Bibliografías temáticas / RANKL

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Literatura académica sobre el tema "RANKL"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 19 de febrero de 2023

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Artículos de revistas sobre el tema "RANKL"

1

Stejskal, David, Josef Bartek, Radmila Pastorkova, Viktor Ruzicka, Ivo Oral y Dalimil Horalik. "OSTEOPROTEGERIN, RANK, RANKL". Biomedical Papers 145, n.º 2 (1 de diciembre de 2001): 61–64. http://dx.doi.org/10.5507/bp.2001.013.

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Nagy, Vanja y Josef M. Penninger. "The RANKL-RANK Story". Gerontology 61, n.º 6 (2015): 534–42. http://dx.doi.org/10.1159/000371845.

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Sale, Craig, David C. Hughes, Julie P. Greeves, Trent Stellingwerff, Craig Ranson, William D. Fraser y Ian Varley. "Rankl/rank/opg Pathway". Medicine & Science in Sports & Exercise 46 (mayo de 2014): 268. http://dx.doi.org/10.1249/01.mss.0000493990.33112.e2.

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Hanada, Reiko, Toshikatsu Hanada, Verena Sigl, Daniel Schramek y Josef M. Penninger. "RANKL/RANK—beyond bones". Journal of Molecular Medicine 89, n.º 7 (29 de marzo de 2011): 647–56. http://dx.doi.org/10.1007/s00109-011-0749-z.

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Boyce, Brendan F. y Lianping Xing. "The RANKL/RANK/OPG pathway". Current Osteoporosis Reports 5, n.º 3 (septiembre de 2007): 98–104. http://dx.doi.org/10.1007/s11914-007-0024-y.

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Hofbauer, L. C. "Bedeutung des RANK/RANKL/OPGSignalwegs für den Knochenstoffwechsel". Osteologie 19, n.º 04 (2010): 354–57. http://dx.doi.org/10.1055/s-0037-1619956.

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ZusammenfassungDie meisten Knochenstoffwechselkrankheiten sind nach heutigem Kenntnisstand Folge einer gesteigerten Knochenresorption durch Osteoklasten. In den letzten 15 Jahren wurden die entscheidenden molekularen und zellulären Regulatoren der Zellbiologie von Osteoklasten entschlüsselt. Receptor activator of NF-κB-Ligand (RANKL) und sein Rezeptor RANK sind essenziell für die Differenzierung und Aktivierung von Osteoklasten und für eine normale Knochenresorption absolut erforderlich. Die Wirkungen von RANKL werden durch den endogenen löslichen Rezeptorantagonisten Osteoprotegerin (OPG) neutralisiert. Die Balance zwischen RANKL und OPG ist im Östrogenmangel oder bei systemischer Glukokortikoidtherapie gestört und dadurch wird der RANKL/OPG-Quotient erhöht, was zum beschleunigten Knochenverlust führt. Angesichts der fundamentalen Rolle des RANKL/RANK/OPG-Signalwegs im Knochenstoffwechsel ist mittlerweile RANKL zum therapeutischen Target geworden. Strategien der RANKL-Blockade wurden in verschiedenen Tiermodellen klinisch relevanter Knochenerkrankungen erfolgreich eingesetzt. Dazu zählen verschiedene Osteoporoseformen sowie Knochenverlust infolge systemischer Entzündung und Tumoren.
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7

Hooshiar, Saeedeh Hosseini, Mohammad Tobeiha y Sadegh Jafarnejad. "Soy Isoflavones and Bone Health: Focus on the RANKL/RANK/OPG Pathway". BioMed Research International 2022 (25 de octubre de 2022): 1–10. http://dx.doi.org/10.1155/2022/8862278.

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Bone remodels via resorption and formation, two phenomena that continuously occur in bone turnover. The RANKL/RANK/OPG pathway is one of the several mechanisms that affect bone turnover. The RANKL/OPG ratio has a substantial role in bone resorption. An imbalance between formation and resorption is related to an increased RANKL/OPG balance. OPG, a member of this system, can bind to RANKL and suppress RANK-RANKL interaction, and subsequently, inhibit further osteoclastogenesis. The serum levels of RANKL and OPG in the bone microenvironment are vital for osteoclasts formation. The RANK/RANKL/OPG system plays a role in the pathogenesis of bone disorders. This system can be considered a new treatment target for bone disorders. Soy isoflavones affect the RANK/RANKL/OPG system through numerous mechanisms. Soy isoflavones decrease RANKL levels and increase OPG levels. Therefore, isoflavones improve bone metabolism and decrease bone resorption. Soy isoflavones decrease serum markers of bone resorption and improve bone metabolism. However, while the available data are promising, the results of several studies reported no change in RANKL and OPG levels with isoflavones supplementation. In this regard, current evidence is insufficient for conclusive approval of the efficacy of isoflavones on RANKL/RANK/OPG and further research, including animal and human studies, are needed to confirm the effect of soy isoflavones on the RANKL/RANK/OPG pathway. This study was a review of available evidence to determine the role of isoflavones in bone hemostasis and the RANK/RANKL/OPG pathway. The identification of the effects of isoflavones on the RANKL/RANK/OPG pathway directs future studies and leads to the development of effective treatment strategies for bone disorders.
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8

Aslan, Figen y Ülkü Küçük. "RANK and RANKL Expression in Salivary Gland Tumors". Ear, Nose & Throat Journal 99, n.º 7 (11 de junio de 2020): 475–80. http://dx.doi.org/10.1177/0145561320930640.

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Objectives: The pathogenesis and molecular basis of salivary gland tumors (SGT) are not well understood. We investigated the expression of receptor activator of nuclear factor κB (RANK) and RANK ligand (RANKL) in benign and malignant SGTs and their relationship with clinicopathological features. Methods: Fifty malignant and 38 benign SGTs were analyzed in this study. We evaluated the correlation between RANK and RANKL expression and benign and malignant tumors, as well as the correlation between clinicopathological prognostic parameters and RANK and RANKL expression. Results: Receptor activator of nuclear factor κB was positive in 82% (41) malignant SGTs and in 34.2% (13) benign SGTs. Receptor activator of nuclear factor κB ligand was expressed in 28% (14) malignant and 5.3% (2) benign tumors. Receptor activator of nuclear factor κB and RANKL expression were significantly different between benign and malignant SGTs ( P < .001, P = .006, respectively). However, a relationship was not found between positive expression of RANK or RANKL and clinicopathological features. Conclusions: In our study, RANK and RANKL expression was found to be higher in malignant SGTs compared to benign SGTs and RANK was more sensitive than RANKL. In addition, RANK and RANKL expression was higher in some malignant histological subtypes. Based on these results, we think that RANK and RANKL expression in SGTs and its potential as a target for treatment should continue to be investigated.
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9

Xing, Lianping, Edward M. Schwarz y Brendan F. Boyce. "Osteoclast precursors, RANKL/RANK, and immunology". Immunological Reviews 208, n.º 1 (diciembre de 2005): 19–29. http://dx.doi.org/10.1111/j.0105-2896.2005.00336.x.

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Boyce, Brendan F. y Lianping Xing. "Biology of RANK, RANKL, and osteoprotegerin". Arthritis Research & Therapy 9, Suppl 1 (2007): S1. http://dx.doi.org/10.1186/ar2165.

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Tesis sobre el tema "RANKL"

1

Navet, Benjamin. "Homéogènes Dlx, signalisation RANK/RANKL et ostéosarcomes". Thesis, Nantes, 2016. http://www.theses.fr/2016NANT1018/document.

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L’ostéosarcome (OS), plus fréquente des tumeurs osseuses primitives malignes, se caractérise par une croissance ostéoïde parfois associée à une ostéolyse. Malgré les avancées thérapeutiques, le taux de survie reste faible (30 % à 5 ans si métastases ou chimiorésis-tances). De nouvelles approches thérapeutiques ciblant la cellule tumorale et son environnement sont néces-saires. Les travaux présentés se sont intéressés aux poten-tiels facteurs pro-tumoraux que sont les gènes Dlx et à une signalisation clé de l’environnement osseux (RANKL/RANK) susceptible d’influer l’agressivité tumo-rale. L’OS étant une tumeur ostéoblastique, la famille Dlx a été choisie, car impliquée dans l’ostéoblasto-genèse, et la signalisation RANKL/RANK, car voie car-dinale du couplage entre ostéoblastes et ostéoclastes. De plus un lien entre Dlx et signalisation RANK était suspecté. Les gènes Dlx1, Dlx4 et Rank non-exprimés dans l’ostéoblaste sain le sont dans les lignées d’OS. Des modulations d’expression des Dlx et de Rank ont été réalisées afin d’en évaluer l’impact sur les cellules tumo-rales. L’implication de la signalisation RANK/RANKL dans le microenvironnement tumoral a été analysée. La perturbation du remodelage est en faveur de la tumeur en participant à l’établissement d’un cercle vicieux entre la tumeur et l’environnement. Les travaux ont établi l’implication des Dlx, surtout Dlx4 pour lequel un nouveau transcrit codant a été ca-ractérisé. Cependant des études supplémentaires sont nécessaires. Concernant la signalisation RANK/RANKL, il s’avère qu’au-delà du cercle vicieux, important au stade d’initiation tumorale, l’expression de RANK par la tumeur s’avère être un facteur pro-métastatique
Osteosarcoma (OS), the most common malignant primary bone tumor, is characterized by an osteoid formation occasionally associated with osteolysis. De-spite therapeutic advances, the 5-years survival rate remains low (30% in case of metastasis or drug-resistance). New therapeutic approaches targeting the tumor cell and its environment are needed. Presented studies focused on potential pro-tumor factors namely Dlx genes and a key signaling pathway of the bone environment (RANKL / RANK) that may influence tumor aggressiveness. The OS is an osteo-blastic tumor and Dlx family was chosen due to its in-volvement in osteoblastogenesis. RANKL / RANK path-way was selected as it constitutes a main element in the coupling between osteoblasts and osteoclasts. A link between Dlx genes and RANK signaling was suspected. Dlx1, Dlx4 and Rank genes are not normally ex-pressed in osteoblasts but are present in the OS cell lines. Dlx and Rank expression modulations were real-ized to assess the impact on tumor cells. RANK / RANKL signaling involvement in the tumor microenvi-ronment was analyzed. Disruption of remodeling is in favor of the tumor taking part in the establishment of a vicious circle between tumor and environment. This work established the involvement of Dlx, espe-cially DLX4 to which a new coding transcript has been characterized. However, additional studies are needed. Regarding the RANK / RANKL signaling, it turns out that beyond the vicious circle, leading to tumor initiation stage, the RANK expression by the tumor proves to be pro-metastatic elements
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2

Yoskovitz, Guy. "Genetic Polymorphisms of RANK, RANKL and their relation to osteoporosis (Polimorfismos genéticos de RANK y RANKL y su relación con la osteoporosis)". Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/98294.

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Osteoporosis is a systemic skeletal disorder and the most common metabolic bone disease. It is recognized as one of the most prevalent problems facing postmenopausal women in western society. The World Health Organization definition of osteoporosis uses bone mineral density (BMD) measurements as the gold standard. The genetic complexity of BMD is incompletely defined. Bone turnover, also called bone remodelling, is a lifelong process that refers to the entire cycle of bone resorption and formation, which determines BMD. In general, the cell biology of an adult bone includes 3 cell types, among others, that have opposite functions: osteoblasts produce the extracellular matrix that becomes mineralized; osteoclasts are responsible for the resorptive actions; and osteocytes are involved in the regulation of both resorption and formation (and are even claimed to dominate the process). A complex signal system between these 3 cell types balances their activities to avoid any over-creation or loss of bone tissue. The bone remodelling equilibrium is in part dominated by a set of protein reactions known as the RANK/RANKL/OPG system. The special importance of the Receptor Activator of NF-kappa-B (RANK) and its interaction with its ligand (RANKL) is that the RANK/RANKL complex is one of the main triggers of osteoclast differentiation and survival. Hence, in-depth analysis of variants in these 2 genes may contribute to the understanding of the genetics of BMD. This study had 4 main objectives: (1) association analysis of putative functional SNPs in evolutionary conserved regions of the RANK and RANKL genes with BMD and the occurrence of fractures in our cohort (BARCOS). (2) Replication of previously associated SNPs, in the BARCOS cohort (3) In-silico study followed by in-vitro functional experiments of the BMD-associated SNP(s) in order to reveal its (their) role(s) in the pathological process of osteoporosis and (4) Characterization of the human RANKL promoter and regulatory regions in-silico and in-vitro. We replicated the association of SNP rs9594738, a genetic variant at 184 kb upstream to RANKL gene, with BMD. Statistical analysis for other SNPs in the RANKL gene failed to be associated with osteoporotic phenotypes. The functional experiments’ results demonstrate that this region surrounding rs9594738, between AKAP11 and RANKL, has the capacity to regulate RANKL, with different effects on its expression in the presence or absence of vitamin D. These results suggest that it may play a role in the RANK/RANKL/OPG equilibrium, and might explain the association between the SNPs in this region and BMD. A transcript of minimum 300 bp (with rs9594738 in a central position) has been detected in this region. The existence of this RNA segment suggests its involvement in alternative functions of the region. We also identified 2 SNPs in the RANK 3’UTR (rs78326403 and rs884205) that are associated with low trauma fractures in our cohort. SNP rs78326403 is associated with wrist/forearm fractures, while SNP rs884205 is associated with spine fractures. In addition, we observed a significant interaction between rs78326403 and the RANKL BMD-associated SNP (rs9594738), highlighting the relevance of both microarchitecture and low BMD as genetically determined predictors of fracture risk that should be assessed using multiple techniques. To conclude, our results highlight the importance of the region between AKAP11 and RANKL on RANKL transcription regulation and suggest that it may play an important role in the RANK/RANKL/OPG equilibrium. Furthermore, the site-dependent associations in the RANK gene might be clinically relevant in the future to better profile a more specific approach to the different types of fractures, both to better understand their underlying mechanisms and to search for site-specific therapeutic strategies.
La osteoporosis es la enfermedad metabólica ósea más frecuente. Está definida como un trastorno esquelético sistémico caracterizado por una disminución de la densidad mineral ósea (DMO) y alteraciones en la microarquitectura del tejido óseo, con un consecuente incremento de la fragilidad ósea y del riesgo de fractura. Su complejidad genética permanece incompletamente definida. La DMO viene marcada por un remodelado óseo basado en ciclos de resorción y formación que suceden a lo largo de toda la vida del organismo. Este proceso, está regulado en parte por un conjunto de reacciones proteicas pertenecientes al sistema conocido como RANK/RANKL/OPG. La especial importancia de RANK, así como la interacción de éste con su ligando RANKL, recae en el hecho que, son factores clave tanto en el desencadenamiento de la diferenciación como de la supervivencia osteoclástica. El estudio se centra en el análisis detallado de variantes pertenecientes a ambos genes, seguido del estudio funcional correspondiente. Se ha replicado la asociación del SNP rs9594738 con la DMO, una variante genética localizada a 184 kb 5' del gen RANKL. Los resultados del estudio funcional muestran que la región que engloba dicha variante actúa como un regulador distal de RANKL, ejerciendo efectos en su expresión que varían en presencia ó ausencia de vitamina D. Además, se identificaron dos SNPs (rs78326403 y rs884205) en el 3’UTR de RANK, asociados con fracturas por bajo traumatismo en nuestra cohorte. Por último, una interacción significativa entre rs78326403 y rs9594738 en la determinación del riesgo de fractura, pone de relieve la importancia de la DMO baja y de la microarquitectura como predictores genéticamente determinados del riesgo de fractura que se deben evaluar con el uso de diversas técnicas.
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3

Hamoudi, Dounia. "Implication de la voie RANK/RANKL/OPG dans la physiopathologie musculaire et potentiel thérapeutique de l’anti-RANKL pour la dystrophie musculaire de Duchenne". Doctoral thesis, Université Laval, 2021. http://hdl.handle.net/20.500.11794/69507.

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La dystrophie musculaire de Duchenne (DMD) est une maladie génétique neuromusculaire provoquée par des mutations du gène codant pour la dystrophine situé sur le chromosome Xp21. L'absence de cette protéine membranaire engendre une dégénérescence progressive des cellules, une augmentation de la concentration du calcium intracellulaire, des dommages oxydatifs, inflammatoires et ultimement une fibrose musculaire. Les patients souffrent également de plusieurs autres anomalies dont les plus importantes sont la cardiomyopathie et l'ostéoporose. Il n'y a actuellement aucune stratégie curative pour la DMD. Les corticostéroïdes sont prescrits pour prolonger la mobilité et l'espérance de vie, mais sont associés à une ostéotoxicité élevée. Bien qu'il existe une association entre l'ostéoporose et la dégénérescence musculaire, nous avons été les premiers à étudier le rôle du récepteur-activateur du facteur nucléaire kB (RANK), son ligand RANKL et du récepteur soluble ostéoprotégérine (OPG), principaux régulateurs du remodelage osseux, dans le contexte des maladies musculaires. Nos travaux antérieurs montrent que les myotubes différenciés secrètent l'OPG, expriment le récepteur RANK à leurs surfaces et dans le contexte de DMD l'expression de l'ARNm de RANK est 4 fois plus élevée dans les muscles de souris dystrophiques comparativement aux muscles sains. L'objectif de la présente thèse vise à exploiter cette voie afin de comprendre le mécanisme d'action de ces cytokines sur la physiopathologie musculaire et d'établir une stratégie thérapeutique pour la DMD en traitement unique ou combinée aux glucocorticoïdes. Dans un premier temps, nous avons investigué l'impact de la neutralisation systémique à long terme de RANKL sur l'intégrité et la fonction musculaire et osseuse dans un modèle sévère de dystrophie déficient en dystrophine/haploinsuffisant en utrophine. Ensuite, nous avons étudié les rôles physiopathologiques de l'OPG sur les tissus musculaires en caractérisant la fonction musculaire de souris déficientes en OPG. Finalement, nous avons débuté une étude sur l'effet de neutralisation systémique de RANKL sur l'ostéoporose associée à un traitement au deflazacort, un glucocorticoïde prescrit pour la DMD. Ainsi nous avons démontré que le traitement à long terme à l'anti-RANKL améliore la fonction et l'intégrité musculaire et osseuse chez les souris dystrophiques et protège contre l'ostéoporose induite par les glucocorticoïdes. À l'opposé, l'absence d'OPG induit, possiblement via RANKL, une faiblesse osseuse et musculaire et une atrophie sélective des fibres musculaires les plus puissantes. Ces avancées repoussent les connaissances au sujet de la voie RANK/RANKL/OPG au sein de la communication muscle-os et appuient l'anti-RANKL comme perspective thérapeutique chez les patients atteints de la DMD.
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Manfrin, Thais Mara [UNESP]. "Imunomarcação das proteínas OPG, RANK e RANKL em dentes reimplantados de rato". Universidade Estadual Paulista (UNESP), 2007. http://hdl.handle.net/11449/101206.

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Made available in DSpace on 2014-06-11T19:31:10Z (GMT). No. of bitstreams: 0 Previous issue date: 2007-12-10Bitstream added on 2014-06-13T19:01:31Z : No. of bitstreams: 1 manfrin_tm_dr_araca.pdf: 3862156 bytes, checksum: dd6ccb05bd3012f8f38552fa7c669deb (MD5)
O sistema OPG, RANK e RANKL é uma das mais importantes descobertas da biologia óssea. Essas proteínas regulam as atividades celulares na remodelação do tecido ósseo e na literatura há diversas investigações nos tecidos dentários. No entanto, no reimplante dentário, ainda não foram encontrados relatos. Foi objetivo deste trabalho, avaliar a imunomarcação das proteínas OPG, RANK e RANKL em dentes reimplantados de rato. Um grupo controle foi formado com quatro ratos no qual o reimplante dentário não foi realizado. Vinte e quatro ratos (Rattus norvegicus, albinus) tiveram seu incisivo superior extraído e depois reimplantado formando os seguintes grupos: grupo I – reimplante imediato; grupo II - reimplante tardio sem tratamento e grupo III - reimplante tardio com tratamento endodôntico (ressecção da papila dentária e preenchimento do canal com pasta de hidróxido de cálcio) e tratamento da superfície radicular (raspagem mecânica do ligamento periodontal necrosado e imersão em solução de flúor fosfato acidulado de sódio a 2,5%). Ao final dos períodos experimentais (10 e 60 dias) os ratos foram eutanasiados. Foram obtidos cortes longitudinais parafinados com 6μm de espessura. Os cortes foram submetidos à reação imunoístoquímica mediante a utilização de anticorpos primários para OPG, RANK e RANKL. Os resultados mostraram que a imunomarcação de OPG e RANKL ocorreu em todos os grupos e períodos estudados, muito embora RANKL não tenha sido observada no grupo reimplante imediato aos 60 dias. RANK foi observada somente aos 10 dias de todos os grupos no qual o reimplante foi realizado. A análise qualitativa dos resultados demonstrou que o sistema OPG, RANK e RANKL apresentou marcação evidente no reimplante tardio, sugerindo a efetiva participação no início do processo de reabsorção radicular, uma vez que aos 60 dias a imunomarcação foi discreta.
The OPG, RANK and RANKL system is one of the most important discoveries in bone biology. These proteins are key regulators of bone remodeling and in the literature there are several studies of tooth resorption. However, in tooth replantation, reports have not been found. The purpose of this study was to determine the immunolabeling of OPG, RANK and RANKL in replanted teeth in rats, using immunohistochemistry methodology. A control group (no replanted teeth) was formed by four rats. Twenty-four rats (Rattus norvegicus, albinus) were submitted to the extraction of their upper right incisors. The replantation was performed according to the groups below: group I – immediate replantation; group II – delay replantation without treatment and group III – delay replantation with endodontic treatment (extirpation of papilla and the root canal filled with calcium hydroxide) and root surface treatment (periodontal ligament was removed with scalpel and teeth were immersed in 2% acidulated phosphate sodium fluoride). The animals were euthanized at the end of the experimental periods (10 and 60 days). Longitudinal 6μm slices embedded in paraffin were obtained. The slices were submitted to immunohistochemistry reaction by means of the primary antibodies for OPG, RANK and RANKL proteins. The results showed the expression of OPG in all groups and periods. RANKL expression was observed in all groups, except in the immediate replanted teeth group (60 days). RANK expression was observed only at 10 days in all groups which replantation was performed. The qualitative analysis of our findings indicated that the system OPG, RANK and RANKL presented strong expression in delayed replantation, suggesting effective participation at the beginning of root resorption, since at 60 days the immunostained cells were discreet.
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Manfrin, Thais Mara. "Imunomarcação das proteínas OPG, RANK e RANKL em dentes reimplantados de rato /". Araçatuba : [s.n.], 2007. http://hdl.handle.net/11449/101206.

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Resumo: O sistema OPG, RANK e RANKL é uma das mais importantes descobertas da biologia óssea. Essas proteínas regulam as atividades celulares na remodelação do tecido ósseo e na literatura há diversas investigações nos tecidos dentários. No entanto, no reimplante dentário, ainda não foram encontrados relatos. Foi objetivo deste trabalho, avaliar a imunomarcação das proteínas OPG, RANK e RANKL em dentes reimplantados de rato. Um grupo controle foi formado com quatro ratos no qual o reimplante dentário não foi realizado. Vinte e quatro ratos (Rattus norvegicus, albinus) tiveram seu incisivo superior extraído e depois reimplantado formando os seguintes grupos: grupo I - reimplante imediato; grupo II - reimplante tardio sem tratamento e grupo III - reimplante tardio com tratamento endodôntico (ressecção da papila dentária e preenchimento do canal com pasta de hidróxido de cálcio) e tratamento da superfície radicular (raspagem mecânica do ligamento periodontal necrosado e imersão em solução de flúor fosfato acidulado de sódio a 2,5%). Ao final dos períodos experimentais (10 e 60 dias) os ratos foram eutanasiados. Foram obtidos cortes longitudinais parafinados com 6μm de espessura. Os cortes foram submetidos à reação imunoístoquímica mediante a utilização de anticorpos primários para OPG, RANK e RANKL. Os resultados mostraram que a imunomarcação de OPG e RANKL ocorreu em todos os grupos e períodos estudados, muito embora RANKL não tenha sido observada no grupo reimplante imediato aos 60 dias. RANK foi observada somente aos 10 dias de todos os grupos no qual o reimplante foi realizado. A análise qualitativa dos resultados demonstrou que o sistema OPG, RANK e RANKL apresentou marcação evidente no reimplante tardio, sugerindo a efetiva participação no início do processo de reabsorção radicular, uma vez que aos 60 dias a imunomarcação foi discreta.
Abstract: The OPG, RANK and RANKL system is one of the most important discoveries in bone biology. These proteins are key regulators of bone remodeling and in the literature there are several studies of tooth resorption. However, in tooth replantation, reports have not been found. The purpose of this study was to determine the immunolabeling of OPG, RANK and RANKL in replanted teeth in rats, using immunohistochemistry methodology. A control group (no replanted teeth) was formed by four rats. Twenty-four rats (Rattus norvegicus, albinus) were submitted to the extraction of their upper right incisors. The replantation was performed according to the groups below: group I - immediate replantation; group II - delay replantation without treatment and group III - delay replantation with endodontic treatment (extirpation of papilla and the root canal filled with calcium hydroxide) and root surface treatment (periodontal ligament was removed with scalpel and teeth were immersed in 2% acidulated phosphate sodium fluoride). The animals were euthanized at the end of the experimental periods (10 and 60 days). Longitudinal 6μm slices embedded in paraffin were obtained. The slices were submitted to immunohistochemistry reaction by means of the primary antibodies for OPG, RANK and RANKL proteins. The results showed the expression of OPG in all groups and periods. RANKL expression was observed in all groups, except in the immediate replanted teeth group (60 days). RANK expression was observed only at 10 days in all groups which replantation was performed. The qualitative analysis of our findings indicated that the system OPG, RANK and RANKL presented strong expression in delayed replantation, suggesting effective participation at the beginning of root resorption, since at 60 days the immunostained cells were discreet.
Orientador: Wilson Roberto Poi
Coorientador: Roberta Okamoto
Banca: Sônia Regina Panzarini Barioni
Banca: Celso Koogi Sonoda
Banca: Luiz Guilherme Brentegani
Banca: Mirian Marubayashi Hidalgo
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Cordeiro, Olga. "From lymph node embryogenesis to homeostasis : new insights into the functions of stromal RANKL (TNFSF11)". Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ075/document.

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RANKL et RANK sont membres de la superfamille des TNF et de la superfamille des TNF-récepteurs, respectivement. Ils sont connus pour jouer un rôle important dans la régulation de la masse osseuse et dans le développement et la fonction du système immunitaire. Cependant des questions restent. Nous avons utilisé des souris génétiquement modifiées pour répondre à certaines de ces questions, en particulier en utilisant une souris dont les cellules stromales réticulaires marginales manquent RANKL dans les ganglions lymphatiques. Les résultats obtenus lors de cette thèse fournissent de nouvelles informations importantes sur l'impact positif de RANKL stromal sur les macrophages des ganglions lymphatiques concomitantes avec une fonction des cellules B amélioré et une pathogénicité virale réduit. Nous avons constaté que RANKL stromal régule l'expression de lymphotoxine et CXCL13, deux molécules clés de l'homéostasie des cellules B et de l'intégrité cellulaire des organes lymphoïdes secondaires. L’activité du RANKL semble suivre une hiérarchie temporelle sur lymphotoxine/TNFα, vu que le phénotype causé par le déficit en RANKL a une pénétrance augmenté avec l'âge. De plus, nous démontrons que RANKL active les cellules endotheliales lymphatiques des ganglions lymphatiques et on a trouvé que l'intégrine ITGA2b est un nouvel indicateur pour les cellules endotheliales lymphatiques activés. Ainsi, avec MAdCAM-1, ITGA2b sert comme un nouveau marqueur pour les cellules endothéliales lymphatiques qui sont constitutivement activés par le RANKL stromal. Au total, les données confirment l'importance de RANKL pour l'homéostasie des ganglions lymphatiques et dévoile les mécanismes ci-inconnus des fonctions de RANKL. À la lumière de cela et le fait que RANKL est sensible aux hormones féminines, nous avons étudié le rôle de RANKL dans le syndrome de Sjögren, une maladie inflammatoire chronique des glandes salivaires et lacrymales avec une forte polarisation de sexe féminin. Nous apportons la preuve que la neutralisation du RANKL réduit la taille des organes lymphoïdes tertiaire. En perspective, une éventuelle diaphonie entre les cellules endothéliales lymphatiques et les macrophages ou les cellules réticulaires marginales reste à clarifier. En outre, d'autres travaux sont nécessaires pour élucider le mécanisme par lequel RANKL stimule les maladies inflammatoires chroniques présentant des structures lymphoïdes tertiaires, afin de faire RANKL une nouvelle cible pour la thérapie
RANKL and RANK are members of the TNF-superfamily and TNF-receptor superfamily, respectively. They are known to play an important role in the regulation of bone mass and in the development and the function of the immune system. However questions still remain. We have used genetically modified mice to address some of these questions, in particular by using a mouse whose lymph node marginal reticular stromal cells lack RANKL. The results obtained during this PhD provide important new insights into the positive impact of stromal RANKL on lymph node macrophages concomitant with enhanced B cell function and reduced viral pathogenicity. We found that stromal RANKL regulates lymphotoxin and CXCL13 expression, two key molecules for B cell homeostasis and secondarylymphoid organ cellular integrity. RANKL activity seems to follow a temporal hierarchy over lymphotoxin/TNFα, as the phenotype caused by stromal RANKL-deficiency has increased penetrance with age. Furthermore, we demonstrate that RANKL activates lymph node lymphatic endothelial cells and found that the integrin ITGA2b is a new indicator for activated lymphatic endothelial cells. Thus, together with MAdCAM-1, ITGA2b serves as a novel marker for those lymphatic endothelial cells that are constitutively activated by stromal RANKL. Altogether, the data reinforce the importance of RANKL for the lymph node homeostasis and uncover here to unknown mechanisms of RANKL functions.In light of this and the fact that RANKL is responsive to female hormones, we studied the role of RANKL in the Sjögrens syndrome, a chronic inflammatory disease of salivary and lacrimal glands with a strong female sex bias. We provide evidence that RANKL neutralization reduces tertiary lymphoid organ size. On the perspective side, a possible cross talk between lymph node lymphatic endothelial cells and macrophages or marginal reticular cells remains to be clarified.Furthermore, further work is required to elucidate the mechanism by which RANKL stimulates chronic inflammatory diseases presenting tertiary lymphoid structures, in order to make RANKL a new target for therapy
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Nascimento, Mariele Andrade do. "Associação entre polimorfismos genéticos em RANK, RANKL e OPG com alterações nas dimensões craniofaciais". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/58/58135/tde-20112017-095844/.

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O objetivo do presente estudo foi avaliar, em humanos, a associação entre polimorfismos genéticos no sistema RANK/RANKL/OPG com as dimensões craniofaciais. Foram incluídos neste estudo um total de 100 indivíduos caucasianos brasileiros não relacionados. O DNA foi extraído da saliva de cada um dos participantes e os polimorfismos rs3826620, rs9594738 e rs2073618 em RANK, RANKL e OPG, respectivamente, foram analisados por PCR em tempo real. Para avaliação das dimensões craniofaciais foram avaliadas três medidas angulares (SNA, SNB e ANB) e quatro medidas lineares (Co-Gn, Go-Pg, Co-Go e PTM-A), obtidas de traçados cefalométricos. Para avaliar a distribuição dos genótipos de acordo com os padrões esqueléticos faciais (Classe I, Classe II e Classe III) foi utilizado o teste do qui-quadrado. Para comparar as médias das dimensões maxilares e mandibulares de acordo com os genótipos utilizou-se o teste de Kruskal-Wallis, com o pós-teste de Dunn para comparações múltiplas, ou ANOVA com pós-teste de Tukey. Foi utilizada a análise de regressão linear multivariada para ajustar a possível influência da idade e do gênero em cada medida. O equilíbrio de Hardy-Weinberg foi avaliado utilizando o teste do qui-quadrado para cada polimorfismo. O nível de significância adotado para todas as análises foi 5%. Os resultados obtidos evidenciaram que não houve associação estatisticamente significante entre a distribuição genotípica de RANK, RANKL e OPG com as médias dos ângulos SNA e SNB, nem com a distribuição fenotípica (padrão esquelético Classe I, II ou III) (p>0,05). Observou-se diferença estatisticamente significante entre a distribuição das medidas do comprimento da base mandibular, de acordo com os genótipos de RANK, onde o genótipo GG apresentou maior medida de Go-Pg (p=0,039). Na análise multivariada, observou-se associação significante para os polimorfismos em RANK e medidas mandibulares (Go-Pg e Co-Gn) (p<0,05). A medida da maxila não foi associada a nenhum polimorfismo. Conclui-se que houve associação entre o polimorfismo genético rs3826620 em RANK com maiores dimensões mandibulares, onde o comprimento da mandíbula (Co-Gn) e o comprimento da base da mandíbula (Go-Pg) estavam aumentados.
The objective of the present study was to evaluate, in humans, the association between genetic polymorphisms in the RANK/ RANKL/OPG system with alterations in craniofacial dimensions. A total of 100 unrelated Brazilian Caucasians were included in this study. DNA was extracted from the saliva of each of the participants and the polymorphisms rs3826620, rs9594738 and rs2073618 in RANK, RANKL and OPG, respectively, were analyzed by real-time PCR. To evaluate the craniofacial dimensions, three angular measurements (SNA, SNB and ANB) and four linear measurements (Co-Gn, Go-Pg, Co-Go and PTM-A) were obtained from cephalometric tracings. To compare the difference between the means of the linear and angular measurements according to the genotype, Kruskal-Wallis followed by Dunn post test or ANOVA followed by the Tukey post test was used. Linear regression analysis was also used to adjust the possible influence of age and gender on each linear maxillary and mandibular measure. The Hardy-Weinberg equilibrium was also evaluated using the chi-square test within each polymorphism. The level of significance was 5%. The results demonstrated that there were no statistically significant association between the genotypic distribution of RANK, RANKL, OPG, and the angules SNA, SNB and according to the phenotypic distribution (Class I, Class II or Class III of skeletal pattern) (p> 0.05). A statistically significant difference was observed between the distribution of mandibular base length measurements according to the RANK genotypes, where the GG genotype showed a higher Go-Pg measurement (p=0.039). In the multivariate analysis, a statistically significant association was found for RANK and mandibular (Go-Pg and Co-Gn) polymorphisms (p<0.05). Measurement of the maxilla was not associated with any polymorphism. It was concluded that there was an association between genetic polymorphism rs3826620 in RANK with a greater mandibular dimension, in which the length of the mandible (Co-Gn) and the length of the base of the mandible (Go-Pg) were increased.
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Dumont, Nicolas. "Atrophie, croissance et fonction musculaire : l'impact des leucocytes et de la triade RANK/RANKL/OPG". Thesis, Université Laval, 2013. http://www.theses.ulaval.ca/2013/29749/29749.pdf.

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L’atrophie et les dysfonctions musculaires sont des problèmes courants et d’origines variées. À titre d’exemple l’alitement prolongé, le SIDA, les cancers, l’hypogravité et le vieillissement peuvent tous entraîner une perte de masse et de force musculaire. Malgré les coûts économiques et sociaux élevés, relativement peu d’efforts ont été investis dans la caractérisation des processus qui gouvernent l’atrophie/dysfonction musculaire et dans le développement de traitements plus efficaces. Conséquemment, cette thèse vise à approfondir les connaissances actuelles sur les mécanismes qui régulent l’atrophie/dysfonction et la récupération des muscles atrophiés par sous-utilisation. Tout d’abord, nous avons caractérisé l’impact des leucocytes impliqués lors de la remise en charge du muscle soléaire atrophié par hypogravité. Ainsi, nous avons démontré que les mastocytes étaient activés par la remise en charge et que leur dégranulation orchestrait le recrutement des neutrophiles et des monocytes/macrophages. Ensuite, nos recherches ont indiqué que l’activité des neutrophiles pouvait être régulée en fonction de leur microenvironnement et que leur présence dans les muscles atrophiés et inflammés n’était pas nécessairement associée à l’induction de dommages secondaires. Par la suite, nous avons établi que la présence des macrophages était importante pour permettre la récupération optimale de la force des muscles atrophiés. Nous avons également démontré que l’activité myogénique des macrophages pouvait être optimisée en favorisant leur phénotype anti-inflammatoire avec le facteur de croissance hématopoïétique « macrophage-colony stimulating factor » (M-CSF). Finalement, nous avons caractérisé l’impact du « receptor activator of NF-kB » (RANK) et de son ligand RANKL, une voie signalétique impliquée dans le remodelage osseux et l’ostéoporose, sur l’atrophie/dysfonction musculaire. Nous avons démontré qu’une déficience de RANK ou le blocage de RANKL par l’ostéoprotégérine protègent contre la perte de force des muscles dénervés ou dystrophiques. Ce phénomène est associé à des modifications dans l’expression des protéines favorisant une recaptation plus efficace du calcium. De plus, RANK participe à la reconversion des fibres rapides vers lentes durant la période de remise charge. Globalement, nos travaux permettent de mieux comprendre les mécanismes entourant l’atrophie, la croissance et les dysfonctions musculaires et ouvrent la voie à de nouvelles pistes de traitement pour plusieurs maladies neuro-musculaires.
Muscle atrophy and dysfunction are characterized by a loss of muscle mass and force, which are commonly found in many pathologies or conditions such as AIDS, cancers, chronic obstructive pulmonary diseases, cast immobilization, hypogravity, bed rest or aging, to name a few. Muscle atrophy/dysfunction have also very high social and economic costs, but very few laboratories have investigated the cellular and molecular mechanisms behind these muscular problems. The aim of this thesis is therefore to enhance our understanding of different mechanisms governing muscle atrophy/dysfunction and regrowth by using different models of disuse and dystrophy. Thus, we have initially explored the roles of different leucocytes in atrophied and reloaded soleus muscle. Firstly, we looked at the role of mast cells and showed that the mechanical stress associated with muscle reloading is able to stimulate mast cell degranulation, which orchestrates the recruitment of neutrophils and monocytes/macrophages. Secondly, our experiments revealed that neutrophil activity is adaptable and that neutrophil-induced tissue damage is dependent on the microenvironment. In atrophied and reloaded muscles, the presence of neutrophils is not associated with secondary damage or promotion of muscle recovery. Thirdly, we demonstrated that the presence of macrophages is essential for optimal muscle force recovery from atrophy. Fourthly, we showed that the macrophage-colony stimulating factor (M-CSF) promote the myogenic activity of macrophages by stimulating their anti-inflammatory phenotype. Finally, we investigated the impact of the receptor activator of NF-kB (RANK) and its ligand RANKL, a signalling pathway involved in bone remodelling and osteoporosis, on muscle atrophy and dysfunction. Our results showed that the specific deletion of RANK in the muscle or the blockage of RANKL with osteoprotegerin increased significantly force production in denervated and dystrophic muscles. These results were associated with various modifications in calcium handling protein expression favouring efficient calcium uptake. Moreover, we also demonstrated that RANK activation gives preference to the reconversion from fast-to-slow muscle fibers following hindlimb unloading/reloading. Overall, our results bring a better understanding of different mechanisms related to muscle atrophy, dysfunction and regrowth and potentially open new avenues for the treatment of several debilitating skeletal muscle conditions.
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Loureiro, Melina Bezerra. "Estudo da associa??o dos genes RANk, RANKL e OPG com a osteopatia diab?tica". Universidade Federal do Rio Grande do Norte, 2014. http://repositorio.ufrn.br/handle/123456789/19413.

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Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior - CAPES
Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico - CNPq
O objetivo do presente trabalho foi avaliar a express?o de RNAm e os polimorfismos dos genes RANK, RANKL e OPG de crian?as, adolescentes e adultos jovens com DM1, bem como estudar a associa??o dos mesmos com o desenvolvimento de altera??es no metabolismo ?sseo.No total, foram inclu?dos no estudo 119 crian?as e adolescentes com DM1 e 161 indiv?duos normoglic?micos (NG) da mesma faixa et?ria. Foram pesquisados os polimorfismos dos genes OPG (1181 G>C e 163 A>G), RANK (575 C>T e 3'UTR C>A) e RANKL (?ntron A>G) e determinadas as express?es g?nicas de OPG, RANK e RANKL. Al?m disso, foram avaliados o controle glic?mico e par?metros laboratoriais de fun??o ?ssea, al?m da densitometria ?ssea. Os indiv?duos com DM1 apresentaram um controle glic?mico insatisfat?rio e valores diminuidos de c?lcio total, propept?deo do col?geno tipo 1 (CTX), como tamb?m baixa densidade mineral ?ssea, quando comparados com os NG (p<0,05). O polimorfismo OPG 1181 G>C pode estar associado com susceptibilidade ao DM1 (p=0,054). Estudando apenas os indiv?duos com DM1, foi observado que os carreadores do gen?tipo OPG 1181 GG apresentaram maiores concentra??es de c?lcio ionizado no modelo recessivo (p<0,05). Esses resultados sugerem que o polimorfismo OPG 1181 G>C pode contribuir para o desenvolvimento do DM1 e da osteopatia diab?tica.
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Camara, Abdouramane. "Control of lymphoid organ CD169+ macrophage differentiation by stromal cells through the RANK-RANKL axis". Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ102.

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Au-delà de leurs rôles de sentinelles, de reconnaissance du danger et d’initiation des réponses protectrices, les signaux et le mécanisme qui gouvernent la formation des macrophages CD169 + sinusoïdaux ganglionnaires sont mal connus. Au cours de ma thèse, j’ai montré que la cytokine Receptor Activator of NF-kB Ligand (RANKL) est requise pour la formation de ces macrophages dès l’embryogenèse jusqu’aux quatre semaines après la naissance. Celle-ci est contrôlée par les cellules endothéliales lymphatiques (LECs) activées par RANKL produite par les cellules mésenchymateuses. Chez l’adulte, les LECs activées par RANKL sont encore nécessaires pour la reconstitution des populations de ces macrophages en cas de déplétion transitoire induite par un stimulus inflammatoire. En complément à cela, j’ai aussi démontré l’importance générale du double signal RANKL & lymphotoxine LTα1β2 dans la formation des macrophages non-ostéoclastiques de la rate et de la moelle osseuse
Lymph node CD169 + sinusoidal macrophages are sentinel cells that recognize the danger signals and initiate the protective immune responses. However, the signals and the mechanism underlying their formation are not well known. During my thesis, I have shown that the cytokine Receptor Activator of NF-kB Ligand (RANKL) is required for their differentiation, starting from the embryogenesis up to four weeks after birth. The lymphatic endothelial cells (LECs) activated by RANKL expressed by mesenchymal cells form the niches for the primary differentiation of these macrophages. Yet, in adults, RANKL-activated LECs are required for their niche replenishment after transient depletion induced by an inflammatory stimulus. Beyond lymph node, my research has revealed a general requirement of the double signal RANKL & lymphotoxin LTα1β2 for the differentiation of non-osteoclastic CD169 + macrophages of spleen and bone marrow
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Libros sobre el tema "RANKL"

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Bingaman, Steven A. The history of American ranks and rank insignia. United States]: [publisher not identified ], 2013.

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group), Fishamble (Theater, ed. Rank. London: Nick Hern Books, 2008.

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Cabban, Peter T. Breaking ranks. Milsons Point, N.S.W: Random House Australia, 2005.

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Aylin, Clyde. Breaking ranks. Braunton: Merlin, 1989.

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Moprofesara ranko. Pretoria: Via Africa, 1992.

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Rōhita, Bōgollāgama y Eksat Jātika Pakṣaya (Sri Lanka), eds. Nāyaka Ranil. Śrī Jayavardhanapura: Eksat Jātika Pakṣaya, 1996.

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Goga, Lamratu M. Inda ranka. Nigeria]: [s.n.], 1999.

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Nakajima, Shigeo. Tadanai rankō. Tōkyō: Rippū Shobō, 1988.

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Schütt, Hans-Dieter. Uta Ranke. Berlin: Elefanten Press, 1993.

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Closing ranks. London: Viking, 1997.

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Capítulos de libros sobre el tema "RANKL"

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Nakashima, Tomoki y Hiroshi Takayanagi. "RANK and RANKL". En Encyclopedia of Signaling Molecules, 4445–54. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_633.

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Leibbrandt, Andreas y Josef M. Penninger. "RANK–RANKL Signaling". En Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4945-2.

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Martemyanov, Kirill A., Pooja Parameswaran, Irene Aligianis, Mark Handley, Marga Gual-Soler, Tomohiko Taguchi, Jennifer L. Stow et al. "RANK and RANKL". En Encyclopedia of Signaling Molecules, 1581–89. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_633.

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Leibbrandt, Andreas y Josef M. Penninger. "RANK–RANKL Signaling". En Encyclopedia of Cancer, 3899–903. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_4945.

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Leibbrandt, Andreas y Josef M. Penninger. "RANK-RANKL Signaling". En Encyclopedia of Cancer, 3165–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4945.

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Stein, Nicola, Martina Rauner y Lorenz C. Hofbauer. "RANKL Inhibition: Clinical Data". En Principles of Osteoimmunology, 217–40. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0520-7_10.

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Sipos, Wolfgang. "RANKL Inhibition: Preclinical Data". En Principles of Osteoimmunology, 197–215. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0520-7_9.

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Hofbauer, Lorenz y Tilman Rachner. "Die Rolle des RANK/RANKL/OPG-Signalwegs im Knochenstoffwechsel". En Fortbildung Osteologie, 118–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-05385-6_26.

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Brown, Julie M., Jian Zhang y Evan T. Keller. "OPG, RANKL, and RANK in Cancer Metastasis: Expression and Regulation". En Cancer Treatment and Research, 149–72. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9129-4_7.

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Leibbrandt, Andreas y Josef M. Penninger. "TNF Conference 2009: Beyond Bones – RANKL/RANK in the Immune System". En Advances in Experimental Medicine and Biology, 5–22. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6612-4_2.

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Actas de conferencias sobre el tema "RANKL"

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Remoto, Júlia Maranghetti, Maria Eduarda Ramos Cezine, Paulo Henrique Cavalcanti De Araújo y Mariana Kiomy Osako. "EXPRESSÃO DE RANK-RANKL-OPG NA DIFERENCIAÇÃO DE CÉLULAS MUSCULARES ESQUELÉTICAS". En I Congresso Nacional On-line de Biologia Celular e Estrutural. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1947.

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Introdução: O sistema RANK-RANKL-OPG é constituído pelo receptor RANK, o ligante RANKL e o receptor solúvel Osteoprotegerina (OPG). Esse sistema tem importante papel na regulação de processos fundamentais ao tecido ósseo, como a remodelação óssea. A literatura descreve o papel da via de sinalização RANK-RANKL na regulação da atividade de retículos sarcoplasmáticos no tecido muscular, bem como a participação de OPG na redução de fraqueza muscular e restauração de fibras em casos de distrofia muscular em camundongos. Dessa forma, destaca-se a relevância de estudos sobre a unidade osso-músculo e a atividade de proteínas solúveis na comunicação e homeostase desses tecidos. Objetivo: Verificar a expressão de RANK-RANKL-OPG ao longo do processo de diferenciação de miotubos in vitro. Materiais e Métodos: A linhagem de mioblastos C2C12 foi cultivada em meio DMEM suplementado com 10% de soro fetal bovino, 100U/ml de penicilina e 100 μg/ml de estreptomicina em estufa a 37ºC e 5% de CO2. A diferenciação em miotubos foi realizada durante cinco dias em DMEM suplementado com 2% soro equino. Estímulos com RANKL foram realizados ao longo da diferenciação, renovados a cada 48h. A análise da expressão gênica e proteica de RANK, RANKL e OPG foram realizadas por RT-qPCR utilizando o kit QuantiFast SYBR® Green (Qiagen®) e western blot, respectivamente. A dosagem de RANKL e OPG no sobrenadante foi realizada pelo kit ELISA Kit (R&D Systems®). Resultados: A expressão proteica de RANK e OPG aumentou, destacando-se a maior expressão de OPG no terceiro dia de diferenciação. Observamos um aumento significativo de OPG no sobrenadante de células no 3º dia de diferenciação, enquanto RANKL foi indetectado. Além do aumento na expressão gênica de OPG, houve aumento na expressão de MyoD e MF20, fundamentais para a diferenciação de miotubos. Conclusão: Os resultados sugerem a ação de RANKL na indução da diferenciação de miotubos e também apontam que RANKL pode atuar como uma osteocina na regulação do músculo esquelético e este, por sua vez, pode regular este estímulo por meio da expressão de OPG. Assim, estes dados preliminares indicam um papel inédito da sinalização RANK-RANKL-OPG em processos fisiológicos da fibra muscular esquelética.
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Sun, Y. "IL-17A-Dependent Lymphoid Neogenesis in COPD Involves RANKL-RANK Expression". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3768.

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Sharma, Bhawna, Michelle L. Varney y Rakesh K. Singh. "Abstract 4968: Chemotherapy up-regulates RANK-RANKL signaling in breast cancer cells." En Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4968.

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Sousa, Sofia, Evelyne Gineyts, Sandra Geraci, Martine Croset y Philippe Clézardin. "Abstract 29: RANK-RANKL signaling inhibition delays early breast cancer bone metastasis formation". En Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-29.

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Intemann, J., C. Wehmeyer, V. Kracke, E. Werbenko, P. Paruzel, I. Kramer, M. Kneissel, T. Pap y B. Dankbar. "P081 Sclerostin affects rankl-mediated osteoclast differentiation". En 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.98.

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Boorsma, Carian, Christina Draijer, Robbert Cool, Corry-Anke Brandsma, George Nossent, Peter Heukels, Bernt Van den Blink, David Brass, Wim Timens y Barbro Melgert. "The RANKL-OPG balance in pulmonary fibrosis". En Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3809.

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Wieser, V., I. Tsibulak, C. Degasper, H. Welponer, K. Leitner, S. Sprung, J. Haybäck, H. Fiegl, C. Marth y AG Zeimet. "RANKL als unabhängiger Prognoseparameter für Patientinnen mit Ovarialkarzinom". En Kongressabstracts zur Wissenschaftlichen Tagung der Arbeitsgemeinschaft für gynäkologische Onkologie (AGO) der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1682001.

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Jacob, A., D. Branstetter, K. Rohrbach, A. Winters, R. Erwert, S. Allred, J. Jones et al. "P3-01-14: RANK and RANK Ligand (RANKL) Expression in Invasive Breast Carcinoma and Human Breast Cancer Cell Lines." En Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p3-01-14.

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van de Luijtgaarden, Addy, Manon Leus, Melissa Roeffen, Uta Flucke, Ingrid van der Geest, Winette van der Graaf y Yvonne Versleijen-Jonkers. "Abstract 655: Prognostic relevance of the RANK/RANKL/OPG triad and the IGF1R pathway in osteosarcoma". En Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-655.

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SILVA, AMANDA LORRAINE PEREIRA y CINTIA GRAZIELY MIRANDA AZEVEDO. "A RELEVÂNCIA DO ESTROGÊNIO NO DESENVOLVIMENTO DA OSTEOPOROSE". En I Congresso Brasileiro de Doenças Crônicas On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/cronics/6633.

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Introdução: A osteoporose é uma doença relacionada à perda de tecido ósseo devido a descompensação no processo de remodelação, o que aumenta a possibilidade de fraturas. O estrogênio atua sobre as células que compõem a matriz óssea modulando a sua função. Objetivo: Discutir e analisar por meio de uma revisão da literatura, como os níveis estrogênio interferem no surgimento da osteoporose. Material e métodos: Foi feito um levantamento bibliográfico no PUBMED entre os anos de 2012 a 2022 com a seleção de 3 artigos em inglês que abordavam a temática. Resultados: O déficit de estrogênio está relacionado com o desenvolvimento da osteoporose devido à distância criada entre a formação óssea e a reabsorção óssea, isto é, aumento da atividade osteoclástica em detrimento da osteoblástica. Essas alterações, possuem mecanismos moleculares que envolvem o aumento da atuação do fator nuclear kappa b (NF-Kb) nos osteoclastos e a elevação da apoptose em osteoblastos. Nesse sentido, o NF-Kb atua no processo de diferenciação e ativação dos osteoclastos, sendo necessário o estímulo via ligante RANKL ao receptor RANK para o seu funcionamento adequado durante a maturação celular, entretanto níveis adequados de estrogênio é capaz de inibir essa ligação favorecendo a diminuição da atividade dessas células com consequente atenuação da reabsorção óssea. A osteoprotegerina é capaz de impedir a ligação RANKL ao receptor RANK. Além disso, o estrogênio promove a manutenção dos osteoblastos, o que contribui para o desenvolvimento ósseo adequado, todavia o baixo nível aumenta a apoptose dessas células. O envelhecimento coopera para reforçar o estresse oxidativo e juntamente com os menores níveis de estrogênio a ampliação da atividade dos osteoclastos e a redução da atividade dos osteoblastos. Conclusão: A redução do nível de estrogênio interfere nos osteoblastos e nos osteoclastos responsáveis pelo desenvolvimento do tecido ósseo e pela reabsorção óssea respectivamente, o que culmina no desenvolvimento da osteoporose.
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Informes sobre el tema "RANKL"

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Bhatia, Pardeep. Study of RANKL Expression in Metastatic Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, junio de 2002. http://dx.doi.org/10.21236/ada405313.

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Bhatia, Pardeep. Study of RANKL Expression in Metastatic Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, junio de 2003. http://dx.doi.org/10.21236/ada418749.

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Hossain, Niamat Ullah Ibne, Farjana Nur, Raed Jaradat, Seyedmohsen Hosseini, Mohammad Marufuzzaman, Stephen Puryear y Randy Buchanan. Metrics for assessing overall performance of inland waterway ports : a Bayesian Network based approach. Engineer Research and Development Center (U.S.), mayo de 2021. http://dx.doi.org/10.21079/11681/40545.

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Because ports are considered to be the heart of the maritime transportation system, thereby assessing port performance is necessary for a nation’s development and economic success. This study proposes a novel metric, namely, “port performance index (PPI)”, to determine the overall performance and utilization of inland waterway ports based on six criteria, port facility, port availability, port economics, port service, port connectivity, and port environment. Unlike existing literature, which mainly ranks ports based on quantitative factors, this study utilizes a Bayesian Network (BN) model that focuses on both quantitative and qualitative factors to rank a port. The assessment of inland waterway port performance is further analyzed based on different advanced techniques such as sensitivity analysis and belief propagation. Insights drawn from the study show that all the six criteria are necessary to predict PPI. The study also showed that port service has the highest impact while port economics has the lowest impact among the six criteria on PPI for inland waterway ports.
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Weber, G. F. y D. L. Laudal. Low-rank coal research. Office of Scientific and Technical Information (OSTI), enero de 1989. http://dx.doi.org/10.2172/7045956.

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Kryzhanivs'kyi, Evstakhii, Liliana Horal, Iryna Perevozova, Vira Shyiko, Nataliia Mykytiuk y Maria Berlous. Fuzzy cluster analysis of indicators for assessing the potential of recreational forest use. [б. в.], octubre de 2020. http://dx.doi.org/10.31812/123456789/4470.

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Cluster analysis of the efficiency of the recreational forest use of the region by separate components of the recreational forest use potential is provided in the article. The main stages of the cluster analysis of the recreational forest use level based on the predetermined components were determined. Among the agglomerative methods of cluster analysis, intended for grouping and combining the objects of study, it is common to distinguish the three most common types: the hierarchical method or the method of tree clustering; the K-means Clustering Method and the two-step aggregation method. For the correct selection of clusters, a comparative analysis of several methods was performed: arithmetic mean ranks, hierarchical methods followed by dendrogram construction, K- means method, which refers to reference methods, in which the number of groups is specified by the user. The cluster analysis of forestries by twenty analytical grounds was not proved by analysis of variance, so the re-clustering of certain objects was carried out according to the nine most significant analytical features. As a result, the forestry was clustered into four clusters. The conducted cluster analysis with the use of different methods allows us to state that their combination helps to select reasonable groupings, clearly illustrate the clustering procedure and rank the obtained forestry clusters.
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Nybom, Martin, Toru Kitagawa y Jan Stuhler. Measurement error and rank correlations. The IFS, abril de 2018. http://dx.doi.org/10.1920/wp.cem.2081.2818.

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Mann, M., M. Johnson, S. Selle y J. Gunderson. Low-rank coal slurry combustion. Office of Scientific and Technical Information (OSTI), mayo de 1988. http://dx.doi.org/10.2172/6936637.

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Cucuringu, Mihai. Sync-rank: Robust Ranking, Constrained Ranking and Rank Aggregation via Eigenvector and SDP Synchronization. Fort Belvoir, VA: Defense Technical Information Center, abril de 2015. http://dx.doi.org/10.21236/ada625017.

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Henry, Marc, Alfred Galichon, Victor Chernozhukov y Marc Hallin. Monge-Kantorovich depth, quantiles, ranks and signs. IFS, enero de 2015. http://dx.doi.org/10.1920/wp.cem.2015.0415.

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Galichon, Alfred, Marc Hallin, Victor Chernozhukov y Marc Henry. Monge-Kantorovich depth, quantiles, ranks and signs. Institute for Fiscal Studies, septiembre de 2015. http://dx.doi.org/10.1920/wp.cem.2015.5715.

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