ZIP2 Protein, a Zinc Transporter, Is Associated with Keratinocyte Differentiation

Inoue, Yu; Hasegawa, Seiji; Ban, Seiji; Yamada, Takaaki; Date, Yasushi; Mizutani, Hiroshi; Nakata, Satoshi; Tanaka, Masahiko; Hirashima, Naohide

doi:10.1074/jbc.m114.560821

Cited by 66 publications

(67 citation statements)

References 25 publications

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“…It is required for differentiation of embryonic skeletal muscle progenitors, for survival of adult skeletal muscle, for promoting myoblast proliferation in mice that were subject to muscle injury, and also for enhancing muscle regeneration in a dystrophic mouse model [26]. ZIP2 is induced by Zn deprivation in monocytes, and is necessary for keratinocyte differentiation [1,27,28]. Experimental evidence suggests a major role in development for ZIP2, as knock-out mice are sensitive to dietary Zn deficiency during pregnancy [29].…”

Section: Introductionmentioning

confidence: 99%

Differential expression of zinc transporters accompanies the differentiation of C2C12 myoblasts

Paskavitz

Quintana

Cangussu

et al. 2018

Journal of Trace Elements in Medicine and Biology

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Zinc transporters facilitate metal mobilization and compartmentalization, playing a key role in cellular development. Little is known about the mechanisms and pathways of Zn movement between Zn transporters and metalloproteins during myoblast differentiation. We analyzed the differential expression of ZIP and ZnT transporters during C2C12 myoblast differentiation. Zn transporters account for a transient decrease of intracellular Zn upon myogenesis induction followed by a gradual increase of Zn in myotubes. Considering the subcellular localization and function of each of the Zn transporters, our findings indicate that a fine regulation is necessary to maintain correct metal concentrations in the cytosol and subcellular compartments to avoid toxicity, maintain homeostasis, and for loading metalloproteins needed during myogenesis. This study advances our basic understanding of the complex Zn transport network during muscle differentiation.

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Section: Introductionmentioning

confidence: 99%

Differential expression of zinc transporters accompanies the differentiation of C2C12 myoblasts

Paskavitz

Quintana

Cangussu

et al. 2018

Journal of Trace Elements in Medicine and Biology

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“…Examples include: the inhibition of keratinocyte differentiation upon ZIP2 knock down (Inoue et al 2014); the systemic zinc deficiency caused by enterocyte-specific deletion of ZIP4 (Geiser et al 2012); the zinc-induced acute pancreatitis observed in pancreas-specific ZIP5 knockout mice (Geiser et al 2013); skeletal and connective tissue abnormalities caused by loss of murine ZIP13, which are also observed in human spondylodysplastic Ehlers-Danlos syndrome patients with mutations in ZIP13 (Fukada et al 2008); the deficits in learning and memory seen in mice lacking ZNT3 (Adlard et al 2010); and the loss of zinc-insulin crystals in the pancreatic beta cells of ZNT8 knockout mice (Wijesekara et al 2010). …”

Section: Introductionmentioning

confidence: 99%

Local and systemic effects of targeted zinc redistribution in Drosophila neuronal and gastrointestinal tissues

Richards

Burke

2015

Biometals

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While the effects of systemic zinc ion deficiency and toxicity on animal health are well documented, the impacts of localized, tissue-specific disturbances in zinc homeostasis are less well understood. Previously we have identified zinc dyshomeostasis scenarios caused by the targeted manipulation of zinc transport genes in the Drosophila eye. Over expression of the uptake transporter dZIP42C.1 (dZIP1) combined with knockdown of the efflux transporter dZNT63C (dZNT1) causes a zinc toxicity phenotype, as does over expression of dZIP71B or dZNT86D. However, all three genotypes result in different morphologies, responses to dietary zinc, and genetic interactions with the remaining zinc transport genes, indicating that each causes a different redistribution of zinc within affected cells. dZNT86D (eGFP) over expression generates a completely different phenotype, interpreted as a Golgi zinc deficiency. Here we assess the effect of each of these transgenes when targeted to a range of Drosophila tissues. We find that dZIP71B is a particularly potent zinc uptake gene, causing early developmental lethality when targeted to multiple different tissue types. dZNT86D over expression (Golgi-only zinc toxicity) is less deleterious, but causes highly penetrant adult cuticle, sensory bristle and wing expansion defects. The dZIP42C.1 over expression, dZNT63C knockdown combination causes only moderate adult cuticle defects and sensitivity to dietary zinc when expressed in the midgut. The Golgi-only zinc deficiency caused by dZNT86D (eGFP) expression results in mild cuticle defects, highly penetrant wing expansion defects and developmental lethality when targeted to the central nervous system and, uniquely, the fat bodies.

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“…The fact that embedded soluble ion-releasing nanoparticles can affect proliferation and migration is not surprising as h-KC migration was previously shown to be affected by the release of iron and zinc ions as specified in the introduction [11], [12], [13], [14], [15], [16]. While KC differentiation, ex vivo, was already described to be induced by topical applications of zinc [16], this parameter has to be studied further in order to supplement the potential effects of our system on the KC behavior.…”

Section: Biological Testingmentioning

confidence: 99%

“…While KC differentiation, ex vivo, was already described to be induced by topical applications of zinc [16], this parameter has to be studied further in order to supplement the potential effects of our system on the KC behavior. While KC rebuild the epidermis and enable the restoration of the homeostasis, FB are recruited on the wound site and proliferate in order to build the granulation tissue.…”

Section: Biological Testingmentioning

confidence: 99%

“…In parallel, the proliferation, migration and differentiation of keratinocytes (KC) contributes to the reepithelialisation of the skin. Hereby zinc was shown to take a part in the KC differentiation mechanisms [16]. Finally the scar tissues are remodelled by a turn over between degradation of type III collagen by MMPs and type I neocollagenesis, where respectively zinc and iron are imperative [11], [12], [13], [15].…”

Section: Introductionmentioning

confidence: 99%

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Water-based, surfactant-free cytocompatible nanoparticle-microgel-composite biomaterials – rational design by laser synthesis, processing into fiber pads and impact on cell proliferation

et al. 2017

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Abstract:This work highlights the laser-based aqueous synthesis and processing of nanocomposites, composed of zinc or iron nanoparticles embedded in a N-Vinylcaprolactam microgel matrix, with potential applicability as ion releasing fiber pads for wound healing. An in situ laser process for microgel synthesis is developed and optimized for high embedded nanoparticle yields, evaluating influences of laser repetition rate and monomer concentration. The impact of the nanoparticles on polymerization was increased by embedded zinc oxide nanoparticles, and reduced in the presence of iron oxide. Furthermore, TEM images verified that the nanoparticles were homogeneously embedded into the polymer matrix. The nanoparticle-loaded microgels were thermally stable up to 429°C, which ensures that the composites maintain their integrity after heat sterilization and during rapid prototyping by thermal polymer processing. The general suitability of the hydrogels as active biomaterial for wound healing was assessed in toxicity, cell proliferation and migration assays using human dermal fibroblasts and keratinocytes, where cytocompatibility was verified, while the proliferation was affected by the gel alone as well as the embedded nanoparticles. The hydrogels were processed to suit their use as a biomaterial for wound coverages via electrospinning resulting in a centimeter scale fully cytocompatible fiber pad with the nanoparticle-filled microgel capsules supported on the fiber's surface.

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ZIP2 Protein, a Zinc Transporter, Is Associated with Keratinocyte Differentiation

Cited by 66 publications

References 25 publications

Differential expression of zinc transporters accompanies the differentiation of C2C12 myoblasts

Differential expression of zinc transporters accompanies the differentiation of C2C12 myoblasts

Local and systemic effects of targeted zinc redistribution in Drosophila neuronal and gastrointestinal tissues

Water-based, surfactant-free cytocompatible nanoparticle-microgel-composite biomaterials – rational design by laser synthesis, processing into fiber pads and impact on cell proliferation

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