VEGF family members and receptors in coronary vessel formation
Authors: Tomanek Robert J. , Holifield Jennifer S. , Reiter Rebecca S. , Sandra Alexander , Lin Jim J.‐C. 
Published: November 2002

AbstractThe specific roles of vascular endothelial growth factor (VEGF) family members and their receptors (VEGFRs) in coronary vessel formation were studied. By using the quail heart explant model, we found that neutralizing antibodies to VEGF‐B or VEGF‐C inhibited tube formation on the collagen gel more than anti–VEGF‐A. Soluble VEGFR‐1, a receptor for VEGF‐A and ‐B, inhibited tube formation by 87%, a finding consistent with that of VEGF‐B inhibition. In contrast, addition of soluble VEGFR‐2, a receptor for VEGF family members A, C, D, and E, inhibited tube formation by only 43%. Acidic FGF‐induced tube formation dependency on VEGF was demonstrated by the attenuating effect of a soluble VEGFR‐1 and ‐2 chimera. The localization of VEGF R‐2 and R‐3 was demonstrated by in situ hybridization of serial sections, which documented marked accumulations of transcripts for both receptors at the base of the truncus arteriosus coinciding with the temporal and spatial formation of the coronary arteries by means of ingrowth of capillary plexuses. This finding suggests that both VEGFR‐2 and R‐3 may play a role in the formation of the coronary artery roots. In summary, these experiments document a role for multiple members of the VEGF family and their receptors in formation of the coronary vascular bed. © 2002 Wiley‐Liss, Inc.
PLEXIN‐D1, a novel plexin family member, is expressed in vascular endothelium and the central nervous system during mouse embryogenesis
Authors: Van Der Zwaag Bert , Hellemons Anita J.C.G.M. , Leenders William P.J. , Burbach J. Peter H. , Brunner Han G. , Padberg George W. , Van Bokhoven Hans 
Published: November 2002

AbstractThe genetic defect in Möbius syndrome 2 (MBS2, MIM 601471), a dominantly inherited disorder characterised by paralysis of the facial nerve, is situated at chromosome 3q21‐q22. We characterised the cDNA and predicted protein, and examined the expression pattern during mouse embryogenesis of a positional candidate gene, PLEXIN‐D1 (PLXND1). The cDNA for PLXND1 is 7095 base pairs in length, coding for a predicted protein of 1925 amino acids. The protein features all known domains of plexin family members, with the exception of the third Met‐related sequence. Northern analysis revealed a very low expression of PLXND1 in adult mouse and adult human tissues. To investigate the expression of PlxnD1 during embryogenesis, RNA in situ hybridisation was performed on mouse embryos from various stages. This investigation revealed expression of PlxnD1 in cells from the central nervous system (CNS) and in vascular endothelium. Early expression in the CNS is located in the ganglia, cortical plate of the cortex, and striatum. At later embryologic stages, neural expression was also seen in the external granular layer of the cerebellum and several nerve nuclei. The expression in the vascular system resides solely in the endothelial cells of developing blood vessels. Based on our results, we suggest that this expression of a member of the plexin family in vascular endothelium could point toward a role in embryonic vasculogenesis. © 2002 Wiley‐Liss, Inc.
Multiple mechanisms of perichondrial regulation of cartilage growth
Authors: Di Nino Dana L. , Crochiere Marsha L. , Linsenmayer Thomas F. 
Published: November 2002

AbstractWe previously observed that the perichondrium (PC) and the periosteum (PO) negatively regulate endochondral cartilage growth through secreted factors. Conditioned medium from cultures of PC and PO cells when mixed (PC/PO‐conditioned medium) and tested on organ cultures of embryonic chicken tibiotarsi from which the PC and PO have been removed (PC/PO‐free cultures) effect negative regulation of growth. Of potential importance, this regulation compensates precisely for removal of the PC and PO, thus mimicking the regulation effected by these tissues in vivo. We have now examined whether two known negative regulators of cartilage growth (retinoic acid [RA] and transforming growth factor‐β1 [TGF‐β1]) act in a manner consistent with this PC/PO‐mediated regulation. The results suggest that RA and TGF‐β1, per se, are not the regulators in the PC/PO‐conditioned medium. Instead, they show that these two factors each act in regulating cartilage growth through an additional, previously undescribed, negative regulatory mechanism(s) involving the perichondrium. When cultures of perichondrial cells (but not periosteal cells) are treated with either agent, they secrete secondary regulatory factors into their conditioned medium, the action of which is to effect precise negative regulation of cartilage growth when tested on the PC/PO‐free organ cultures. This negative regulation through the perichondrium is the only activity detected with TGF‐β1. Whereas, RA shows additional regulation on the cartilage itself. However, this regulation by RA is not “precise” in that it produces abnormally shortened cartilages. Overall, the precise regulation of cartilage growth effected by the action of the perichondrial‐derived factor(s) elicited from the perichondrial cells by treatment with either RA or TGF‐β1, when combined with our previous results showing similar—yet clearly different—“precise” regulation by the PC/PO‐conditioned medium suggests the existence of multiple mechanisms involving the perichondrium, possibly interrelated or redundant, to ensure the proper growth of endochondral skeletal elements. © 2002 Wiley‐Liss, Inc.
PI‐3 kinase activity is required for epithelial‐mesenchymal transformation during palate fusion
Authors: Kang Pei , Svoboda Kathy K.H. 
Published: November 2002

AbstractEpithelial‐mesenchymal transformation (EMT) is the primary mechanism for the disappearance of medial edge epithelia (MEE) during palate fusion. This phenotype transition is highly regulated by growth factors, extracellular matrix, cell surface receptors, and a variety of intracellular signaling. Phosphatidylinositol‐3 (PI‐3) kinase regulates cytoskeleton reorganization, cell migration, and transforming growth factor (TGF) β–regulated EMT. Therefore, we investigated the role of PI‐3 kinase in EMT during palatal fusion in vitro. Palatal shelves from embryonic (E) 13.5 day mouse embryos were collected and cultured for up to 72 hr. A specific PI‐3 kinase inhibitor, LY294002, was added to the medium at concentrations of 100 ηM, 1 μM, and 10 μM. The fate of midline epithelia was traced by carboxyfluorescence labeling and analyzed by confocal microscopy. Harvested tissues were also processed for immunohistochemical analysis of a specific marker for basal lamina (laminin). Palatal fusion stages were scored on a scale of 1 to 5, with 1 equal to complete nonfusion and 5 equal to complete fusion. The mean fusion score (MFS) was calculated for each treatment group. Palatal shelves fused after 72 hr of culture in control and 100 ηM LY294002 inhibitor‐treated groups, with MFS of 4.67 and 4.5, respectively. Laminin was absent in the midline and epithelia transformed into mesenchyme. However, when cultured palates were treated with 1 and 10 μM LY294002, MEE persisted in the midline and the basal lamina remained intact after 72 hr. The MFS was significantly less in the 1 and 10 μM LY294002‐treated tissues at 2.08 and 1.33, respectively. Our results demonstrate that EMT during palatal fusion in vitro is dependent on PI‐3 kinase activity. © 2002 Wiley‐Liss, Inc.
VEGF signaling is required for the assembly but not the maintenance of embryonic blood vessels
Authors: Argraves W. Scott , Larue Amanda C. , Fleming Paul A. , Drake Christopher J. 
Published: November 2002

AbstractHere we investigated the importance of vascular endothelial growth factor (VEGF) signaling to the de novo formation of embryonic blood vessels, vasculogenesis, as opposed to the maintenance of blood vessels. We found that antagonizing the activity of the VEGF signaling pathway by using soluble VEGF receptor 1 (sFlt1) or VEGF antibodies inhibited vasculogenesis that occurs in embryos and in cultures of 7.5 days postcoitus prevascular mesoderm. Antagonist treatment resulted in the formation of clusters of endothelial cells not normally observed during vasculogenesis. In contrast, when embryos with established vasculatures or cultures of vascularized mesoderm were treated with sFlt1 or VEGF antibodies, no discernible alterations to the preexisting blood vessels were observed. These observations indicate that, although VEGF signaling is required to promote the mesenchymal to epithelial transition by which angioblasts assemble into nascent endothelial tubes, it is not required by endothelial cells to maintain their organization as an endothelium. © 2002 Wiley‐Liss, Inc.
Prox1 is a master control gene in the program specifying lymphatic endothelial cell fate
Authors: Hong Young‐Kwon , Harvey Natasha , Noh Yun‐Hee , Schacht Vivien , Hirakawa Satoshi , Detmar Michael , Oliver Guillermo 
Published: November 2002

AbstractEarly during development, one of the first indications that lymphangiogenesis has begun is the polarized expression of the homeobox gene Prox1 in a subpopulation of venous endothelial cells. It has been shown previously that Prox1 expression in the cardinal vein promotes and maintains the budding of endothelial cells that will form the lymphatic vascular system. Prox1‐deficient mice are devoid of lymphatic vasculature, and in these animals endothelial cells fail to acquire the lymphatic phenotype; instead, they remain as blood vascular endothelium. To investigate whether Prox1 is sufficient to induce a lymphatic fate in blood vascular endothelium, Prox1 cDNA was ectopically expressed by adenoviral gene transfer in primary human blood vascular endothelial cells and by transient plasmid cDNA transfection in immortalized microvascular endothelial cells. Transcriptional profiling combined with quantitative real‐time reverse transcription‐polymerase chain reaction and Western blotting analyses revealed that Prox1 expression up‐regulated the lymphatic endothelial cell markers podoplanin and vascular endothelial growth factor receptor‐3. Conversely, genes such as laminin, vascular endothelial growth factor‐C, neuropilin‐1, and intercellular adhesion molecule‐1, whose expression has been associated with the blood vascular endothelial cell phenotype, were down‐regulated. These results were confirmed by the use of specific antibodies against some of these markers in sections of embryonic and adult tissues. These findings validate our previous proposal that Prox1 is a key player in the molecular pathway leading to the formation of lymphatic vasculature and identify Prox1 as a master switch in the program specifying lymphatic endothelial cell fate. That a single gene product was sufficient to re‐program the blood vascular endothelium toward a lymphatic phenotype corroborates the close relationship between these two vascular systems and also suggests that during evolution, the lymphatic vasculature originated from the blood vasculature by the additional expression of only a few gene products such as Prox1. © 2002 Wiley‐Liss, Inc.
Evidence that nitric oxide regulates cell‐cycle progression in the developing chick neuroepithelium
Authors: Traister Alexandra , Abashidze Soulico , Gold Veronica , Plachta Nicolas , Karchovsky Esther , Patel Ketan , Weil Miguel 
Published: November 2002

AbstractIn all developing epithelia, the nuclei continually migrate between the apical and basal sides of the cell during the cell cycle, with S phase occurring basally and mitosis occurring apically. The purpose and mechanism of this nuclear migration are unknown. Here, we show that nitric oxide (NO) is endogenously produced in the developing chicken neural tube, where it apparently regulates cell‐cycle progression. We provide evidence that high NO levels promote entry into S phase basally, whereas low levels of NO facilitate entry into mitosis apically. © 2002 Wiley‐Liss, Inc.
Embryonic retinal gene expression in sonic‐you mutant zebrafish
Authors: Stenkamp Deborah L. , Frey Ruth A. , Mallory Dianne E. , Shupe Emily E. 
Published: November 2002

AbstractHedgehog (Hh) signaling is required for proper eye development in vertebrates; known roles for Hh in the zebrafish include regulation of eye morphogenesis, ganglion cell neurogenesis, and photoreceptor differentiation. To gain insight into the mechanisms by which Hh signaling influences these developmental events, we have examined proliferation, cell death, and expression patterns of several retinal genes in the eyes of embryonic zebrafish lacking the sonic hedgehog gene. We find that features of the eye phenotype of the sonic‐you (syu) mutant are consistent with multiple roles for the Hh signal during retinal development. Most interestingly, half of the mutant retinas failed to initiate cell differentiation and, instead, retained a neuroepithelial appearance. In the other half of the mutants, retinal cell differentiation was initiated, but not fully propagated. We also find that Hh signaling is important for retinal cell proliferation and retinal cell survival; together, these functions provide an explanation for progressive microphthalmia in the syu‐/‐ mutant. © 2002 Wiley‐Liss, Inc.
Expression of the ETS transcription factor ER81 in the developing chick and mouse hindbrain
Authors: Zhu Yan , Guthrie Sarah 
Published: November 2002

AbstractER81 is an ETS domain‐containing transcription factor, which is expressed in various developing tissues and organs of the embryo and in pools of developing spinal motor neurons and proprioceptive sensory neurons. Analysis of mice lacking ER81 function showed that this gene played an important role in the establishment of sensory‐motor circuitry in the spinal cord. Here, we investigate the expression pattern of er81 in the hindbrain of both chick and mouse embryos. We find that er81 is expressed in a subpopulation of inferior olive neurons, which send their projections to the caudal cerebellum. © 2002 Wiley‐Liss, Inc.
Prep2: Cloning and expression of a new prep family member
Authors: Haller Klaus , Rambaldi Isabel , Kovács Erzsébet Nagy , Daniels Eugene , Featherstone Mark 
Published: November 2002

AbstractWe describe Prep2, a new murine homeobox‐containing gene closely related to Prep1. The PREP2 protein belongs to the three amino acid loop extension (TALE) superclass of homeodomain‐containing proteins and encodes a polypeptide of 462 residues. As for PREP1, PREP2 binds an appropriate site on DNA as a heterodimer with PBX1A. Northern analysis, immunoblotting, immunohistochemistry, and in situ hybridization show widespread Prep2 expression during organogenesis and in the adult. The data suggest that Prep2 functions to varying degrees in a broad array of tissues and developmental processes. © 2002 Wiley‐Liss, Inc.
Tooth development is independent of a Hox patterning programme
Authors: James Chela T. , Ohazama Atsushi , Tucker Abigail S. , Sharpe Paul T. 
Published: November 2002

AbstractHox genes have a critical role in controlling the patterning processes of many tissues by imparting positional information in embryogenesis. Patterning of the pharyngeal component of the skull (the visceroskeleton) has been proposed to be influenced by this “Hox code.” Recently, it has been shown that Hox genes are associated with the evolution of jaws, loss of Hox gene expression in the first branchial arch being necessary for the transition from the agnathan condition to the gnathostome condition. Teeth develop on the first branchial arch in mammals and, therefore, might be expected to be under the control of Hox genes in a manner similar to that of the cranial skeletal elements. However, we show that, unlike cartilage and bone, the development of teeth is not affected by alterations in Hoxa2 expression. Tooth development in the first arch was unaffected by overexpression of Hoxa2, whereas recombinations of second arch mesenchyme with first arch epithelium led to tooth development within a Hoxa2‐positive environment. These data demonstrate that teeth develop from local interactions and that tooth formation is not under the axial patterning program specified by the Hox genes. We propose that the evolutionary development of teeth in the first branchial arch is independent of the loss of Hox expression necessary for the development of the jaw. © 2002 Wiley‐Liss, Inc.
Surface imaging microscopy, an automated method for visualizing whole embryo samples in three dimensions at high resolution
Authors: Ewald Andrew J. , Mcbride Helen , Reddington Mark , Fraser Scott E. , Kerschmann Russell 
Published: November 2002

AbstractModern biology is faced with the challenge of understanding the specification, generation, and maintenance of structures ranging from cells and tissues to organs and organisms. By acquiring images directly from the block face of an embedded sample, surface imaging microscopy (SIM) generates high‐resolution volumetric images of biological specimens across all of these scales. Surface imaging microscopy expands our range of imaging tools by generating three‐dimensional reconstructions of embryo samples at high resolution and high contrast. SIM image quality is not limited by depth or the optical properties of overlying tissue, and intrinsic or extrinsic alignment markers are not required for volume reconstruction. These volumes are highly isotropic, enabling them to be virtually sectioned in any direction without loss of image quality. Surface imaging microscopy provided a more accurate three‐dimensional representation of a chick embryo than confocal microscopy of the same sample. SIM offers excellent imaging of embryos from three major vertebrate systems in developmental biology: mouse, chicken, and frog. Immediate applications of this technology are in visualizing and understanding complex morphogenetic events and in making detailed comparisons between normal and genetically modified embryos. © 2002 Wiley‐Liss, Inc.
An amphioxus winged helix/forkhead gene,AmphiFoxD: Insights into vertebrate neural crest evolution
Authors: Yu Jr‐Kai , Holland Nicholas D. , Holland Linda Z. 
Published: November 2002

AbstractDuring amphioxus development, the neural plate is bordered by cells expressing many genes with homologs involved in vertebrate neural crest induction. However, these amphioxus cells evidently lack additional genetic programs for the cell delaminations, migrations, and differentiations characterizing definitive vertebrate neural crest. We characterize an amphioxus winged helix/forkhead gene (AmphiFoxD) closely related to vertebrateFoxDgenes. Phylogenetic analysis indicates that theAmphiFoxDis basal to vertebrateFoxD1,FoxD2,FoxD3,FoxD4, andFoxD5. One of these vertebrate genes (FoxD3) consistently marks neural crest during development. Early in amphioxus development,AmphiFoxDis expressed medially in the anterior neural plate as well as in axial (notochordal) and paraxial mesoderm; later, the gene is expressed in the somites, notochord, cerebral vesicle (diencephalon), and hindgut endoderm. However, there is never any expression in cells bordering the neural plate. We speculate that anAmphiFoxDhomolog in the common ancestor of amphioxus and vertebrates was involved in histogenic processes in the mesoderm (evagination and delamination of the somites and notochord); then, in the early vertebrates, descendant paralogs of this gene began functioning in the presumptive neural crest bordering the neural plate to help make possible the delaminations and cell migrations that characterize definitive vertebrate neural crest. © 2002 Wiley‐Liss, Inc.
Ultrasonic imaging with narrow aperture phased array
Authors: Takizawa Naoki , Ohya Akihisa , Akiyama Iwaki 
Published: November 2002

AbstractThis paper describes the method of narrow aperture phased array ultrasonic computed tomography (NAPA‐CT), conceived for three‐dimensional imaging with increased resolution and speed in the field of clinical diagnosis. By reducing the size of the transducer in the thickness direction, a beam is formed such that the focal region of the phased array is a circular arc. This arc focus is scanned in a sector and is further rotated about the sound axis to acquire an echo. Then, the scatterer distribution on a hemisphere containing the arc as its part can be reconstructed by the inverse Radon transform. The feasibility of the proposed method is investigated by simulation and experiment. © 2002 Wiley Periodicals, Inc. Electron Comm Jpn Pt 3, 86(2): 72–81, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecjc.10029
Design of nonlinear adaptive digital filter by wavelet shrinkage
Authors: Tokairin Tomoya , Sato Yoshiharu 
Published: November 2002

AbstractThe wavelet shrinkage method is a nonlinear signal denoising procedure to remove noise by shrinking the empirical wavelet coefficients in the wavelet domain. In this paper, we apply the wavelet shrinkage method to nonlinear adaptive digital filters, and we propose the adaptive wavelet shrinkage filter which updates the threshold levels adaptively by the LMS algorithm according to the reference signal. The adaptive wavelet shrinkage filter is robust and has the property that one can control the filter easily by modifying the threshold levels. We describe the theorems concerning the convergence of the LMS algorithm for updating the threshold levels, and demonstrate several examples of the adaptive wavelet shrinkage filter. © 2002 Wiley Periodicals, Inc. Electron Comm Jpn Pt 3, 86(2): 59–71, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecjc.10032