ORCID Profile
0000-0002-1438-0783
Current Organisations
University of South Australia
,
South Australian Health and Medical Research Institute
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Publications
Imaging Blood Vessels in the Zebrafish
Publisher: Elsevier
Date: 2010
Human and Mouse Homologues of the Drosophila melanogaster tweety (tty) Gene: A Novel Gene Family Encoding Predicted Transmembrane Proteins
Publisher: Elsevier BV
Date: 08-2000
Imaging blood vessels and lymphatic vessels in the zebrafish
Publisher: Elsevier
Date: 2016
DOI: 10.1016/BS.MCB.2016.03.023
Abstract: Blood vessels supply tissues and organs with oxygen, nutrients, cellular, and humoral factors, while lymphatic vessels regulate tissue fluid homeostasis, immune trafficking, and dietary fat absorption. Understanding the mechanisms of vascular morphogenesis has become a subject of intense clinical interest because of the close association of both types of vessels with pathogenesis of a broad spectrum of human diseases. The zebrafish provides a powerful animal model to study vascular morphogenesis because of their small, accessible, and transparent embryos. These unique features of zebrafish embryos permit sophisticated high-resolution live imaging of even deeply localized vessels during embryonic development and even in adult tissues. In this chapter, we summarize various methods for blood and lymphatic vessel imaging in zebrafish, including nonvital resin injection-based or dye injection-based vessel visualization, and alkaline phosphatase staining. We also provide protocols for vital imaging of vessels using microangiography or transgenic fluorescent reporter zebrafish lines.
Essential and overlapping roles for laminin α chains in notochord and blood vessel formation
Publisher: Elsevier BV
Date: 2006
DOI: 10.1016/J.YDBIO.2005.10.006
Abstract: Laminins are major constituents of basement membranes and have wide ranging functions during development and in the adult. They are a family of heterotrimeric molecules created through association of an alpha, beta and gamma chain. We previously reported that two zebrafish loci, grumpy (gup) and sleepy (sly), encode laminin beta1 and gamma1, which are important both for notochord differentiation and for proper intersegmental blood vessel (ISV) formation. In this study we show that bashful (bal) encodes laminin alpha1 (lama1). Although the strongest allele, bal(m190), is fully penetrant, when compared to gup or sly mutant embryos, bal mutants are not as severely affected, as only anterior notochord fails to differentiate and ISVs are unaffected. This suggests that other alpha chains, and hence other isoforms, act redundantly to laminin 1 in posterior notochord and ISV development. We identified cDNA sequences for lama2, lama4 and lama5 and disrupted the expression of each alone or in mutant embryos also lacking laminin alpha1. When expression of laminin alpha4 and laminin alpha1 are simultaneously disrupted, notochord differentiation and ISVs are as severely affected as sly or gup mutants. Moreover, live imaging of transgenic embryos expressing enhanced green fluorescent protein in forming ISVs reveals that the vascular defects in these embryos are due to an inability of ISV sprouts to migrate correctly along the intersegmental, normally laminin-rich regions.
Imaging Blood Vessels in the Zebrafish
Publisher: Elsevier
Date: 2004
Molecular distinction between arteries and veins
Publisher: Springer Science and Business Media LLC
Date: 10-2003
DOI: 10.1007/S00441-003-0771-8
Abstract: The vertebrate vascular system is essential for the delivery and exchange of gases, hormones, metabolic wastes and immunity factors. These essential functions are carried out in large part by two types of anatomically distinct blood vessels, namely arteries and veins. Previously, circulatory dynamics were thought to play a major role in establishing this dichotomy, but recently it has become clear that arterial and venous endothelial cells are molecularly distinct even before the output of the first embryonic heartbeat, thus revealing the existence of genetic programs coordinating arterial-venous differentiation. Here we review some of the molecular mechanisms involved in this process.
Lysosomal N-acetyltransferase interacts with ALIX and is detected in extracellular vesicles
Publisher: Elsevier BV
Date: 10-2018
DOI: 10.1016/J.BBAMCR.2018.07.001
Abstract: Heparan acetyl CoA: α-glucosaminide N-acetyltransferase (HGSNAT) is a lysosomal multi-pass transmembrane protein whose deficiency may lead to an accumulation of heparan sulphate and the neurodegenerative lysosomal storage disorder mucopolysaccharidosis (MPS) IIIC. In this study, HGSNAT activity was detected in extracellular vesicles isolated from both human urine and culture medium conditioned with HEK 293T cells. We also demonstrate that HGSNAT co-immunoprecipitates with antibodies to ALIX, which is associated with the endosomal sorting complexes required for transport (ESCRT) proteins, and is implicated in the targeting of proteins to intraluminal vesicles of multivesicular bodies, the origin of exosomes. Furthermore, mutation of a putative LYPX
Aminoacyl-Transfer RNA Synthetase Deficiency Promotes Angiogenesis via the Unfolded Protein Response Pathway
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 04-2016
DOI: 10.1161/ATVBAHA.115.307087
Abstract: Understanding the mechanisms regulating normal and pathological angiogenesis is of great scientific and clinical interest. In this report, we show that mutations in 2 different aminoacyl-transfer RNA synthetases, threonyl tRNA synthetase (tars y58 ) or isoleucyl tRNA synthetase (iars y68 ) , lead to similar increased branching angiogenesis in developing zebrafish. The unfolded protein response pathway is activated by aminoacyl-transfer RNA synthetase deficiencies, and we show that unfolded protein response genes atf4, atf6 , and xbp1 , as well as the key proangiogenic ligand vascular endothelial growth factor (vegfaa) , are all upregulated in tars y58 and iars y68 mutants. Finally, we show that the protein kinase RNA-like endoplasmic reticulum kinase–activating transcription factor 4 arm of the unfolded protein response pathway is necessary for both the elevated vegfaa levels and increased angiogenesis observed in tars y58 mutants. Our results suggest that endoplasmic reticulum stress acts as a proangiogenic signal via unfolded protein response pathway–dependent upregulation of vegfaa.
Live Imaging Innate Immune Cell Behavior During Normal Development, Wound Healing and Infection
Publisher: WORLD SCIENTIFIC
Date: 08-2010
Eukaryotic elongation factor 2 kinase upregulates the expression of proteins implicated in cell migration and cancer cell metastasis
Publisher: Wiley
Date: 27-12-2017
DOI: 10.1002/IJC.31210
Abstract: Eukaryotic elongation factor 2 kinase (eEF2K) negatively regulates the elongation phase of mRNA translation and hence protein synthesis. Increasing evidence indicates that eEF2K plays an important role in the survival and migration of cancer cells and in tumor progression. As demonstrated by two-dimensional wound-healing and three-dimensional transwell invasion assays, knocking down or inhibiting eEF2K in cancer cells impairs migration and invasion of cancer cells. Conversely, exogenous expression of eEF2K or knocking down eEF2 (the substrate of eEF2K) accelerates wound healing and invasion. Importantly, using LC-HDMS
Quantitative Non-canonical Amino Acid Tagging (QuaNCAT) Proteomics Identifies Distinct Patterns of Protein Synthesis Rapidly Induced by Hypertrophic Agents in Cardiomyocytes, Revealing New Aspects of
Publisher: Elsevier BV
Date: 10-2016
SOLH, a Human Homologue of theDrosophila melanogaster small optic lobesGene Is a Member of the Calpain and Zinc-Finger Gene Families and Maps to Human Chromosome 16p13.3 nearCATM(Cataract with Microph
Publisher: Elsevier BV
Date: 07-1998
Abstract: Mutations in the Drosophila melanogaster small optic lobes (sol) gene cause a sever reduction in the neuropiles of the medulla and lobula complexes of the adult optic lobes. The predicted protein product of sol contains zinc-finger-like repeats, a calpain-like protease domain, and a C-terminal region of unknown function. We have isolated human brain cDNA for SOLH, a human homologue of sol. The human SOLH gene consists of 14 exons distributed over more than 45 kb of genomic DNA. The encoded SOLH protein of 1086 amino acids has strong similarity to the D. melanogaster protein. The calpain-like domain and C-terminal region are highly conserved (58% identity), and similar Cys2-Cys2 zinc fingers are present in the N-terminal region. A reported Caenorhabditis elegans homologue contains the calpain domain and C-terminal region, but appears to lack the zinc finger region. A single copy of the zinc finger sequence is present in adjacent C. elegans genomic cosmid DNA sequence, and we show that it is part of the C. elegans sol-like transcript. Northern analysis of human tissues revealed a SOLH transcript of approximately 5 kb that was strongest in human brain. We have mapped the SOLH gene to chromosome 16p13.3 by in situ hybridization. SOLH is a candidate gene for CATM (hereditary cataracts with microphthalmia), which maps in this region.
CDP-diacylglycerol synthetase-controlled phosphoinositide availability limits VEGFA signaling and vascular morphogenesis
Publisher: American Society of Hematology
Date: 12-07-2012
DOI: 10.1182/BLOOD-2012-02-408328
Abstract: Understanding the mechanisms that regulate angiogenesis and translating these into effective therapies are of enormous scientific and clinical interests. In this report, we demonstrate the central role of CDP-diacylglycerol synthetase (CDS) in the regulation of VEGFA signaling and angiogenesis. CDS activity maintains phosphoinositide 4,5 bisphosphate (PIP2) availability through resynthesis of phosphoinositides, whereas VEGFA, mainly through phospholipase Cγ1, consumes PIP2 for signal transduction. Loss of CDS2, 1 of 2 vertebrate CDS enzymes, results in vascular-specific defects in zebrafish in vivo and failure of VEGFA-induced angiogenesis in endothelial cells in vitro. Absence of CDS2 also results in reduced arterial differentiation and reduced angiogenic signaling. CDS2 deficit-caused phenotypes can be successfully rescued by artificial elevation of PIP2 levels, and excess PIP2 or increased CDS2 activity can promote excess angiogenesis. These results suggest that availability of CDS-controlled resynthesis of phosphoinositides is essential for angiogenesis.
Aminoglycoside-induced premature stop codon read-through of mucopolysaccharidosis type i patient Q70X and W402X mutations in cultured cells
Publisher: Springer Berlin Heidelberg
Date: 2014
Solh, the Mouse Homologue of the Drosophila melanogaster small optic lobes Gene: Organization, Chromosomal Mapping, and Localization of Gene Product to the Olfactory Bulb
Publisher: Elsevier BV
Date: 02-2000
Long-Term Time-Lapse Fluorescence Imaging of Developing Zebrafish
Publisher: Mary Ann Liebert Inc
Date: 08-2005
Abstract: A variety of different transgenic zebrafish lines have been generated expressing green fluorescent protein (GFP) or other fluorescent proteins in different organs and tissues, permitting dynamic visualization of development of these organs and tissues in living animals via time-lapse imaging. Although methods have been devised for short- to medium-term time-lapse imaging of transgenic zebrafish, these methods are not suitable for longer term imaging because of poor control over temperature, evaporation, and anoxia. We describe a new imaging chamber that provides continuously circulating flow of warm, oxygenated aqueous media. We show that the chamber can be used for multiphoton time-lapse imaging of developing blood vessels in the trunk of Fli1-EGFP transgenic zebrafish for 5 days without developmental delay, loss of viability, or evident reduction in strength of circulatory flow. This imaging chamber provides an important new tool for long-term dynamic imaging of transgenic zebrafish.
fused‐somites–like mutants exhibit defects in trunk vessel patterning
Publisher: Wiley
Date: 10-04-2006
DOI: 10.1002/DVDY.20814
Abstract: We identified four mutants in two distinct loci exhibiting similar trunk vascular patterning defects in an F3 genetic screen for zebrafish vascular mutants. Initial vasculogenesis is not affected in these mutants, with proper specification and differentiation of endothelial cells. However, all four display severe defects in the growth and patterning of angiogenic vessels in the trunk, with ectopic branching and disoriented migration of intersegmental vessels. The four mutants are allelic to previously characterized mutants at the fused-somites (fss) and beamter (bea) loci, and they exhibit comparable defects in trunk somite boundary formation. The fss locus has been shown to correspond to tbx24 we show here that bea mutants are defective in the zebrafish dlC gene. Somitic expression of known vascular guidance factors efnb2a, sema3a1, and sema3a2 is aberrantly patterned in fss and bea mutants, suggesting that the vascular phenotype is due to loss of proper guidance cues provided by these factors.
pak2a mutations cause cerebral hemorrhage in redhead zebrafish
Publisher: Proceedings of the National Academy of Sciences
Date: 28-08-2007
Abstract: The zebrafish is a powerful model for studying vascular development, demonstrating remarkable conservation of this process with mammals. Here, we identify a zebrafish mutant, redhead ( rhd mi149 ), that exhibits embryonic CNS hemorrhage with intact gross development of the vasculature and normal hemostatic function. We show that the rhd phenotype is caused by a hypomorphic mutation in p21-activated kinase 2a ( pak2a ). PAK2 is a kinase that acts downstream of the Rho-family GTPases CDC42 and RAC and has been implicated in angiogenesis, regulation of cytoskeletal structure, and endothelial cell migration and contractility among other functions. Correction of the Pak2a-deficient phenotype by Pak2a overexpression depends on kinase activity, implicating Pak2 signaling in the maintenance of vascular integrity. Rescue by an endothelial-specific transgene further suggests that the hemorrhage seen in Pak2a deficiency is the result of an autonomous endothelial cell defect. Reduced expression of another PAK2 ortholog, pak2b , in Pak2a-deficient embryos results in a more severe hemorrhagic phenotype, consistent with partially overlapping functions for these two orthologs. These data provide in vivo evidence for a critical function of Pak2 in vascular integrity and demonstrate a severe disease phenotype resulting from loss of Pak2 function.
Lysosomal LAMP1 immunoreactivity exists in both diffuse and neuritic amyloid plaques in the human hippocampus.
Publisher: Wiley
Date: 02-04-2018
DOI: 10.1111/EJN.13913
Abstract: Lysosomal vesicles around neuritic plaques are thought to drive Alzheimer's disease by providing ideal microenvironments for generation of amyloid-β. Although lysosomal vesicles are present at every amyloid plaque in mouse models of Alzheimer's disease, the number of amyloid plaques that contain lysosomal vesicles in the human brain remains unknown. This study aimed to quantify lysosomal vesicles at amyloid plaques in the human hippoc us. Lysosome-associated membrane protein 1 (LAMP1)-positive vesicles accumulated in both diffuse (Aβ42-positive/AT8-negative) and neuritic (Aβ42-positive/AT8-positive) plaques in all regions were analysed. In contrast to mouse models of Alzheimer's disease, however, not all amyloid plaques accumulated LAMP1-positive lysosomal vesicles. Even at neuritic plaques, LAMP1 immunoreactivity was more abundant than phospho-tau (AT8). Further, lysosomal vesicles colocalised weakly with phospho-tau such that accumulation of lysosomal vesicles and phospho-tau appeared to be spatially distinct events that occurred within dystrophic neurites. This quantitative study shows that diffuse plaques, as well as neuritic plaques, contain LAMP1 immunoreactivity in the human hippoc us.
Endothelial tubes assemble from intracellular vacuoles in vivo
Publisher: Springer Science and Business Media LLC
Date: 21-06-2006
DOI: 10.1038/NATURE04923
Abstract: The formation of epithelial tubes is crucial for the proper development of many different tissues and organs, and occurs by means of a variety of different mechanisms. Morphogenesis of seamless, properly patterned endothelial tubes is essential for the development of a functional vertebrate circulatory system, but the mechanism of vascular lumenization in vivo remains unclear. Evidence dating back more than 100 years has hinted at an important function for endothelial vacuoles in lumen formation. More than 25 years ago, in some of the first endothelial cell culture experiments in vitro, Folkman and Haudenschild described "longitudinal vacuoles" that "appeared to be extruded and connected from one cell to the next", observations confirmed and extended by later studies in vitro showing that intracellular vacuoles arise from integrin-dependent and cdc42/Rac1-dependent pinocytic events downstream of integrin-extracellular-matrix signalling interactions. Despite compelling data supporting a model for the assembly of endothelial tubes in vitro through the formation and fusion of vacuoles, conclusive evidence in vivo has been lacking, primarily because of difficulties associated with imaging the dynamics of subcellular endothelial vacuoles deep within living animals. Here we use high-resolution time-lapse two-photon imaging of transgenic zebrafish to examine how endothelial tubes assemble in vivo, comparing our results with time-lapse imaging of human endothelial-cell tube formation in three-dimensional collagen matrices in vitro. Our results provide strong support for a model in which the formation and intracellular and intercellular fusion of endothelial vacuoles drives vascular lumen formation.
Reciprocal signaling between mTORC1 and MNK2 controls cell growth and oncogenesis
Publisher: Springer Science and Business Media LLC
Date: 13-03-2020
Related Organisations
National Institute Of Child Health And Human Development
Location: No location found
South Australian Health And Medical Research Institute
Location: Australia
National Institute Of Child Health And Human Development
Location: United States of America
Related Funding Activities
No related grants have been discovered for Makoto Kamei.