Relevant bibliographies by topics / Sclerostina

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Sclerostina'

Author: Grafiati
Published: 9 March 2023
Last updated: 11 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Sclerostina.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Sclerostina"

1

Boschert, V., C. Frisch, J. W. Back, et al. "The sclerostin-neutralizing antibody AbD09097 recognizes an epitope adjacent to sclerostin's binding site for the Wnt co-receptor LRP6." Open Biology 6, no. 8 (2016): 160120. http://dx.doi.org/10.1098/rsob.160120.

Full text
Abstract:
The glycoprotein sclerostin has been identified as a negative regulator of bone growth. It exerts its function by interacting with the Wnt co-receptor LRP5/6, blocks the binding of Wnt factors and thereby inhibits Wnt signalling. Neutralizing anti-sclerostin antibodies are able to restore Wnt activity and enhance bone growth thereby presenting a new osteoanabolic therapy approach for diseases such as osteoporosis. We have generated various Fab antibodies against human and murine sclerostin using a phage display set-up. Biochemical analyses have identified one Fab developed against murine sclerostin, AbD09097 that efficiently neutralizes sclerostin's Wnt inhibitory activity. In vitro interaction analysis using sclerostin variants revealed that this neutralizing Fab binds to sclerostin's flexible second loop, which has been shown to harbour the LRP5/6 binding motif. Affinity maturation was then applied to AbD09097, providing a set of improved neutralizing Fab antibodies which particularly bind human sclerostin with enhanced affinity. Determining the crystal structure of AbD09097 provides first insights into how this antibody might recognize and neutralize sclerostin. Together with the structure–function relationship derived from affinity maturation these new data will foster the rational design of new and highly efficient anti-sclerostin antibodies for the therapy of bone loss diseases such as osteoporosis.
APA, Harvard, Vancouver, ISO, and other styles
2

Shum, Ka To, Celine Chan, Ching-Man Leung, and Julian A. Tanner. "Identification of a DNA aptamer that inhibits sclerostin's antagonistic effect on Wnt signalling." Biochemical Journal 434, no. 3 (2011): 493–501. http://dx.doi.org/10.1042/bj20101096.

Full text
Abstract:
Sclerostin is an extracellular negative regulator of bone formation that is a recognized therapeutic target for osteoporosis therapy. In the present study, we performed DNA aptamer selection against sclerostin, then characterized aptamer–sclerostin binding and the ability to inhibit sclerostin function in cell culture. We show that a selected DNA aptamer was highly selective for binding to sclerostin with affinities in the nanomolar range as determined by solid-phase assays and by isothermal titration calorimetry. Binding between sclerostin and the aptamer was exothermic and enthalpically driven. CD confirmed that the aptamer had temperature-dependent parallel G-quadruplex characteristics. The aptamer was stabilized with 3′ inverted thymidine to investigate efficacy at inhibiting sclerostin function in cell culture. The stabilized DNA aptamer showed potent and specific dose-dependent inhibition of sclerostin's antagonistic effect on Wnt activity using a reporter assay. Taken together, the present findings suggest an alternative approach to inhibiting sclerostin function with therapeutic potential.
APA, Harvard, Vancouver, ISO, and other styles
3

Kim, Soohyun P., Julie L. Frey, Zhu Li, et al. "Sclerostin influences body composition by regulating catabolic and anabolic metabolism in adipocytes." Proceedings of the National Academy of Sciences 114, no. 52 (2017): E11238—E11247. http://dx.doi.org/10.1073/pnas.1707876115.

Full text
Abstract:
Sclerostin has traditionally been thought of as a local inhibitor of bone acquisition that antagonizes the profound osteoanabolic capacity of activated Wnt/β-catenin signaling, but serum sclerostin levels in humans exhibit a correlation with impairments in several metabolic parameters. These data, together with the increased production of sclerostin in mouse models of type 2 diabetes, suggest an endocrine function. To determine whether sclerostin contributes to the coordination of whole-body metabolism, we examined body composition, glucose homeostasis, and fatty acid metabolism in Sost−/− mice as well as mice that overproduce sclerostin as a result of adeno-associated virus expression from the liver. Here, we show that in addition to dramatic increases in bone volume, Sost−/− mice exhibit a reduction in adipose tissue accumulation in association with increased insulin sensitivity. Sclerostin overproduction results in the opposite metabolic phenotype due to adipocyte hypertrophy. Additionally, Sost−/− mice and those administered a sclerostin-neutralizing antibody are resistant to obesogenic diet-induced disturbances in metabolism. This effect appears to be the result of sclerostin’s effects on Wnt signaling and metabolism in white adipose tissue. Since adipocytes do not produce sclerostin, these findings suggest an unexplored endocrine function for sclerostin that facilitates communication between the skeleton and adipose tissue.
APA, Harvard, Vancouver, ISO, and other styles
4

Vasiliadis, Elias S., Dimitrios-Stergios Evangelopoulos, Angelos Kaspiris, Ioannis S. Benetos, Christos Vlachos, and Spyros G. Pneumaticos. "The Role of Sclerostin in Bone Diseases." Journal of Clinical Medicine 11, no. 3 (2022): 806. http://dx.doi.org/10.3390/jcm11030806.

Full text
Abstract:
Sclerostin has been identified as an important regulator of bone homeostasis through inhibition of the canonical Wnt-signaling pathway, and it is involved in the pathogenesis of many different skeletal diseases. Many studies have been published in the last few years regarding sclerostin’s origin, regulation, and mechanism of action. The ongoing research emphasizes the potential therapeutic implications of sclerostin in many pathological conditions with or without skeletal involvement. Antisclerostin antibodies have recently been approved for the treatment of osteoporosis, and several animal studies and clinical trials are currently under way to evaluate the effectiveness of antisclerostin antibodies in the treatment of other than osteoporosis skeletal disorders and cancer with promising results. Understanding the exact role of sclerostin may lead to new therapeutic approaches for the treatment of skeletal disorders.
APA, Harvard, Vancouver, ISO, and other styles
5

Leupin, Olivier, Elke Piters, Christine Halleux, et al. "Bone Overgrowth-associated Mutations in the LRP4 Gene Impair Sclerostin Facilitator Function." Journal of Biological Chemistry 286, no. 22 (2011): 19489–500. http://dx.doi.org/10.1074/jbc.m110.190330.

Full text
Abstract:
Humans lacking sclerostin display progressive bone overgrowth due to increased bone formation. Although it is well established that sclerostin is an osteocyte-secreted bone formation inhibitor, the underlying molecular mechanisms are not fully elucidated. We identified in tandem affinity purification proteomics screens LRP4 (low density lipoprotein-related protein 4) as a sclerostin interaction partner. Biochemical assays with recombinant proteins confirmed that sclerostin LRP4 interaction is direct. Interestingly, in vitro overexpression and RNAi-mediated knockdown experiments revealed that LRP4 specifically facilitates the previously described inhibitory action of sclerostin on Wnt1/β-catenin signaling. We found the extracellular β-propeller structured domain of LRP4 to be required for this sclerostin facilitator activity. Immunohistochemistry demonstrated that LRP4 protein is present in human and rodent osteoblasts and osteocytes, both presumed target cells of sclerostin action. Silencing of LRP4 by lentivirus-mediated shRNA delivery blocked sclerostin inhibitory action on in vitro bone mineralization. Notably, we identified two mutations in LRP4 (R1170W and W1186S) in patients suffering from bone overgrowth. We found that these mutations impair LRP4 interaction with sclerostin and its concomitant sclerostin facilitator effect. Together these data indicate that the interaction of sclerostin with LRP4 is required to mediate the inhibitory function of sclerostin on bone formation, thus identifying a novel role for LRP4 in bone.
APA, Harvard, Vancouver, ISO, and other styles
6

Silverman, Stuart L. "Sclerostin." Journal of Osteoporosis 2010 (2010): 1–3. http://dx.doi.org/10.4061/2010/941419.

Full text
Abstract:
The striking clinical benefits of intermittent parathyroid hormone in osteoporosis have begun a new era of skeletal anabolic agents. One potential new agent is monoclonal antibody to sclerostin, a potent inhibitor of osteoblastogenesis.
APA, Harvard, Vancouver, ISO, and other styles
7

Honasoge, Mahalakshmi, Ajay D. Rao, and Sudhaker D. Rao. "Sclerostin." Current Opinion in Endocrinology & Diabetes and Obesity 21, no. 6 (2014): 437–46. http://dx.doi.org/10.1097/med.0000000000000114.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Holdsworth, Gill, Scott J. Roberts, and Hua Zhu Ke. "Novel actions of sclerostin on bone." Journal of Molecular Endocrinology 62, no. 2 (2019): R167—R185. http://dx.doi.org/10.1530/jme-18-0176.

Full text
Abstract:
The discovery that two rare autosomal recessive high bone mass conditions were caused by the loss of sclerostin expression prompted studies into its role in bone homeostasis. In this article, we aim to bring together the wealth of information relating to sclerostin in bone though discussion of rare human disorders in which sclerostin is reduced or absent, sclerostin manipulation via genetic approaches and treatment with antibodies that neutralise sclerostin in animal models and in human. Together, these findings demonstrate the importance of sclerostin as a regulator of bone homeostasis and provide valuable insights into its biological mechanism of action. We summarise the current state of knowledge in the field, including the current understanding of the direct effects of sclerostin on the canonical WNT signalling pathway and the actions of sclerostin as an inhibitor of bone formation. We review the effects of sclerostin, and its inhibition, on bone at the cellular and tissue level and discuss new findings that suggest that sclerostin may also regulate adipose tissue. Finally, we highlight areas in which future research is expected to yield additional insights into the biology of sclerostin.
APA, Harvard, Vancouver, ISO, and other styles
9

Romejko, Katarzyna, Aleksandra Rymarz, Katarzyna Szamotulska, Zbigniew Bartoszewicz, and Stanisław Niemczyk. "Relationships between Sclerostin, Leptin and Metabolic Parameters in Non-Dialysis Chronic Kidney Disease Males." Journal of Personalized Medicine 13, no. 1 (2022): 31. http://dx.doi.org/10.3390/jpm13010031.

Full text
Abstract:
Sclerostin is an inhibitor of the Wnt-beta-catenin pathway. The relationship between sclerostin and adipose tissue or between sclerostin and nutritional status has been the subject of research interest in the last decade. Sclerostin concentrations are elevated in patients with chronic kidney disease (CKD). Leptin is an adipocytokine which inhibits food intake by stimulating the satiety center in the hypothalamus. Leptin concentrations rise with the reduction of eGFR (glomerular filtration rate). The aim of this study was to investigate the possible association between sclerostin and leptin, between sclerostin and selected poor prognostic factors of CKD progression, and between sclerostin and nutritional parameters in non-dialysis CKD male patients. 101 men with non-dialysis CKD stage 3–5 were included in the study. Bioimpedance spectroscopy (BIS) was used to measure body composition. Blood samples were drawn to measure the serum concentrations of sclerostin, leptin, creatinine, hemoglobin (Hgb), parathormone (PTH), inflammatory markers, and markers of nutritional status. We also measured homeostatic model assessment of insulin resistance (HOMA-IR) as well as blood pressure. We observed a significant, positive relationship between sclerostin and age, leptin, and glycated hemoglobin (HgbA1c) concentrations. A significant, negative association was observed between sclerostin and eGFR. Sclerostin is associated with leptin in non-dialysis CKD male patients. Sclerostin is also related to metabolic disturbances such as hyperglycemia in this population.
APA, Harvard, Vancouver, ISO, and other styles
10

Liu, Wen, Zhenyu Wang, Jun Yang, et al. "Osteocyte TSC1 promotes sclerostin secretion to restrain osteogenesis in mice." Open Biology 9, no. 5 (2019): 180262. http://dx.doi.org/10.1098/rsob.180262.

Full text
Abstract:
Osteocytes secrete the glycoprotein sclerostin to inhibit bone formation by osteoblasts, but how sclerostin production is regulated in osteocytes remains unclear. Here, we show that tuberous sclerosis complex 1 (TSC1) in osteocytes promotes sclerostin secretion through inhibition of mechanistic target of rapamycin complex 1 (mTORC1) and downregulation of Sirt1. We generated mice with DMP1 -Cre-directed Tsc1 gene deletion ( Tsc1 CKO) to constitutively activate mTORC1 in osteocytes. Although osteocyte TSC1 disruption increased RANKL expression and osteoclast formation, it markedly reduced sclerostin production in bone, resulting in severe osteosclerosis with enhanced bone formation in mice. Knockdown of TSC1 activated mTORC1 and decreased sclerostin, while rapamycin inhibited mTORC1 and increased sclerostin mRNA and protein expression levels in MLO-Y4 osteocyte-like cells. Furthermore, mechanical loading activated mTORC1 and prevented sclerostin expression in osteocytes. Mechanistically, TSC1 promotes sclerostin production and prevents osteogenesis through inhibition of mTORC1 and downregulation of Sirt1, a repressor of the sclerostin gene Sost . Our findings reveal a role of TSC1/mTORC1 signalling in the regulation of osteocyte sclerostin secretion and bone formation in response to mechanical loading in vitro . Targeting TSC1 represents a potential strategy to increase osteogenesis and prevent bone loss-related diseases.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Sclerostina"

1

MAGARO', MARIA SARA. "Crosstalk tra muscolo e osso: identificazione di Sclerostina come una presunta nuova miochina." Doctoral thesis, Università degli studi di Modena e Reggio Emilia, 2020. http://hdl.handle.net/11380/1200030.

Full text
Abstract:
L'osso e il muscolo striato sono stati riconosciuti come organi endocrini poiché producono e secernono "fattori simil-ormonali" attraverso i quali possono influenzarsi a vicenda ed agire su altri tessuti, dando vita ad un "crosstalk muscolo-scheletrico". Nel nostro studio, abbiamo utilizzato una linea cellulare miogenica (cellule C2C12) ed una osteogenica (cellule 2T3) per studiare gli effetti dei fattori prodotti dalle cellule muscolari sul processo di maturazione degli osteoblasti. Abbiamo evidenziato che il medium miogenico ha effetti inibitori sulla differenziazione degli osteoblasti: questo dato ci ha spinto ad analizzare il contenuto dei terreni condizionati da mioblasti/miotubi e, così facendo, abbiamo identificato Sclerostina come una delle miochine prodotte dalle cellule muscolari. Sclerostina è una glicoproteina secreta espressa principalmente dalle cellule ossee/cartilaginee ed è considerata un regolatore negativo della crescita ossea poiché agisce come antagonista della via di segnalazione Wnt/β-catenina. Si è scoperto anche che inibisce le prime fasi del differenziamento degli osteoblasti in pre-osteociti in vitro. Dato il ruolo inibitorio di questa proteina nell'osso, abbiamo approfondito l’analisi dell'espressione di Sclerostina da parte delle cellule muscolari e come essa possa influenzare la formazione e l'omeostasi dell’osso. Inizialmente, si è caratterizzata e quantificata la sintesi di Sclerostina in mioblasti murini (C2C12) tramite Western Blot, Real Time PCR, Immunofluorescenza ed ELISA. Successivamente, si è passati all’analisi della produzione di Sclerostina muscolare in vivo. Abbiamo esaminato la sua sintesi in muscoli di topi di età diversa: giovani (6 settimane), adulti (5 mesi) e anziani (18 mesi). Per ogni età abbiamo studiato: i) un muscolo composto da fibre fasiche o glicolitiche (Gastrocnemio); ii) un muscolo composto da fibre toniche o ossidative (Soleo), che sono soggette al carico meccanico e al movimento; iii) un muscolo dorsale (Latissimus dorsi), con meno carico in ragione dell'attività fasica degli arti, per verificare se il tipo di lavoro muscolare/carico influisce sulla produzione di Sclerostina. Inoltre, è stato isolato un muscolo dell'arto superiore (Triceps brachii), per confrontarlo con i muscoli dell'arto inferiore. Infine, allo scopo di delineare il ruolo di Sclerostina muscolare abbiamo espresso in modo transiente la proteina nei seguenti muscoli: quadricipite femorale, gastrocnemio e tibiale anteriore di giovani topi (2 settimane di età) attraverso l'elettroporazione di un plasmide contenente il gene SOST. Questo esperimento mira a valutare sia gli effetti paracrini della Sclerostina muscolare sui segmenti scheletrici adiacenti sia la sua azione endocrina sull'intero scheletro.
Bone and muscle have been recognized as endocrine organs since they produce and secrete “hormone like factors” that can mutually influence each other and other tissues, giving rise to a “bone-muscle crosstalk”. In our study, we made use of a myogenic (C2C12 cells) and an osteogenic (2T3 cells) cell line to investigate the effects of muscle cell-produced factors on the maturation process of osteoblasts. We found that the myogenic medium has inhibitory effects on bone cells differentiation: this datum prompted us to analyze the content of myoblast/myotube-conditioned media and, by so doing, we identified Sclerostin as one of the myokines produced by muscle cells. Sclerostin is a secreted glycoprotein mainly expressed by bone/cartilage cells and is considered a negative regulator of bone growth due to its role as an antagonist of the Wnt/β-catenin pathway. It has also been found to inhibit the early stages of in vitro osteoblasts-to-preosteocytes differentiation. Given the inhibitory role of this protein in bone, we analyzed deeper the expression of Sclerostin by muscle cells and how it affects bone formation and homeostasis. Firstly, we characterized and quantified Sclerostin synthesis by a murine myoblast cell line (C2C12) by Western Blot, Real Time PCR, Immunofluorescence and ELISA assay. Next, we moved on to the in vivo muscular production of Sclerostin. We examined its synthesis in muscles of differently aged mice: young (6 weeks), adult (5 months) and old (18 months). For each age we studied: i) a muscle composed of fast/phasic or glycolytic fibers (Gastrocnemius); ii) a muscle composed of slow/tonic or oxidative fibers (Soleus), which are subjected to mechanical loading and movement; iii) a back muscle (Latissimus dorsi), less loaded according to the phasic activity of the limbs, to check if the type of muscular work/load affects the Sclerostin production. Also, a muscle of the upper limb (Triceps brachii) was isolated, to compare it with the muscles of the lower limb. Finally, we transiently expressed Sclerostin in Quadriceps femoris, Gastrocnemius and Tibialis anterior muscles of young mice (2 weeks of age) via electroporation of a plasmid containing the SOST gene, in order to investigate the effects of a muscle-specific overproduction of the protein. This experiment was aimed at evaluating the paracrine effects of muscular Sclerostin on the adjacent skeletal segments and its endocrine action on the whole skeleton.
APA, Harvard, Vancouver, ISO, and other styles
2

Kim-Weroha, Nellie A. Johnson Mark L. "Regulation of sclerostin expression in osteocytes by mechanical loading." Diss., UMK access, 2008.

Abstract:
Thesis (M.S.)--School of Dentistry. University of Missouri--Kansas City, 2008.
"A thesis in oral biology." Advisor: Mark L. Johnson. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed Aug. 07, 2008. Includes bibliographical references (leaves 57-65). Online version of the print edition.
APA, Harvard, Vancouver, ISO, and other styles
3

Moustafa, Alaa M. "Mechanical loading effects on sclerostin expression in mouse bone in vivo." Thesis, Royal Veterinary College (University of London), 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558978.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Galea, Galea. "The regulation in bone cells of Sost/sclerostin by mechanical strain." Thesis, University of Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.629122.

Full text
Abstract:
Under normal circumstances bones are kept strong enough to withstand mechanical loads without fracture because bone cells sense the deformation that occurs when they are loaded and adjust bone structure accordingly. This process of functional adaptation allows us to lead active lives without a high incidence of fracture. The situation changes in later life when age-related bone loss occurs, leading to osteoporosis. Current treatments are unable to recover the bone lost with age, nor can they selectively target bone formation to regions of the skeleton under the greatest strain. Clinical trials are currently investigating the potential of blocking sclerostin, an endogenous inhibitor of bone formation which is down-regulated by loading, to cause bone formation. However, the mechanisms by which sclerostin expression is controlled by loading are not known. The experiments in this thesis were designed to establish how osteocyte-like cells translate the mechanical strain signals they encounter during loading into appropriate down-regulation of Sostlsclerostin. These studies delineate novel mechanisms whereby prostaglandin and oestrogen receptor signalling, previously known to influence bone's adaptation to loading, cooperate to promote Sost down-regulation following strain. We demonstrate that sclerostin inhibits the proliferation of osteoblast-like cells following strain, providing a mechanism whereby blocking sclerostin may lead to new bone formation. In the absence of sclerostin, osteoblastic cells' proliferation following strain requires the oestrogen receptor a and protein kinase Ca. Strain also orients the division of these cells through Planar Cell Polarity signalling, thereby potentially influencing bone architecture. These findings identify new mechanisms whereby loading stimulates bone cells to produce a structure strong enough to resist fracture. Deciphering the cellular processes by which sclerostin is naturally down-regulated following loading may lead to the development of improved treatment regimens for bone loss diseases based on the combination of sclerostin blocking therapies with other bone-strengthening strategies such as exercise.
APA, Harvard, Vancouver, ISO, and other styles
5

Chan, Sze-lai Celine, and 陳思例. "Sclerostin: a negative regulator of bone formation and a target for osteoporosis therapy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B4189702X.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Lyu, Quanxia. "Therapeutic potential of nucleic acid aptamers against sclerostin in the treatment of osteoporosis." HKBU Institutional Repository, 2017. https://repository.hkbu.edu.hk/etd_oa/431.

Full text
Abstract:
Osteoporosis is a skeletal disease characterized with poor bone quality and low bone mineral density. The pathogenesis of osteoporosis is the imbalance of bone resorption and bone formation. Two strategies can be employed to cure osteoporosis. One is to inhibit bone resorption and the other is to stimulate bone formation. Currently, therapeutic drugs approved by FDA are mainly antiresorptive agents. Till now, there is only one bone anabolic agent approved. Obviously, more efforts should be poured into the development of bone anabolic agents. Sclerostin is a key negative regulator of osteoblast Wnt signaling making it a promising therapeutic target for bone anabolic therapy. Anti-sclerostin humanized monoclonal antibody romosozumab, which could effectively promote bone formation, has been accepted by the FDA for the review of biologic license application in 2017. However, there are several concerns about the humanized anti-sclerostin antibody, including immunogenicity, high cost of production and relative low stability. Nucleic acid aptamers are short single stranded oligonucleotides. They can bind to their targets with similar high affinity as antibodies. Moreover, aptamers have some superior advantages compared to antibodies, such as no immunogenicity, easily synthesized, and high stability. Aptamers against sclerostin could be a promising alternative to antibodies in terms of promotion of bone formation and reversal of osteoporosis. In this thesis, 20 rounds of SELEX were performed to select aptamers with high binding affinity and specificity to sclerostin. The inhibition potency of aptamer candidates to the antagonistic effect of sclerostin on Wnt signaling was also evaluated. Low KD and EC50 values of aptamer candidates against sclerostin implied a great potential of sclerostin aptamer being novel agents to promote bone formation. The study establishes the foundation for the next stage of preclinical studies and it will benefit the development of novel bone anabolic agents to reverse osteoporosis.
APA, Harvard, Vancouver, ISO, and other styles
7

Chan, Sze-lai Celine. "Sclerostin a negative regulator of bone formation and a target for osteoporosis therapy /." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4189702X.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

ABU, HAMDAN NATALIE. "SCLEROSTIN IMMUNOREACTIVITY INCREASES WITHIN THE CORTICAL BONE OSTEOCYTES IN THE FEMUR OF AGING MICE." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/612463.

Full text
Abstract:
Sclerostin, a secreted glycoprotein, is known to down-regulate osteocyte differentiation from osteoblasts and acts as a negative modulator of bone formation. It is well established that serum sclerostin levels increase with age but the relationship between changes of cellular expression of sclerostin with age is not well known. Immunohistochemical staining and confocal microscopic analysis of sclerostin immunoreactivity (sclerostin-IR) in the femurs of 4, 9, and 24 month old adult C3H/HeJ male mice was performed. Detectable levels of sclerostin-IR were found in cortical bone osteocytes of the femur in all age groups using an antibody directed against sclerostin. Phalloidin and DAPI were used to mark all osteocytes in cortical bone to detect osteocyte/ sclerostin-IR colocalization. Sclerostin-negative and sclerostin-positive expressing osteocytes were detected in close proximity throughout the cortical bone. Only a subset of osteocytes expressed sclerostin and this ratio of sclerostin positive osteocytes increased with age, from 38.5 ± 1.6% to 43 ± 3.6% to 49 ± 2.3% in young, middle-aged, and old mice, respectively. Understanding the potential mechanisms that drive these age-related changes may influence the therapeutic potential of age-related diseases like osteoporosis.
APA, Harvard, Vancouver, ISO, and other styles
9

York, Spencer. "Impact of Mechanically-Induced Microdamage and Gap Junctional Intercellular Communication on MLO-Y4 Viability and Sclerostin Expression." University of Akron / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=akron1415272760.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Kruck, Bettina [Verfasser]. "Die Behandlung mit Sclerostin-neutralisierenden Antikörpern fördert die Knochenbildung, kann jedoch eine mechanisch bedingte Heilungsverzögerung nicht ausgleichen / Bettina Kruck." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1206185724/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Sclerostina"

1

Cipriani, Cristiana, and John P. Bilezikian. "Sclerostin Inhibition." In Osteoporosis. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-83951-2_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kosacka, M., I. Porębska, and A. Brzecka. "Sclerostin in Obstructive Sleep Apnea." In Respiratory Medicine and Science. Springer International Publishing, 2015. http://dx.doi.org/10.1007/5584_2015_202.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

van Lierop, Antoon H., and Socrates E. Papapoulos. "Circulating Sclerostin in Bone Sclerosing Disorders." In Biomarkers in Bone Disease. Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7693-7_39.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

van Lierop, Antoon H., and Socrates E. Papapoulos. "Circulating Sclerostin in Bone Sclerosing Disorders." In Biomarkers in Bone Disease. Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7745-3_39-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Baron, Roland, Francesca Gori, and Benjamin Z. Leder. "Sclerostin Inhibition in the Treatment of Osteoporosis." In Osteoporosis. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-69287-6_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Kocijan, Roland, Sebastian Dinu, and Christian Muschitz. "Serum Sclerostin as Biomarker in Osteogenesis Imperfecta." In Biomarkers in Bone Disease. Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7693-7_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kocijan, Roland, Sebastian Dinu, and Christian Muschitz. "Serum Sclerostin as Biomarker in Osteogenesis Imperfecta." In Biomarkers in Bone Disease. Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7745-3_5-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Apetrii, Mugurel, and Adrian Covic. "Wnt/Sclerostin and the Relation with Vitamin D in Chronic Kidney Disease." In Vitamin D in Chronic Kidney Disease. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32507-1_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Findlay, David M., and Gerald J. Atkins. "TWEAK and TNF Regulation of Sclerostin: A Novel Pathway for the Regulation of Bone Remodelling." In Advances in Experimental Medicine and Biology. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6612-4_34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

van Bezooijen, Rutger L., Socrates E. Papapoulos, Neveen A. T. Hamdy, and Clemens W. G. M. Löwik. "SOST/Sclerostin." In Principles of Bone Biology. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-12-373884-4.00014-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Sclerostina"

1

SHARBA, Intisar Razzaq, та Arshad Noori AL-DUJAILI. "ASSESSMENT OF SERUM SCLEROSTIN LEVEL AS A BIOMARKER ASSOCIATED WITH BONE DISORDERS IN Β-THALASSEMIA PATIENTS IN AL- NAJAF CITY, IRAQ". У SOUTHERN BRAZILIAN JOURNAL OF CHEMISTRY 2021 INTERNATIONAL VIRTUAL CONFERENCE. DR. D. SCIENTIFIC CONSULTING, 2022. http://dx.doi.org/10.48141/sbjchem.21scon.05_abstract_sharba.pdf.

Full text
Abstract:
Aim of the study: To assess serum sclerostin in female patients with beta-thalassemia and compare with the healthy controls and to predict its complication associated with the bone pathophysiology, for designed improvement the lifestyle goodliness for these patients. Material and methods: Sixty-nine female beta-thalassemia (βT) patients (54 βT major and 15 βT Intermedia), aged 8-40 years who dependent on transfused blood, and 20 healthy controls were evaluated serum sclerostin, and was examined the relationship with hematological parameters RBC, Hb, PCV, WBC, PLT, BMI, splenic status, iron, and ferritin levels. The information of beta-thalassemia patients was collected and recorded by the questioner. Results: A significantly increased serum sclerostin level (mean 26.80±0.91) pg/ml was shown in βT patients compared with the healthy controls (10.03±0.68, p < 0.001) pg/ml. Furthermore, a significant decrease (p<0.05) of the sclerostin level was observed in β-thalassemia major compared to intermedia β-thalassemia patients. Serum sclerostin level revealed a significant increase in progress age; it is highest in the age group (30-40) year as compared with age group (8-18) and (19-29) year respectively. Sclerostin showed no associations with the RBC, Hb, PCV, and significantly positively correlated (p<0.05) with serum iron, ferritin levels, WBC, and PLT count. Significantly higher sclerostin levels in splenectomized and underweight groups were observed compared to unsplenectomized and normal-weight groups (p<0.05) of βT patients. Conclusion: Sclerostin plays an important role in beta-thalassemia patients and can serve as a biomarker associated with the bone pathophysiology and indicator to prevent the continuation of such serious diseases caused by iron overload in these patients.
APA, Harvard, Vancouver, ISO, and other styles
2

Pap, T. "SP0135 Myostatin, sclerostin, syndecan and more." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7261.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Biasin, V., J. Hoffmann, E. Gschwandtner, W. Klepetko, B. Obermayer-Pietsch, and G. Kwapiszewska. "Sclerostin: moving from bone to lung." In 1. MuSkITYR Symposium. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1700631.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Intemann, J., C. Wehmeyer, V. Kracke, et al. "P081 Sclerostin affects rankl-mediated osteoclast differentiation." In 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Intemann, J., C. Wehmeyer, DJ de Gorter, et al. "P082/O24 Sclerostin deficiency affects RANKL-mediated osteoclast differentiation." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.71.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bitzer, A., J. Wallwitz, E. Gadermaier, G. Berg, and G. Himmler. "Bioactive Sclerostin: better analyte definition in the measurement of bone remodeling." In OSTEOLOGIE 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680030.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Elmallah, R., E. EL Attar, D. Farrag, and D. Samaha. "AB0787 Study of serum sclerostin levels in association to enthesial ultrasonography in egyptian psoriatic arthritis patients." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1317.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ciccia, F., G. Guggino, A. Rizzo, et al. "OP0309 Intestinal sclerostin/serotonin axis is modulated by dysbiosis and regulates ilc3 expansion in as patients." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3995.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Lloyd, William R., Benjamin P. Sinder, Joseph Salemi, et al. "Tissue level material composition and mechanical properties in Brtl/+ mouse model of Osteogenesis Imperfecta after sclerostin antibody treatment." In SPIE BiOS, edited by Bernard Choi, Nikiforos Kollias, Haishan Zeng, et al. SPIE, 2015. http://dx.doi.org/10.1117/12.2080261.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Brandy-Garcia, Anahy, Melania Martínez-Morillo, Roxana Coras, et al. "FRI0481 MEDIATORS OF BONE METABOLISM (DKK1, OPG SCLEROSTIN AND RANKL) IN A COHORT OF PATIENTS WITH ELDERLY-ONSET ARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5305.

Full text
APA, Harvard, Vancouver, ISO, and other styles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography