RESUMEN
Mild acidification caused by transcutaneous administration of carbon dioxide (CO2 ) has been reported to improve some epidermal skin impairments, such as desquamation and inflammation; however, its effects on dermal tissue remain unclear. Here, we examined the effect and mechanism of mild acidity on extracellular matrix (ECM) protein production in normal human dermal fibroblasts (NHDFs). To achieve this, the skin permeability of CO2 and its effect on intradermal pH were evaluated by treating reconstructed human skin equivalents (HSEs) with a CO2 -containing formulation. Additionally, NHDFs were cultured in a pH-adjusted medium (pH 6.5). CO2 successfully permeated HSEs and reduced the intradermal pH. Decreased extracellular pH activated CREB, upregulated TGF-ß1 expression, promoted the production of elastic and collagen fibres, and increased hyaluronan concentration in NHDFs. Additionally, the low pH-induced increase in TGF-ß1 expression was attenuated via the RNAi-mediated suppression of the expression of CREB1 and proton-sensing G protein-coupled receptors (GPCRs), including GPR4 and GPR65. Moreover, low pH-induced CREB activation was suppressed by the inhibition of the cAMP/PKA and PLC/PKC signalling pathways. Taken together, a CO2 -induced decrease in intradermal pH may promote ECM production in NHDFs via the upregulation of TGF-ß1 expression, which was mediated by the activation of the GPCR signalling pathway and CREB, indicating that CO2 could be used to treat ultraviolet radiation-induced photoaging, intrinsic ageing and ECM deterioration.
Asunto(s)
Dióxido de Carbono , Matriz Extracelular , Factor de Crecimiento Transformador beta1 , Humanos , Dióxido de Carbono/farmacología , Células Cultivadas , Matriz Extracelular/metabolismo , Fibroblastos/metabolismo , Concentración de Iones de Hidrógeno , Factor de Crecimiento Transformador beta1/metabolismo , Rayos UltravioletaRESUMEN
Cell migration-inducing hyaluronidase 1 (CEMIP), also known as hyaluronan (HA)-binding protein involved in HA depolymerization (HYBID), plays a role in HA degradation. CEMIP2, also known as transmembrane protein 2 (TMEM2), possessing a sequence similarity with HYBID, is reported as a hyaluronidase in mice. However, the expression of these molecules in osteoarthritic synovium and their involvement in HA degradation in synovial fluid (SF) from patients with knee osteoarthritis remain elusive. This study examined their expression in synovial tissue and the relationship with molecular weight of HA in SF in knee osteoarthritis patients. Quantification of mRNA demonstrated that HYBID expression is significantly (5.5-fold) higher in osteoarthritic synovium than in normal control synovium, whereas TMEM2 expression level is similar between the two groups. By immunohistochemistry, HYBID was localized mainly to CD68-negative and fibroblast-specific protein 1-positive synovial lining cells and sublining fibroblasts in osteoarthritic synovium. The mRNA expression levels of HYBID, but not TMEM2, in osteoarthritic synovium positively correlated with distribution of lower-molecular-weight HA with below 1000 kDa in SF. HA-degrading activity in osteoarthritic synovial fibroblasts was abrogated by siRNA-mediated knockdown of HYBID. Among the 12 factors examined, IL-6 significantly up-regulated the HYBID expression and HA-degrading activity in osteoarthritic synovial fibroblasts. These data suggest that HYBID overexpressed by IL-6-stimulated synovial fibroblasts is implicated in HA degradation in osteoarthritic synovium.
Asunto(s)
Fibroblastos/metabolismo , Ácido Hialurónico/metabolismo , Hialuronoglucosaminidasa/metabolismo , Proteínas de la Membrana/metabolismo , Osteoartritis de la Rodilla/metabolismo , Anciano , Femenino , Humanos , Masculino , Osteoartritis de la Rodilla/patología , Membrana Sinovial/metabolismo , Membrana Sinovial/patologíaRESUMEN
BACKGROUND: Establishing a noninvasive method to estimate skin damage immediately after ultraviolet (UV) exposure is required to minimize the anticipated severe symptoms triggered by early phase UV-induced reactions in the skin. To develop a suitable method, we focused on ultraweak photon emission (UPE) immediately after UV exposure to characterize the relationship of UPE to skin photodamage caused by the UV exposure. MATERIALS AND METHODS: Analysis of the correlation between UV-induced UPE and erythema formation characterized by skin redness was conducted in a clinical study. To clarify the source of UPE, time-dependent lipid oxidation was analyzed in human epidermal keratinocytes in vitro using a fluorescence indicator as well as the lipid hydroperoxide (LPO) assay. RESULTS: The average amount of UV-induced long-lasting UPE per second, especially from 1 to 3 minutes compared to other time periods after the UV radiation, increased in a dose-dependent manner and was highly correlated with the intensity of cutaneous redness 24 hours after UV exposure. In addition, cellular examinations elucidated that both the long-lasting UPE signals and the increased amounts of LPO 2 minutes after UV radiation were significantly suppressed by Trolox (a vitamin E derivative), which has been shown to inhibit UV-induced erythema formation in human skin. CONCLUSION: Long-lasting UPE generated between 1 and 3 minutes immediately after UV exposure, which is associated with LPO production, is a valuable indicator to estimate and/or avoid severe cutaneous photodamage.
Asunto(s)
Estrés Oxidativo , Piel , Humanos , Fotones , Piel/metabolismo , Rayos Ultravioleta/efectos adversosRESUMEN
Melanin in the epidermis is known to ultimately regulate human skin pigmentation. Recently, we exploited a phenotypic-based screening system composed of ex vivo human skin cultures to search for effective materials to regulate skin pigmentation. Since a previous study reported the potent inhibitory effect of metformin on melanogenesis, we evaluated several biguanide compounds. The unexpected effect of phenformin, once used as an oral anti-diabetic drug, on cutaneous darkening motivated us to investigate its underlying mechanism utilizing a chemical genetics approach, and especially to identify alternatives to phenformin because of its risk of severe lactic acidosis. Chemical pull-down assays with phenformin-immobilized beads were performed on lysates of human epidermal keratinocytes, and subsequent mass spectrometry identified 7-dehydrocholesterol reductase (DHCR7). Consistent with this, AY9944, an inhibitor of DHCR7, was found to decrease autophagic melanosome degradation in keratinocytes and to intensely darken skin in ex vivo cultures, suggesting the involvement of cholesterol biosynthesis in the metabolism of melanosomes. Thus, our results validated the combined utilization of the phenotypic screening system and chemical genetics as a new approach to develop promising materials for brightening/lightening and/or tanning technologies.
Asunto(s)
Queratinocitos/metabolismo , Melanocitos/metabolismo , Melanosomas/metabolismo , Fenformina/farmacología , Pigmentación de la Piel/efectos de los fármacos , Colesterol/biosíntesis , Femenino , Humanos , Queratinocitos/citología , Masculino , Melanocitos/citología , Oxidorreductasas actuantes sobre Donantes de Grupo CH-CH/antagonistas & inhibidores , Oxidorreductasas actuantes sobre Donantes de Grupo CH-CH/metabolismo , Diclorhidrato de trans-1,4-Bis(2-clorobenzaminometil)ciclohexano/farmacologíaRESUMEN
Ultraviolet (UV)-induced skin photoaging is caused by qualitative and quantitative degradation of dermal extracellular matrix components such as collagen and elastic fibers. Elastic fibers are important for maintaining cutaneous elasticity, despite their small amount in the skin. Previously, microfibril-associated protein 4 (MFAP-4), which is downregulated in photoaging dermis, has been found to be essential for elastic fiber formation by interaction with both fibrillin-1 and elastin, which are core components of elastic fiber. In addition, enhanced cutaneous MFAP-4 expression in a human skin-xenografted murine photoaging model protects against UV-induced photodamage accompanied by the prevention of elastic fiber degradation and aggravated elasticity. We therefore hypothesized that the upregulation of MFAP-4 in dermal fibroblasts may more efficiently accelerate elastic fiber formation. We screened botanical extracts for MFAP-4 expression-promoting activity in normal human dermal fibroblasts (NHDFs). We found that rosemary extract markedly promotes early microfibril formation and mature elastic fiber formation along with a significant upregulation of not only MFAP-4 but also fibrillin-1 and elastin in NHDFs. Furthermore, rosmarinic acid, which is abundant in rosemary extract, accelerated elastic fiber formation via upregulation of transforming growth factor ß-1. This was achieved by the induction of cAMP response element-binding protein phosphorylation, demonstrating that rosmarinic acid represents one of the active ingredients in rosemary extract. Based on the findings in this study, we conclude that rosemary extract and rosmarinic acid represent promising materials that exert a preventive or ameliorative effect on skin photoaging by accelerating elastic fiber formation.
Asunto(s)
Cinamatos , Depsidos , Tejido Elástico , Elastina , Fibrilina-1 , Fibroblastos , Extractos Vegetales , Ácido Rosmarínico , Envejecimiento de la Piel , Humanos , Fibroblastos/efectos de los fármacos , Fibroblastos/metabolismo , Fibroblastos/efectos de la radiación , Depsidos/farmacología , Fibrilina-1/metabolismo , Cinamatos/farmacología , Extractos Vegetales/farmacología , Elastina/metabolismo , Tejido Elástico/efectos de los fármacos , Tejido Elástico/metabolismo , Envejecimiento de la Piel/efectos de los fármacos , Envejecimiento de la Piel/efectos de la radiación , Células Cultivadas , Rosmarinus/química , Regulación hacia Arriba/efectos de los fármacos , Proteína de Unión a Elemento de Respuesta al AMP Cíclico/metabolismo , Piel/efectos de los fármacos , Piel/efectos de la radiación , Piel/citología , Piel/patología , Piel/metabolismo , Dermis/citología , Dermis/efectos de los fármacos , Dermis/metabolismo , Rayos Ultravioleta/efectos adversos , Proteínas de la Matriz Extracelular/metabolismo , AdipoquinasRESUMEN
The content and distribution of melanin in the epidermis determines the wide variety of skin colors associated with ethnic/racial diversity. Although it was previously reported that qualitative changes in keratinocyte-derived exosomes regulate melanocyte pigmentation in vitro, their practical involvement, especially in skin color development in vivo, has remained unclear. To address this unexplained scientific concern, the correlation of epidermal exosomes isolated from human skin tissues with melanosomal protein expression levels was demonstrated in this study for the first time. After confirming the quantitative effect of human keratinocyte-derived exosomes on human melanocyte activation, even in the absence of ultraviolet B (UV-B) exposure, the impact of exosomes secreted from UV-B-irradiated keratinocytes on melanogenesis was consistently detected, which suggests their constitutive role in regulating cutaneous pigmentation. Additionally, both a specific exosome secretion inducer and a suppressor were consistently found to significantly control melanin synthesis in a co-culture system composed of keratinocytes and melanocytes as well as in an ex vivo skin culture system. These results suggest that quantitative changes, in addition to already known qualitative changes, in exosomes secreted from human epidermal keratinocytes homeostatically regulate melanogenic activity in a paracrine manner, which leads to skin color determination.
Asunto(s)
Exosomas/metabolismo , Queratinocitos/metabolismo , Melaninas/biosíntesis , Melanosomas/metabolismo , Comunicación Paracrina , Pigmentación de la Piel , Adulto , Compuestos de Anilina/farmacología , Compuestos de Bencilideno/farmacología , Técnicas de Cocultivo , Dihidroxifenilalanina/metabolismo , Epidermis/metabolismo , Exosomas/ultraestructura , Femenino , Flavonoides/farmacología , Hemostasis , Humanos , Queratinocitos/efectos de los fármacos , Queratinocitos/efectos de la radiación , Melanocitos/efectos de los fármacos , Factor de Transcripción Asociado a Microftalmía/metabolismo , Monofenol Monooxigenasa/metabolismo , Norbornanos/farmacología , Fosfatidilinositoles/farmacología , Inhibidores de Fosfodiesterasa/farmacología , Inhibidores de Proteínas Quinasas/farmacología , Transducción de Señal/efectos de los fármacos , Pigmentación de la Piel/efectos de los fármacos , Tiocarbamatos/farmacología , Técnicas de Cultivo de Tejidos , Rayos Ultravioleta , Regulación hacia Arriba/efectos de los fármacos , Antígeno gp100 del Melanoma/metabolismoRESUMEN
BACKGROUND: Hyaluronan (HA) is an essential constituent of extracellular matrix in the skin. HA reduction in the dermis and overexpression of HYBID (KIAA1199), a key molecule for HA degradation in skin fibroblasts, are implicated in facial skin wrinkling. AIMS: We aimed to obtain anti-wrinkle agent(s) by screening for inhibition of HYBID-mediated HA degradation. METHODS: Various plant extracts were screened for inhibition of HA degradation in HYBID-stable transfectants in HEK293 (HYBID/HEK293). Inhibition of HA-degrading activity and HYBID mRNA and protein expression by Geranium thunbergii extract was studied in skin fibroblasts and HYBID/HEK293 cells. Size distribution of newly produced HA was evaluated by preparing metabolically radiolabeled HA in skin fibroblasts. A double-blind, randomized, and placebo-controlled study was performed in healthy Japanese women (n = 21) by topically treating each side of the face with a lotion formulated with G. thunbergii extract or placebo for 8 weeks. RESULTS: Among the plant extracts tested, only G. thunbergii extract abolished HA depolymerization in skin fibroblasts and HYBID/HEK293 cells by down-regulating HYBID mRNA and protein expression and by inhibiting HYBID-mediated HA-degrading activity. Although untreated skin fibroblasts produced polydispersed HA, G. thunbergii extract-treated cells produced high-molecular-weight HA. Treatment with G. thunbergii extract-formulated lotion significantly improved skin elasticity and reduced skin wrinkling scores at the outer eye corner compared with the placebo formulation. CONCLUSIONS: Geranium thunbergii extract inhibited HYBID-mediated HA degradation in vitro and showed anti-wrinkle activity in vivo accompanying the improvement in skin elasticity. Our study provides a possible strategy for anti-wrinkle care through inhibition of HYBID-mediated HA degradation.
Asunto(s)
Geranium/química , Ácido Hialurónico/metabolismo , Hialuronoglucosaminidasa/antagonistas & inhibidores , Extractos Vegetales/administración & dosificación , Envejecimiento de la Piel/efectos de los fármacos , Administración Cutánea , Adulto , Método Doble Ciego , Evaluación Preclínica de Medicamentos , Elasticidad/efectos de los fármacos , Cara , Femenino , Fibroblastos/efectos de los fármacos , Fibroblastos/metabolismo , Células HEK293 , Voluntarios Sanos , Humanos , Hialuronoglucosaminidasa/metabolismo , Persona de Mediana Edad , Piel/citología , Piel/efectos de los fármacos , Piel/metabolismo , Resultado del TratamientoRESUMEN
The homeodomain-containing protein Hex acts as an activator as well as a repressor of transcription in animals. While its repression domain has been mapped to the amino-terminal region, the activation domain has never been identified. Here, we show that the homeodomain and the acidic carboxyl-terminal region are necessary for full activation of the sodium-dependent bile acid cotransporter gene promoter in a cell type-independent manner, suggesting that the carboxyl-terminal region comprising residues 197 to 271 functions as the activation domain. In addition, we observed that a Hex mutant without this activation domain acts as a dominant-negative mutant as to the transactivating function of Hex.
Asunto(s)
Proteínas de Homeodominio/genética , Activación Transcripcional , Animales , Secuencia de Bases , Ácidos y Sales Biliares/metabolismo , Proteínas de Homeodominio/metabolismo , Humanos , Luciferasas/metabolismo , Datos de Secuencia Molecular , Mutación , Regiones Promotoras Genéticas/fisiología , Proteínas Recombinantes de Fusión/genética , Proteínas Recombinantes de Fusión/metabolismo , Sodio/farmacología , Factores de Transcripción/fisiología , Células Tumorales CultivadasRESUMEN
Hex is one of the homeobox genes suggested to be important for hematopoietic cell differentiation. However, its biological function and mechanism of transcriptional regulation in hematopoietic cells remain elusive. We have identified the regulatory region necessary for transcription of the mouse Hex gene in K562 leukemia cells through transient reporter assays involving various deletion mutants. This region, comprising +775 to +1177 in the first intron, had enhancer-like properties and showed high activity in other hematopoietic cell lines such as U937, HEL, and RAW264.7, but little activity in other Hex-expressing cell lines such as MH(1)C(1) and H4IIE hepatoma cells, suggesting that this region functions as a hematopoietic cell-specific enhancer-like element. Binding site mutation of hematopoietic transcription factors, such as GATAs and c-Myb present in the enhancer-like element, significantly decreased the luciferase reporter gene expression in K562 cells. Electrophoretic mobility shift assays showed that GATA-1, GATA-2, or c-Myb actually binds to three of these putative binding sites, and also suggested that several unidentified factors might interact with the enhancer-like element. Overexpression of GATA-1, GATA-2, or c-Myb stimulated the enhancer-like activity via these three binding sites. Thus, we conclude that Hex expression in hematopoietic cells is mainly regulated by GATA-1, GATA-2, and c-Myb via this intronic enhancer-like element.
Asunto(s)
Elementos de Facilitación Genéticos , Genes Homeobox , Sistema Hematopoyético/citología , Proteínas de Homeodominio/genética , Animales , Secuencia de Bases , Sitios de Unión , Diferenciación Celular , Línea Celular , Ensayo de Cambio de Movilidad Electroforética/métodos , Genes Reporteros , Sistema Hematopoyético/metabolismo , Humanos , Células K562 , Luciferasas/genética , Luciferasas/metabolismo , Ratones , Mutación , Proteínas Proto-Oncogénicas c-myb/metabolismo , Transactivadores/metabolismo , Factores de Transcripción/metabolismoRESUMEN
The signaling of stem cell factor (SCF) through its receptor Kit is known to play an important role in regulating cutaneous melanogenesis. In the course of UVB-induced pigmentation, the expression of membrane-bound SCF by epidermal keratinocytes is upregulated at an early phase and subsequently activates neighboring melanocytes via their Kit receptors. In order to identify effective skin-lightening materials, we screened botanical extracts to determine their abilities to diminish Kit expression in melanocytes. A Platycodon root extract was consequently found to have a remarkable inhibitory activity on Kit expression. When the extract was applied to three-dimensional human skin substitutes in vitro and to human skin in vivo after UVB irradiation, their pigmentation was significantly reduced, confirming the substantial contribution of the suppression of SCF/Kit signaling to preventing or inhibiting melanin synthesis. These data demonstrate that a Platycodon root extract is a promising material for a skin-lightening product to improve pigmentation-related diseases.
Asunto(s)
Platycodon , Proteínas Proto-Oncogénicas c-kit/metabolismo , Preparaciones para Aclaramiento de la Piel/farmacología , Pigmentación de la Piel/efectos de los fármacos , Animales , Células Cultivadas , Humanos , Melanocitos/efectos de los fármacos , Melanocitos/metabolismo , Extractos Vegetales/química , Extractos Vegetales/farmacología , Raíces de Plantas/química , Factor de Células Madre/farmacología , Rayos UltravioletaRESUMEN
BACKGROUND: Tyrosinase, the rate-limiting enzyme required for melanin production, has been targeted to develop active brightening/lightening materials for skin products. Unexpected depigmentation of the skin characterized with the diverse symptoms was reported in some subjects who used a tyrosinase-competitive inhibiting quasi-drug, rhododendrol. OBJECTIVE: To investigate the mechanism underlying the depigmentation caused by rhododendrol-containing cosmetics, this study was performed. METHODS: The mechanism above was examined using more than dozen of melanocytes derived from donors of different ethnic backgrounds. The RNAi technology was utilized to confirm the effect of tyrosinase to induce the cytotoxicity of rhododendrol and liquid chromatography-tandem mass spectrometry was introduced to detect rhododendrol and its metabolites in the presence of tyrosinase. RESULTS: Melanocyte damage was related to tyrosinase activity at a certain threshold. Treatment with a tyrosinase-specific siRNA was shown to dramatically rescue the rhododendrol-induced melanocyte impairment. Hydroxyl-rhododendrol was detected only in melanocytes with higher tyrosinase activity. When an equivalent amount of hydroxyl-rhododendrol was administered, cell viability was almost equally suppressed even in melanocytes with lower tyrosinase activity. CONCLUSION: The generation of a tyrosinase-catalyzed hydroxyl-metabolite is one of the causes for the diminishment of the melanocyte viability by rhododendrol.
Asunto(s)
Blanqueadores/química , Butanoles/química , Melanocitos/efectos de los fármacos , Monofenol Monooxigenasa/metabolismo , Supervivencia Celular , Humanos , Hipopigmentación/metabolismo , Melaninas/biosíntesis , Melanocitos/citología , Monofenol Monooxigenasa/antagonistas & inhibidores , Monofenol Monooxigenasa/química , ARN Interferente Pequeño/metabolismo , Piel/metabolismo , Pigmentación de la Piel/efectos de los fármacosRESUMEN
UVB-induced cutaneous photodamage/photoaging is characterized by qualitative and quantitative deterioration in dermal extracellular matrix (ECM) components such as collagen and elastic fibers. Disappearance of microfibrillar-associated protein 4 (MFAP-4), a possible limiting factor for cutaneous elasticity, was documented in photoaged dermis, but its function is poorly understood. To characterize its possible contribution to photoprotection, MFAP-4 expression was either augmented or inhibited in a human skin xenograft photodamage murine model and human fibroblasts. Xenografted skin with enhanced MFAP-4 expression was protected from UVB-induced photodamage/photoaging accompanied by the prevention of ECM degradation and aggravated elasticity. Additionally, remarkably increased or decreased fibrillin-1-based microfibril development was observed when fibroblasts were treated with recombinant MFAP-4 or with MFAP-4-specific siRNA, respectively. Immunoprecipitation analysis confirmed direct interaction between MFAP-4 and fibrillin-1. Taken together, our findings reveal the essential role of MFAP-4 in photoprotection and offer new therapeutic opportunities to prevent skin-associated pathologies.
Asunto(s)
Proteínas Portadoras/metabolismo , Proteínas de la Matriz Extracelular/metabolismo , Glicoproteínas/metabolismo , Piel/metabolismo , Animales , Proteínas Portadoras/antagonistas & inhibidores , Proteínas Portadoras/genética , Proteínas Portadoras/farmacología , Elasticidad , Proteínas de la Matriz Extracelular/antagonistas & inhibidores , Proteínas de la Matriz Extracelular/genética , Proteínas de la Matriz Extracelular/farmacología , Fibrilina-1 , Fibrilinas , Glicoproteínas/antagonistas & inhibidores , Glicoproteínas/genética , Glicoproteínas/farmacología , Homeostasis , Humanos , Ratones , Proteínas de Microfilamentos/metabolismo , ARN Interferente Pequeño/genética , Proteínas Recombinantes/farmacología , Piel/efectos de los fármacos , Piel/efectos de la radiación , Envejecimiento de la Piel/fisiología , Fenómenos Fisiológicos de la Piel , Trasplante Heterólogo , Rayos Ultravioleta/efectos adversosRESUMEN
The signaling of stem cell factor (SCF) and its receptor KIT (membrane-bound KIT; m-KIT) plays an important role in melanocyte development, survival, proliferation, and melanogenesis. It has been demonstrated in other systems that a soluble form of m-KIT released from the cell surface (s-KIT) regulates SCF signaling, although there have been no reports pertaining to the existence and the biological role of s-KIT in melanocytes. In this study, we therefore examined the involvement of s-KIT in melanogenesis. Western blotting analysis revealed that treatment with phorbol 12-myristate-13-acetate (PMA) or 4-aminophenylmercuric acetate (APMA) induced s-KIT production in cultured human melanocytes. Inhibitors of tumor necrosis factor-alpha-converting enzyme (TACE) and metalloproteinases (MMPs) muted this release of s-KIT into the media. Human recombinant s-KIT added to melanocytes inhibited SCF-induced phosphorylation of m-KIT, resulting in suppression of SCF-induced melanogenesis. Additionally, APMA-induced s-KIT production abolished SCF-induced melanogenesis as effectively as a KIT-neutralizing antibody. Concomitantly, APMA and TACE inhibitors significantly decreased and increased melanin synthesis, respectively, in an in vitro skin model. Taken together, these findings provided an insight into the elaborate mechanism of SCF/m-KIT signaling in human melanocytes and suggested that production of s-KIT contributes to the regulation of human skin pigmentation. Journal of Investigative Dermatology (2008) 128, 1763-1772; doi:10.1038/jid.2008.9; published online 31 January 2008.
Asunto(s)
Melaninas/biosíntesis , Melanocitos/metabolismo , Proteínas Proto-Oncogénicas c-kit/fisiología , Factor de Células Madre/antagonistas & inhibidores , Proteínas ADAM/fisiología , Proteína ADAM17 , Células Cultivadas , Humanos , Metaloproteinasas de la Matriz/fisiología , Fosforilación , Transducción de Señal , Piel/metabolismo , Pigmentación de la Piel , Factor de Células Madre/fisiologíaRESUMEN
A new nickel polyborate, NiB12O14(OH)10 was synthesized using boric acid as a flux. This material has two-dimensional borate layers with a quasi-square lattice of Ni2+. The Ni2+ ions locate in the plane of the two-dimensional layer, bridged through BnO(n+1) chains in the plane and connected with the three-membered ring borate groups out of the plane. The dc and ac magnetic susceptibility, magnetization and specific heat measurements show that this material undergoes a weak ferromagnetic phase transition at Tc = 5.8 K. At T < Tc, a metamagnetic phase transition is observed at about 5 T, associated by a spin-flop, suggesting the ferromagnetic ordering is induced by an antiferromagnetic interaction. A broad maximum in the ac susceptibility at TM = 23-24 K indicates an intermediate short-range ordering.