bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endogenous distribution of retinoids during normal development and teratogenesis in the mouse embryo
Authors: Horton Claire , Maden Malcolm 
Published: February 2005

AbstractWe have analysed the endogenous retinoids present in whole mouse embryos from day 9 to day 14 of development and in individual components of the embryo at two stages, day 10.5 and day 13, by HPLC. We can only detect two retinoids, all‐trans ‐RA (tRA) and all‐trans ‐retinol (t‐retinol), and t‐retinol is 5‐10‐fold in excess over tRA. We cannot detect 9‐cis ‐RA or any didehydroretinoids; thus mammalian embryos seem to differ in their retinoid content from other embryos such as chick, Xenopus, and fish. The levels of tRA do not change significantly over the 6 days of development analysed, whereas t‐retinol rises sharply as the liver develops. Within the embryo, tRA is present at high levels in the developing spinal cord and at very low levels in the forebrain; indeed there is a gradient of endogenous tRA from the forebrain to the spinal cord. Other parts of the embryo had intermediate levels of tRA. When a teratogenic dose of RA was administered to day 10.5 embryos, the levels of tRA present in individual tissues of the embryo rose dramatically—from 175‐fold to 1,400‐fold—and the levels rose in all tissues not in any exclusive areas. We then determined which areas of the embryo were malformed by such a teratogenic dose. The lower jaw, palate, vertebrae, tail, and limbs were consistently abnormal, and since these areas received a dose of tRA no higher than any other it was concluded that cell‐specific factors must determine the teratogenic response of these tissues. We then considered whether cellular retinoic acid‐binding protein I or II (CRABP I or II) played any role in this response by determining their relative levels in each of the tissues analysed. There was no correlation between the presence of CRABP I and II and the distribution of administered RA. Neither was there a clear correlation in detail between the presence of CRABP I and II and the sites of teratogenesis. We therefore conclude that other factors, for example, nuclear factors, must be responsible for the teratogenic response to RA. © 1995 Wiley‐Liss, Inc.
Novel mouse endothelial cell surface marker is suppressed during differentiation of the blood brain barrier
Authors: Hallmann R. , Mayer D. N. , Berg E. L. , Broermann R. , Butcher E. C. 
Published: February 2005

AbstractFew markers specific for mouse endothelium exist. We describe here one such marker, MECA‐32, a monoclonal antibody which shows high specificity for mouse endothelium in both embryonic and mature tissues. The MECA‐32 antigen has a Mr of 50−55 − 103 under reducing conditions and Mr of 100−120 − 103 under nonreducing conditions. It is expressed on most endothelial cells in the embryonic and in the adult mouse, with the exception of the brain, skeletal, and cardiac muscle, where it has a more restricted distribution. In skeletal and cardiac muscle only small arterioles and venules express the MECA‐32 antigen, while in the brain its expression is negatively correlated with the differentiation of the vasculature to form the blood brain barrier. Interestingly, during embryonic development the antigen occurs on the brain vasculature up to day 16 of gestation (E16), whereupon it disappears. The embryonic brain is an avascular organ anlage which is vascularized by ingrowth of external blood vessels. Differentiation of the vasculature to form the blood brain barrier occurs at approximately E16 in the mouse. This differentiation correlates with the downregulation of MECA‐32 antigen expression. Between E12 and E16 MECA‐32 detects most endothelial cell surfaces of the blood vessels in the brain. No MECA‐32 antigen is found in the brain at E17 or any later stage of development with the exception of the vasculature of the circumventricular organs. The results suggest that MECA‐32 antigen expression is temporally and spatially correlated with the development of the blood brain barrier. © 1995 Wiley‐Liss, Inc.
Posterior extension of the chick nephric (Wolffian) duct: The role of fibronectin and NCAM polysialic acid
Authors: Bellairs Ruth , Lear Pamela , Yamada Kenneth M. , Rutishauser Urs , Lash James W. 
Published: February 2005

AbstractThe nephric duct of the chick embryo starts to form at about stage 10 of Hamburger and Hamilton ([1951] J. Morphol. 88:49–92) and extends posteriorly, fusing with the cloaca at about the end of the third day of incubation (HH stage 17). Evidence from the literature suggests that the extension involves active migration of the posterior tip. This investigation concerned some molecules that might control this migration: fibronectin, vitronectin, the β1 integrin receptor, and NCAM polysialic acid. The concentration of fibronectin in the extracellular matrix was found by immunocytochemistry to be negligible at the posterior end of the duct; treatment of the living embryo with GRGDS failed to halt further extension of the duct; SEM examination of embryos treated with the synthetic peptides of fibronectin GRGDS, GRDGS, SDGR, and GRGES, or with vitronectin, revealed negligible morphological effects on the duct. It is concluded that there is yet no evidence that fibronectin is an important factor in duct migration. NCAM polysialic acid had a similar distribution to fibronectin, but treatment of the living embryo with Endo‐N caused cessation of extension of the duct. Endo‐N is an enzyme that specifically degrades PSA without affecting the NCAM polypeptide itself. It is suggested therefore that PSA may play an important role in duct extension. The synthetic peptides of fibronectin each produced distinctive patterns of blebbing on the surfaces of cells in trunk mesoderm, but the duct cells were unaffected. GRGES and SDGR caused blebbing on cells in the somites and the anterior segmental plate, though not on cells in the posterior segmental plate. This suggests that integrin receptors change in the anterior segmental plate as the mesoderm forms somites from somitomeres. © 1995 Wiley‐Liss, Inc.
Muscle cell death during the development of head and neck muscles in the chick embryo
Authors: McClearn Deedra , Medville Richard , Noden Drew 
Published: February 2005

AbstractDegenerating myofibers have been reported in the embryos and neonates of a number of birds and mammals, but neither the pervasiveness of the phenomenon nor the spatiotemporal patterns of degeneration has been examined in detail. Using transmission electron microscopy, we determined the patterns of muscle cell death in the chick biventer cervicis, a head extensor muscle. Cell death is most pronounced at incubation days 10 through 15, and occurs throughout the muscle. This is the period during which many myofiber clusters segregate into individual fibers, each with a separate basal lamina, and secondary myofibers become demarcated. Cells of largest diameter, presumably the primary myofibers, are preferentially affected. Degenerating cells exhibit a cohort of cytological features consistent with apoptosis, including the presence of dense, darkly‐staining, hypercontracted myofibrils, misshapen nuclei with irregular chromatin condensations along the nuclear envelope, and scores of cytoplasmic vesicles and vacuoles. In cross section some large diameter muscle cells are characterized by sparse, flocculent cytoplasm that is devoid of myofibrils and organelles. Some show disintegrating cell membranes. In longitudinal section 200–300 μm long regions of hypercontracted myofibrils alternate with areas devoid of fibrils; this arrangement suggests that the myofibrils break into segments that are in register along one part of a muscle fiber and entirely absent from the adjacent length of fiber. We have observed similar patterns of muscle cell degeneration in the complexus, splenius cervicis, depressor mandibulae, and branchiomandibularis muscles. By day 18 of incubation most signs of degeneration are absent and by hatching (day 21) the muscle fibers all appear healthy. Many of these cytological changes in embryonic head muscle cells are characteristic of programmed cell death. We hypothesize that large‐scale death of myocytes is a normal part of avian myogenesis and an important mechanism for affecting the transformation from embryonic to hatching muscle patterning. © 1995 Wiley‐Liss, Inc.
92‐kDa type IV collagenase and TIMP‐3, but not 72‐kDa type IV collagenase or TIMP‐1 or TIMP‐2, are highly expressed during mouse embryo implantation
Authors: Reponen Paula , Leivo Ilmo , Sahlberg Carin , Apte Suneel S. , Thesleff Irma , Olsen Björn R. , Tryggvason Karl 
Published: February 2005

AbstractExpression of 72 kDa and 92 kDa type IV collagenases and the metalloproteinase inhibitors TIMPs 1, 2, and 3 was studied by in situ hybridization in implanting mouse embryos of days 5.5 to 7.5. The 92 kDa type IV collagenase was strongly expressed in invading trophoblasts, signals above background not being observed in the embryonic proper or placental tissue. In contrast, signals above background were not seen for the 72 kDa enzyme in any cells of the implantation region, including trophoblasts and stromal cells of the decidual tissue. Only cells in the mucosal stroma outside the decidual region displayed some expression. TIMP‐3 was intensily expressed in maternal cells in the area surrounding the invading embryonic tissue. No expression was observed for TIMP‐1 or TIMP‐2 in the embryo proper, trophoblasts, or the area of the uterine decidual reactin. Weak signals appeared for TIMP‐1 only in the circular layer of myometrial smooth muscle and in some uterine stroma cells distant from the site of embryo implantation. The results suggest a central role for 92 kDa type IV collagenase and TIMP‐3 in the extracellular proteolysis associated with implantation of the early embryo. © 1995 Wiley‐Liss, Inc.
Differential expression of the chicken Pax‐1 and Pax‐9 Gene: In situ hybridization and immunohistochemical analysis
Authors: Peters Heiko , Doll Uwe , Niessing Jürgen 
Published: February 2005

AbstractWe report the cloning, partial sequence analysis, and spatiotemporal expression of the chicken Pax‐1 (chPax‐1) and Pax‐9 (chPax‐9) gene, two closely related members of the paired box‐containing (PAX) gene family. The chPax‐1 gene encodes RNAs of 2.0 and 4.3 kb and a 42 kD protein while the gene products of chPax‐9 are represented by 1.9 and 3.1 kb transcripts and a 39 kD protein. In situ hybridization and immunohistochemical analyses reveal chPax‐1 expression in the developing pectoral girdle, in cells of the ventral part of sclerotomes, in sclerotome cells of the perichordal tube, and, later in development, in sclerotome‐derived cells of the intervertebral disks. Other chPax‐1 expression domains detected in the mesenchyme surrounding the atlas and axis and in chondrocytes of immature vertebral bodies, so far unreported for mouse Pax‐1, correlate with as yet unexplained malformations in the mouse Pax‐1 mutant undulated and Undulated‐short tail. Overlapping expression of chPax‐1 and chPax‐9 is detected in epithelial cells of the embryonic and adult thymus and in cells of the developing intervertebral disks. Unlike chPax‐1, however, chPax‐9 is not expressed in those perichordal sclerotome cells which are thought to give rise to vertebral bodies. Furthermore, chPax‐9 gene products are detected in circumscribed areas of mesenchyme in the metatarsus and in entodermal derivatives, i.e., in the lining epithelium of the developing pharynx and of the embryonic and adult esophagus. ©1995 Wiley‐Liss, Inc.
Pattern of muscle fiber type formation in the pig
Authors: Lefaucheur L. , Edom F. , Ecolan P. , Butler‐Browne G. S. 
Published: February 2005

AbstractThe aim of this study was to analyze the temporal sequence of expression of the myosin isoforms in the populations of muscle fibers in the pig and to bring more information on the origin of the strikingly different pattern of fiber composition and distribution between the deep medial red (oxido‐glycolytic) and superficial white (glycolytic) portions of semitendinosus (ST) muscle. Muscle samples were taken from 49‐, 55‐, 75‐, 90‐, 103‐, and 113‐ (birth) day‐old fetuses, from 6‐, 11‐, 21‐, 35‐, 50‐, and 80‐day‐old piglets, and from a 3‐year‐old pig. Our results confirm the sequential formation of primary and secondary generation fibers. The use of immunohistochemistry and heterologous monoclonal antibodies (mAb) directed against specific myosin heavy chain (MHC) isoforms revealed a different pattern of gene expression between the two portions of the ST muscle for both generations of fibers. By 75 days of gestation (dg), primary myotubes from the deep medial portion stained positively for the anti‐slow MHC mAb and negatively for the adult anti‐fast MHC, whereas the opposite was observed in the superficial portion. Secondary fibers never expressed slow MHC until late gestation. Instead, they expressed an adult fast MHC isoform as soon as they formed in the deep medial portion and later on in the superficial portion. From late gestation to the first 3 postnatal weeks, slow MHC began to be expressed in a subpopulation of secondary fibers. These fibers were in the direct vicinity of primary myotubes in the deep medial portion, whereas their location could not be established in the superficial portion. The remaining secondary fibers matured to type IIA in the direct vicinity of these type I fibers and to type IIB at the periphery of the islets. In both portions of the muscle, a subpopulation of secondary fibers, the first ones to express slow MHC, also transitorily expressed a MHC that was identical or closely related to the αcardiac MHC during the early postnatal period. A third generation of small diameter fibers was observed shortly after birth and reacted with the anti‐fetal MHC mAb; their destiny remains to be established. The present work reveals a remarkable pattern of MHC gene expression in the pig and raises many questions on the real nature of these isoforms. In order to answer these questions, we have undertaken to make a cDNA library of pig skeletal muscle and to screen this library with the same mAbs used in the present study. ©1995 Wiley‐Liss, Inc.
Developmentally regulated neural protein EAP‐300 is expressed by myocardium and cardiac neural crest during chick embryogenesis
Authors: McCabe Craig F. , Gourdie Robert G. , Thompson Robert P. , Cole Gregory J. 
Published: February 2005

AbstractThe spatiotemporal distribution of EAP‐300 (embryonic avian polypeptide of 300 kDa) was analyzed in embryonic chick heart using immunohistochemistry and confocal microscopy. EAP‐300 is a developmentally regulated protein initially characterized in neural cells from chick retina. Myocardial cells all along the early tubular heart were ubiquitously immunolabeled for EAP‐300 by embryonic day 2 (E2, Stage 13). At E5 (Stage 24), myocardial EAP‐300 expression levels remained significant in both atrial and ventricular myocardium. At E6 (Stage 28), distinct populations of EAP‐300 immunolabeled cells were also observed external to the heart, in septal mesenchymal tissue and neural ganglia adjacent to the outflow tract; these cell populations were confirmed as neural crest‐derived by co‐localization of EAP‐300 and HNK‐1. At E13 (Stage 39), myocardial immunolabeling for EAP‐300 was no longer ubiquitous, but increasingly restricted to conduction tissues, including the atrioventricular bundle and subendocardial Purkinje cells. This restriction of immunolabeling could be demonstrated definitively at E15 (stage 41), by which stage subendocardial and periarterial Purkinje fibers were clearly immunoreactive for EAP‐300 and several known markers of chick conduction tissue, including specific myosin heavy chain isoforms and connexin42, a gap junctional protein preferentially expressed by Purkinje fibers. Just prior to hatching at E21 (Stage 46), immunolabeling of conduction tissues was reduced, although still above that of non‐conductile myocardium. This spatiotemporal map of cardiac EAP‐300 expression indicates that it is independently and transiently expressed in early myocardium, cardiac conduction tissue, and neural crest derivatives during development. ©1995 Wiley‐Liss, Inc.
Expression of runt in the mouse embryo
Authors: Simeone Antonio , Daga Antonio , Calabi Franco 
Published: February 2005

AbstractThe Drosophila runt locus controls early events in embryogenesis. A human homologue (CBFA2) was criginally identified because of its involvement in the t(8;21) associated with a subtype of acute myeloid leukaemia. The phylogenetically conserved region (runt box) was reported to correspond to a DNA binding domain. In order to investigate whether runt also plays a role in mammalian development, we have conducted a preliminary survey of its expression in the mouse embryo. Expression in embryonic tissues was detected starting from day 9.2 post coitum. From day 10.5 post coitum, highest levels are found in the neural tube, sensory ganglia, specialised sensory epithelial structures (olfactory and gustatory mucosa, follicles of the vibrissae), all chondrogenic centres (both of neural crest and of mesodermal origin), and the genital system (the gonad, the paramesonephros, and the genital tubercle). Unambiguous expression in the haemo‐poietic system could be established for the thymus. The data suggest a pleiotropic role for mammalian runt in embryogenesis. ©1995 Wiley‐Liss, Inc.
Distribution of vitronectin mRNA during murine development
Authors: Seiffert Dietmar , Iruela‐Arispe Maria Luisa , Sage E. Helene , Loskutoff David J. 
Published: February 2005

AbstractVitronectin (Vn) is not only a major adhesive glycoprotein in plasma but also regulates cell‐mediated proteolytic enzyme cascades, including the complement, coagulation, and fibrinolytic systems. This broad functional activity suggests that Vn may also play a critical role in development. To begin to investigate this possibility, we studied Vn gene expression during murine embryogenesis. In situ hybridization analysis of embryonic tissues revealed Vn mRNA primarily in the liver and the central nervous system (CNS). In the liver, Vn mRNA was detected by day 10, the level increasing at later developmental stages. In the CNS, Vn mRNA was also detected as early as day 10 and was confined to the floor plate. However, as development proceeded, high levels of Vn transcripts became prominent in the meninges of the cortex and spinal cord, and in close proximity to brain capillaries. The perikarya of most neurons lacked Vn mRNA. Unexpectedly, high levels of Vn mRNA were associated with capillaries of the CNS, but not with blood vessels of peripheral organs. These results indicate that Vn is expressed in a spatially and temporally distinct pattern during murine embryogenesis, and suggest that the Vn transcript may be a CNS‐specific vascular marker. ©1995 Wiley‐Liss, Inc.
Inhibitory effects of ouabain on early heart development and cardiomyogenesis in the chick embryo
Authors: Linask Kersti K. , Gui Yong‐Hao 
Published: February 2005

AbstractPericardial cavity formation and epithelialization of the cardiac precursor cell population constitute a critical developmental period that precedes stable cardiac cell commitment and differentiation. These events delineate the myocardial and endocardial precursor population in the embryo. Restriction of Na/K‐ATPase (the sodium pump) expression to the pre‐cardiomyocyte lateral membranes coincides with these events. Na/K‐ATPase has been implicated developmentally in cavitation and in maintaining membrane potential. Experiments were undertaken to determine if the effects of perturbing sodium pump activity will affect pericardial cavity formation and, in turn, whether heart formation and/or cardiac cell commitment will be affected. We incubated whole chick embryos in vitro between stages 5 to 8 in the presence of the highly specific Na/K‐ATPase inhibitor ouabain. Exposure of whole embryos to 10 μM ouabain (10−5 M) demonstrated that heart development and precardiomyocyte differentiation are inhibited principally between stage 5 through stage 7. In each stage the degree of inhibition follows a rostrocaudal gradient as development proceeds along the anterior to posterior axis. After stage 8 ouabain no longer affects heart development or cardiomyogenesis. The inhibition is concentration‐ and developmental stage‐dependent. The inhibition is reversible by elevating the outside potassium ion concentration [Ko] in the culture medium or by transferring the embryos into normal medium minus ouabain even after 20 hr of ouabain exposure. The results also suggest that the regulation of the formation of the three‐dimensional organ is independent from regulation of myogenesis. ©1995 Wiley‐Liss, Inc.
Steel and c‐kit in the development of avian melanocytes: A study of normally pigmented birds and of the hyperpigmented mutant silky fowl
Authors: Lecoin Laure , Lahav Ronit , Martin Francis H. , Teillet Marie‐Aimée , Le Douarin Nicole M. 
Published: February 2005

AbstractWe describe here the expression of c‐kit and Steel (Sl) genes during the development of melanocytes in normally pigmented strains of chick and quail compared to unpigmented (White Leghorn) and hyperpigmented (Silky Fowl) strains of chickens. By using the quail/chick chimera system, we found that the neural crest cells, which migrate dorso‐laterally in the subectodermal mesenchyme to give rise to the melanocytes, express c‐kit as early as E4, that is about 2 days after they have left the neural primordium. The Sl gene is expressed from E4 onward in the epidermis but not at all in the dermis at any developmental stage. As feather buds develop, Sl mRNA becomes restricted to the apical region of the feather filaments. During formation of the barbs and barbules of the down feather, production of the Steel factor is restricted to the external epidermal cells of the barbules. The cell bodies of the c‐kit‐positive melanocytes are then located in the internal border of the epidermal ridges and extend their processes toward the source of the Steel factor. We propose that the spatial restriction of Sl gene activity at that stage accounts for the morphology of the melanocytes and their vectorial secretion of melanin to the external barbule cells. As a whole, these results show that during skin development c‐kit positive cells are present in the Steel factor‐producing areas at the time when melanoblasts proliferate and differentiate. Interestingly, in the mouse, previous studies showed that the Sl gene is activated in the dermis where melanoblasts undergo most of their expansion (Nishikawa et al. [1991] EMBO J. 10:2111‐2118). In the unpigmented and hyperpigmented mutants that we studied, expression of the Sl message, as judged quantitatively in Northern blots (for the SF embryos) or spatially by in situ hybridization, is similar to that observed in normal birds. In SF embryos the c‐kit expressing melanoblasts migrate initially in the dorso‐lateral migration pathway as in normal birds. However their number increases considerably in the dermis from E5 onward. From E7, they invade mesodermally derived organs that do not express the Sl gene. This suggests that another, still unknown, factor(s) is responsible for the survival, the proliferation, and the extensive spreading of melanocytic cells within the mesoderm of this mutant. ©1995 Wiley‐Liss, Inc.