for Journals by Title or ISSN
for Articles by Keywords
Followed Journals
Journal you Follow: 0
Sign Up to follow journals, search in your chosen journals and, optionally, receive Email Alerts when new issues of your Followed Journals are published.
Already have an account? Sign In to see the journals you follow.
Journal Cover Journal of Developmental Biology
  [2 followers]  Follow
  This is an Open Access Journal Open Access journal
   ISSN (Online) 2221-3759
   Published by MDPI Homepage  [151 journals]
  • JDB, Vol. 5, Pages 4: Moving the Shh Source over Time: What Impact on
           Neural Cell Diversification in the Developing Spinal Cord'

    • Authors: Cathy Danesin, Cathy Soula
      First page: 4
      Abstract: A substantial amount of data has highlighted the crucial influence of Shh signalling on the generation of diverse classes of neurons and glial cells throughout the developing central nervous system. A critical step leading to this diversity is the establishment of distinct neural progenitor cell domains during the process of pattern formation. The forming spinal cord, in particular, has served as an excellent model to unravel how progenitor cells respond to Shh to produce the appropriate pattern. In recent years, considerable advances have been made in our understanding of important parameters that control the temporal and spatial interpretation of the morphogen signal at the level of Shh-receiving progenitor cells. Although less studied, the identity and position of Shh source cells also undergo significant changes over time, raising the question of how moving the Shh source contributes to cell diversification in response to the morphogen. Here, we focus on the dynamics of Shh-producing cells and discuss specific roles for these time-variant Shh sources with regard to the temporal events occurring in the receiving field.
      PubDate: 2017-04-12
      DOI: 10.3390/jdb5020004
      Issue No: Vol. 5, No. 2 (2017)
  • JDB, Vol. 5, Pages 5: Special Issue on HOX Genes in Development

    • Authors: Vincenzo Zappavigna
      First page: 5
      Abstract: n/a
      PubDate: 2017-05-10
      DOI: 10.3390/jdb5020005
      Issue No: Vol. 5, No. 2 (2017)
  • JDB, Vol. 5, Pages 6: Sonic Hedgehog Signaling and Development of the

    • Authors: Maisa Seppala, Gareth Fraser, Anahid Birjandi, Guilherme Xavier, Martyn Cobourne
      First page: 6
      Abstract: Sonic hedgehog (Shh) is an essential signaling peptide required for normal embryonic development. It represents a highly-conserved marker of odontogenesis amongst the toothed vertebrates. Signal transduction is involved in early specification of the tooth-forming epithelium in the oral cavity, and, ultimately, in defining tooth number within the established dentition. Shh also promotes the morphogenetic movement of epithelial cells in the early tooth bud, and influences cell cycle regulation, morphogenesis, and differentiation in the tooth germ. More recently, Shh has been identified as a stem cell regulator in the continuously erupting incisors of mice. Here, we review contemporary data relating to the role of Shh in odontogenesis, focusing on tooth development in mammals and cartilaginous fishes. We also describe the multiple actions of this signaling protein at the cellular level.
      PubDate: 2017-05-31
      DOI: 10.3390/jdb5020006
      Issue No: Vol. 5, No. 2 (2017)
  • JDB, Vol. 5, Pages 1: Acknowledgement to Reviewers of Journal of
           Developmental Biology in 2016

    • Authors: JDB Editorial Office
      First page: 1
      Abstract: n/a
      PubDate: 2017-01-11
      DOI: 10.3390/jdb5010001
      Issue No: Vol. 5, No. 1 (2017)
  • JDB, Vol. 5, Pages 2: Sonic Hedgehog—‘Jack-of-All-Trades’ in Neural
           Circuit Formation

    • Authors: Nikole Zuñiga, Esther Stoeckli
      First page: 2
      Abstract: As reflected by the term morphogen, molecules such as Shh and Wnts were identified based on their role in early development when they instruct precursor cells to adopt a specific cell fate. Only much later were they implicated in neural circuit formation. Both in vitro and in vivo studies indicated that morphogens direct axons during their navigation through the developing nervous system. Today, the best understood role of Shh and Wnt in axon guidance is their effect on commissural axons in the spinal cord. Shh was shown to affect commissural axons both directly and indirectly via its effect on Wnt signaling. In fact, throughout neural circuit formation there is cross-talk and collaboration of Shh and Wnt signaling. Thus, although the focus of this review is on the role of Shh in neural circuit formation, a separation from Wnt signaling is not possible.
      PubDate: 2017-02-08
      DOI: 10.3390/jdb5010002
      Issue No: Vol. 5, No. 1 (2017)
  • JDB, Vol. 5, Pages 3: Canonical Sonic Hedgehog Signaling in Early Lung

    • Authors: Hugo Fernandes-Silva, Jorge Correia-Pinto, Rute Moura
      First page: 3
      Abstract: The canonical hedgehog (HH) signaling pathway is of major importance during embryonic development. HH is a key regulatory morphogen of numerous cellular processes, namely, cell growth and survival, differentiation, migration, and tissue polarity. Overall, it is able to trigger tissue-specific responses that, ultimately, contribute to the formation of a fully functional organism. Of all three HH proteins, Sonic Hedgehog (SHH) plays an essential role during lung development. In fact, abnormal levels of this secreted protein lead to severe foregut defects and lung hypoplasia. Canonical SHH signal transduction relies on the presence of transmembrane receptors, such as Patched1 and Smoothened, accessory proteins, as Hedgehog-interacting protein 1, and intracellular effector proteins, like GLI transcription factors. Altogether, this complex signaling machinery contributes to conveying SHH response. Pulmonary morphogenesis is deeply dependent on SHH and on its molecular interactions with other signaling pathways. In this review, the role of SHH in early stages of lung development, specifically in lung specification, primary bud formation, and branching morphogenesis is thoroughly reviewed.
      PubDate: 2017-03-13
      DOI: 10.3390/jdb5010003
      Issue No: Vol. 5, No. 1 (2017)
  • JDB, Vol. 1, Pages 186-202: The Epicardium and Coronary Artery Formation

    • Authors: Adriana Pires-Gomes, José Pérez-Pomares
      Pages: 186 - 202
      Abstract: The coronary system is the network of blood vessels that nourishes the heart muscle. After birth, proper coronary blood circulation is required to support heart homeostasis, and altered coronary function frequently leads to myocardial ischemia, infarction and heart failure. The epicardium plays a pivotal role during coronary blood vessel embryonic development, contributing cells to the coronary vasculature, but also secreting diffusible signals that regulate coronary morphogenesis and secondarily impact on ventricular compact myocardium growth. Accordingly, anomalous epicardium development gives rise to the multiple congenital defects of the coronary vascular system and the heart walls. In this review, we will summarize and discuss our current knowledge on the embryogenesis of coronary blood vessels, as related to epicardial development, and attempt to highlight the biomedical relevance of this tissue.
      PubDate: 2013-10-18
      DOI: 10.3390/jdb1030186
      Issue No: Vol. 1, No. 3 (2013)
  • JDB, Vol. 1, Pages 64-81: Development of the Serosal Mesothelium

    • Authors: Nichelle Winters, David Bader
      Pages: 64 - 81
      Abstract: Mesothelia in the adult vertebrate are the simple squamous epithelia covering all coelomic organs and body cavities. Until recently, analysis of the generation and differentiative potential of mesothelia in organogenesis has largely focused on development of visceral mesothelium of the heart; the epicardium and its progenitor, the proepicardium. Here, we review emerging data on the development and differentiation of serosal mesothelium, the covering of the gastrointestinal tract. This literature demonstrates that serosal mesothelium is generated through a completely different mechanism than that seen in the heart suggesting that commitment of progenitors to this cell lineage does not follow a common pathway. The differentiative potential of serosal mesothelium is also discussed in comparison to that observed for progeny of the proepicardium/epicardium. In our review of the literature, we point out gaps in our understanding of serosal mesothelial development and that of mesothelial development as a whole.
      PubDate: 2013-06-26
      DOI: 10.3390/jdb1020064
      Issue No: Vol. 1, No. 2 (2013)
  • JDB, Vol. 1, Pages 82-91: Induction of the Proepicardium

    • Authors: Lisandro Maya-Ramos, James Cleland, Michael Bressan, Takashi Mikawa
      Pages: 82 - 91
      Abstract: The proepicardium is a transient extracardiac embryonic tissue that gives rise to the epicardium and a number of coronary vascular cell lineages. This important extracardiac tissue develops through multiple steps of inductive events, from specification of multiple cell lineages to morphogenesis. This article will review our current understanding of inductive events involved in patterning of the proepicardium precursor field, specification of cell types within the proepicardium and their extension and attachment to the heart.
      PubDate: 2013-07-01
      DOI: 10.3390/jdb1020082
      Issue No: Vol. 1, No. 2 (2013)
  • JDB, Vol. 1, Pages 92-111: Transcriptional Control of Cell Lineage
           Development in Epicardium-Derived Cells

    • Authors: Caitlin Braitsch, Katherine Yutzey
      Pages: 92 - 111
      Abstract: Epicardial derivatives, including vascular smooth muscle cells and cardiac fibroblasts, are crucial for proper development of the coronary vasculature and cardiac fibrous matrix, both of which support myocardial integrity and function in the normal heart. Epicardial formation, epithelial-to-mesenchymal transition (EMT), and epicardium-derived cell (EPDC) differentiation are precisely regulated by complex interactions among signaling molecules and transcription factors. Here we review the roles of critical transcription factors that are required for specific aspects of epicardial development, EMT, and EPDC lineage specification in development and disease. Epicardial cells and subepicardial EPDCs express transcription factors including Wt1, Tcf21, Tbx18, and Nfatc1. As EPDCs invade the myocardium, epicardial progenitor transcription factors such as Wt1 are downregulated. EPDC differentiation into SMC and fibroblast lineages is precisely regulated by a complex network of transcription factors, including Tcf21 and Tbx18. These and other transcription factors also regulate epicardial EMT, EPDC invasion, and lineage maturation. In addition, there is increasing evidence that epicardial transcription factors are reactivated with adult cardiac ischemic injury. Determining the function of reactivated epicardial cells in myocardial infarction and fibrosis may improve our understanding of the pathogenesis of heart disease.
      PubDate: 2013-07-03
      DOI: 10.3390/jdb1020092
      Issue No: Vol. 1, No. 2 (2013)
  • JDB, Vol. 1, Pages 112-125: Epicardium Formation as a Sensor in Toxicology

    • Authors: Peter Hofsteen, Jessica Plavicki, Richard Peterson, Warren Heideman
      Pages: 112 - 125
      Abstract: Zebrafish (Danio rerio) are an excellent vertebrate model for studying heart development, regeneration and cardiotoxicity. Zebrafish embryos exposed during the temporal window of epicardium development to the aryl hydrocarbon receptor (AHR) agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exhibit severe heart malformations. TCDD exposure prevents both proepicardial organ (PE) and epicardium development. Exposure later in development, after the epicardium has formed, does not produce cardiac toxicity. It is not until the adult zebrafish heart is stimulated to regenerate does TCDD again cause detrimental effects. TCDD exposure prior to ventricular resection prevents cardiac regeneration. It is likely that TCDD-induced inhibition of epicardium development and cardiac regeneration occur via a common mechanism. Here, we describe experiments that focus on the epicardium as a target and sensor of zebrafish heart toxicity.
      PubDate: 2013-07-24
      DOI: 10.3390/jdb1020112
      Issue No: Vol. 1, No. 2 (2013)
  • JDB, Vol. 1, Pages 126-140: Left-Right Asymmetrical Development of the

    • Authors: Jan Schlueter, Thomas Brand
      Pages: 126 - 140
      Abstract: The proepicardium (PE) is a cluster of cells that forms on the cardiac inflow tract and gives rise to the epicardium and connective tissue and largely contributes to the coronary vasculature. In many vertebrates, the PE undergoes left-right asymmetrical development. While PE cells and marker genes can be initially found on both sides, only the right-sided PE will fully develop and ultimately deliver cells to the heart. Several signalling inputs, like FGF and BMP signals, are involved in PE induction in the lateral plate mesoderm, as well as during inflow tract formation and, also, control asymmetric PE development. These signalling events will be put into the context of embryonic left-right asymmetry determination. Finally, it will be discussed whether PE development may serve as a readout for asymmetric inflow tract morphogenesis.
      PubDate: 2013-07-26
      DOI: 10.3390/jdb1020126
      Issue No: Vol. 1, No. 2 (2013)
  • JDB, Vol. 1, Pages 141-158: Epicardial Lineages and Cardiac Repair

    • Authors: Manvendra Singh, Jonathan Epstein
      Pages: 141 - 158
      Abstract: The death of cardiac myocytes resulting from myocardial infarction is a major cause of heart failure worldwide. Effective therapies for regenerating lost cardiac myocytes are lacking. Recently, the epicardium has been implicated as a source of inflammatory cytokines, growth factors and progenitor cells that modulate the response to myocardial injury. During embryonic development, epicardially-derived cells have the potential to differentiate into multiple cardiac lineages, including fibroblasts, vascular smooth muscle and potentially other cell types. In the healthy adult heart, epicardial cells are thought to be generally quiescent. However, injury of the adult heart results in reactivation of a developmental gene program in the epicardium, which leads to increased epicardial cell proliferation and differentiation of epicardium-derived cells (EPDCs) into various cardiac lineages. Recent work suggests that epicardial reactivation after injury is accompanied by, and contributes to, a robust inflammatory response. In this review, we describe the current status of research related to epicardial biology in cardiac development and regeneration, highlighting important recent discoveries and ongoing controversies.
      PubDate: 2013-08-26
      DOI: 10.3390/jdb1020141
      Issue No: Vol. 1, No. 2 (2013)
  • JDB, Vol. 1, Pages 159-185: Soluble VCAM-1 Alters Lipid Phosphatase
           Activity in Epicardial Mesothelial Cells: Implications for Lipid Signaling
           During Epicardial Formation

    • Authors: Manjari Ranganathan, Danijela Dokic, Sonia Sterrett, Kathryn Dwyer, Robert Dettman
      Pages: 159 - 185
      Abstract: Epicardial formation involves the attachment of proepicardial (PE) cells to the heart and the superficial migration of mesothelial cells over the surface of the heart. Superficial migration has long been known to involve the interaction of integrins expressed by the epicardium and their ligands expressed by the myocardium; however, little is understood about signals that maintain the mesothelium as it migrates. One signaling pathway known to regulate junctional contacts in epithelia is the PI3K/Akt signaling pathway and this pathway can be modified by integrins. Here, we tested the hypothesis that the myocardially expressed, integrin ligand VCAM-1 modulates the activity of the PI3K/Akt signaling pathway by activating the lipid phosphatase activity of PTEN. We found that epicardial cells stimulated with a soluble form of VCAM-1 (sVCAM-1) reorganized PTEN from the cytoplasm to the membrane and nucleus and activated PTEN’s lipid phosphatase activity. Chick embryonic epicardial mesothelial cells (EMCs) expressing a shRNA to PTEN increased invasion in collagen gels, but only after stimulation by TGFβ3, indicating that loss of PTEN is not sufficient to induce invasion. Expression of an activated form of PTEN was capable of blocking degradation of junctional complexes by TGFβ3. This suggested that PTEN plays a role in maintaining the mesothelial state of epicardium and not in EMT. We tested if altering PTEN activity could affect coronary vessel development and observed that embryonic chick hearts infected with a virus expressing activated human PTEN had fewer coronary vessels. Our data support a role for VCAM-1 in mediating critical steps in epicardial development through PTEN in epicardial cells.
      PubDate: 2013-09-18
      DOI: 10.3390/jdb1020159
      Issue No: Vol. 1, No. 2 (2013)
  • JDB, Vol. 1, Pages 3-19: Evolutionary Origin of the Proepicardium

    • Authors: Elena Cano, Rita Carmona, Ramón Muñoz-Chápuli
      Pages: 3 - 19
      Abstract: The embryonic epicardium and the cardiac mesenchyme derived from it are critical to heart development. The embryonic epicardium arises from an extracardiac progenitor tissue called the proepicardium, a proliferation of coelomic cells located at the limit between the liver and the sinus venosus. A proepicardium has not been described in invertebrates, and the evolutionary origin of this structure in vertebrates is unknown. We herein suggest that the proepicardium might be regarded as an evolutionary derivative from an ancient pronephric external glomerulus that has lost its excretory role. In fact, we previously described that the epicardium arises by cell migration from the primordia of the right pronephric external glomerulus in a representative of the most primitive vertebrate lineage, the lamprey Petromyzon marinus. In this review, we emphasize the striking similarities between the gene expression profiles of the proepicardium and the developing kidneys, as well as the parallelisms in the signaling mechanisms involved in both cases. We show some preliminary evidence about the existence of an inhibitory mechanism blocking glomerular differentiation in the proepicardium. We speculate as to the possibility that this developmental link between heart and kidney can be revealing a phylogenetically deeper association, supported by the existence of a heart-kidney complex in Hemichordates. Finally, we suggest that primitive hematopoiesis could be related with this heart-kidney complex, thus accounting for the current anatomical association of the hematopoietic stem cells with an aorta-gonad-mesonephros area. In summary, we think that our hypothesis can provide new perspectives on the evolutionary origin of the vertebrate heart.
      PubDate: 2013-05-30
      DOI: 10.3390/jdb1010003
      Issue No: Vol. 1, No. 1 (2013)
  • JDB, Vol. 1, Pages 20-31: Role of Prokineticin Receptor-1 in Epicardial
           Progenitor Cells

    • Authors: Thu Nguyen, Adelin Gasser, Canan Nebigil
      Pages: 20 - 31
      Abstract: G protein-coupled receptors (GPCRs) form a large class of seven transmembrane (TM) domain receptors. The use of endogenous GPCR ligands to activate the stem cell maintenance or to direct cell differentiation would overcome many of the problems currently encountered in the use of stem cells, such as rapid in vitro differentiation and expansion or rejection in clinical applications. This review focuses on the definition of a new GPCR signaling pathway activated by peptide hormones, called “prokineticins”, in epicardium-derived cells (EPDCs). Signaling via prokineticin-2 and its receptor, PKR1, is required for cardiomyocyte survival during hypoxic stress. The binding of prokineticin-2 to PKR1 induces proliferation, migration and angiogenesis in endothelial cells. The expression of prokineticin and PKR1 increases during cardiac remodeling after myocardial infarction. Gain of function of PKR1 in the adult mouse heart revealed that cardiomyocyte-PKR1 signaling activates EPDCs in a paracrine fashion, thereby promoting de novo vasculogenesis. Transient PKR1 gene therapy after myocardial infarction in mice decreases mortality and improves heart function by promoting neovascularization, protecting cardiomyocytes and mobilizing WT1+ cells. Furthermore, PKR1 signaling promotes adult EPDC proliferation and differentiation to adopt endothelial and smooth muscle cell fate, for the induction of de novo vasculogenesis. PKR1 is expressed in the proepicardium and epicardial cells derived from mice kidneys. Loss of PKR1 causes deficits in EPDCs in the neonatal mice hearts and kidneys and impairs vascularization and heart and kidney function. Taken together, these data indicate a novel role for PKR1 in heart-kidney complex via EPDCs.
      PubDate: 2013-06-18
      DOI: 10.3390/jdb1010020
      Issue No: Vol. 1, No. 1 (2013)
  • JDB, Vol. 1, Pages 32-46: Epicardial Lineages

    • Authors: Franziska Greulich, Andreas Kispert
      Pages: 32 - 46
      Abstract: The epicardium is the mono-layered epithelium that covers the outer surface of the myocardium from early in cardiac development. Long thought to act merely passively to protect the myocardium from frictional forces in the pericardial cavity during the enduring contraction and expansion cycles of the heart, it is now considered to be a crucial source of cells and signals that direct myocardial growth and formation of the coronary vasculature during development and regeneration. Lineage tracing efforts in the chick, the mouse and the zebrafish unambiguously identified fibroblasts in interstitial and perivascular locations as well as coronary smooth muscle cells as the two major lineages that derive from epithelial-mesenchymal transition and subsequent differentiation from individual epicardial cells. However, controversies exist about an additional endothelial and myocardial fate of epicardial progenitor cells. Here, we review epicardial fate mapping efforts in three vertebrate model systems, describe their conceptual differences and discuss their methodological limitations to reach a consensus of the potential of (pro-)epicardial cells in vitro and in vivo.
      PubDate: 2013-06-21
      DOI: 10.3390/jdb1010032
      Issue No: Vol. 1, No. 1 (2013)
  • JDB, Vol. 1, Pages 47-63: Microsurgical Procedures for Studying the
           Developmental Significance of the Proepicardium and Epicardium in Avian
           Embryos: PE-Blocking, PE-Photoablation, and PE-Grafting

    • Authors: Jörg Männer
      Pages: 47 - 63
      Abstract: The epicardium is the outer skin of the mature vertebrate heart. Its embryonic origin and its possible roles in the developing and mature heart did not receive much recognition during the 19th and most of the 20th century. During the past 25 years, however, the epicardium came into the focus of developmental biology and regenerative medicine. Clinical researchers usually prefer genetically modified mouse models when they want to gain insight into developmental or pathological processes. The story of research on the embryonic epicardium, however, nicely demonstrates the value of non-mammalian species, namely avian species, for elucidating fundamental processes in embryonic and fetal development. Studies on chick and quail embryos have not only led to the identification of the primarily extracardiac source of the epicardium—presently called the proepicardium (PE)—they have also significantly contributed to our current knowledge about the developmental significance of the embryonic epicardium. In this review article, I describe three “classical” microsurgical experiments that have been developed for studying the developmental significance of the PE/epicardium in avian embryos (mechanical PE-blocking, PE-photoablation, orthotopic PE-grafting). Furthermore, I show how these microsurgical experiments have contributed to our current knowledge about the roles of the PE/epicardium in cardiac development. There are still some unsolved aspects in the physiology of the developing epicardium, which may be clarified with the aid of these “classical” microsurgical experiments.
      PubDate: 2013-06-21
      DOI: 10.3390/jdb1010047
      Issue No: Vol. 1, No. 1 (2013)
  • JDB, Vol. 1, Pages 1-2: Developmental Biology — Expanding the

    • Authors: Andy Wessels
      Pages: 1 - 2
      Abstract: Developmental biology is arguably the most exciting field of study within the biological sciences. To elucidate how complex organisms develop from a single cell into a complex organism is a quest that has captured the minds of many great scientists. [...]
      PubDate: 2012-09-25
      DOI: 10.3390/jdb1010001
      Issue No: Vol. 1, No. 1 (2012)
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
Tel: +00 44 (0)131 4513762
Fax: +00 44 (0)131 4513327
Home (Search)
Subjects A-Z
Publishers A-Z
Your IP address:
About JournalTOCs
News (blog, publications)
JournalTOCs on Twitter   JournalTOCs on Facebook

JournalTOCs © 2009-2016