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    Sost sclerostin [ Rattus norvegicus (Norway rat) ]

    Gene ID: 80722, updated on 2-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    The Possible Role of Sclerostin in the Pathogenesis of Tympanosclerosis.

    The Possible Role of Sclerostin in the Pathogenesis of Tympanosclerosis.
    Huang Y, Wang X, Wu F, Lu Y, Liang G, Liu A.

    07/3/2021
    Changes in the intra- and peri-cellular sclerostin distribution in lacuno-canalicular system induced by mechanical unloading.

    Changes in the intra- and peri-cellular sclerostin distribution in lacuno-canalicular system induced by mechanical unloading.
    Osumi R, Wang Z, Ishihara Y, Odagaki N, Iimura T, Kamioka H.

    04/13/2021
    Sclerostin as Regulatory Molecule in Vascular Media Calcification and the Bone-Vascular Axis.

    Sclerostin as Regulatory Molecule in Vascular Media Calcification and the Bone-Vascular Axis.
    De Maré A, Maudsley S, Azmi A, Hendrickx JO, Opdebeeck B, Neven E, D'Haese PC, Verhulst A., Free PMC Article

    09/5/2020
    The combination of ZOL and the osteoanabolic sclerostin antibody was more effective than either agent alone.

    Systemic sclerostin antibody treatment increases osseointegration and biomechanical competence of zoledronic-acid-coated dental implants in a rat osteoporosis model.
    Korn P, Kramer I, Schlottig F, Tödtman N, Eckelt U, Bürki A, Ferguson SJ, Kautz A, Schnabelrauch M, Range U, Kneissel M, Stadlinger B.

    05/30/2020
    More surprisingly SOST and DKK1 were overexpressed from day 6 and followed by a dramatic decrease in bone formation from day 8. At the time of arthritis onset, SOST and DKK1 returned to control values, but frizzled related protein 1 (SFRP1), proinflammatory cytokines, and MMPs started to increase.

    Early sclerostin expression explains bone formation inhibition before arthritis onset in the rat adjuvant-induced arthritis model.
    Courbon G, Lamarque R, Gerbaix M, Caire R, Linossier MT, Laroche N, Thomas M, Thomas T, Vico L, Marotte H., Free PMC Article

    09/14/2019
    beta-GP induced VSMC calcification by activating the Wnt/beta-catenin signaling pathway. Sclerostin and Lrp4 were involved in beta-GP-induced VSMC calcification and play an important role. GBE could alleviate VSMC calcification induced by beta-GP through inhibiting the Wnt/beta-catenin signaling pathway.

    Sclerostin/Receptor Related Protein 4 and Ginkgo Biloba Extract Alleviates β-Glycerophosphate-Induced Vascular Smooth Muscle Cell Calcification By Inhibiting Wnt/β-Catenin Pathway.
    Wang J, Qiu X, Xu T, Sheng Z, Yao L., Free PMC Article

    05/4/2019
    alleviated the osteogenic differentiation of ectomesenchymal stem cells (EMSCs), and LNGFR enhanced the osteogenic differentiation of EMSCs by decreasing SOST

    SOST, an LNGFR target, inhibits the osteogenic differentiation of rat ectomesenchymal stem cells.
    Li G, Liu J, Zhao M, Wang Y, Yang K, Liu C, Xiao Y, Wen X, Liu L., Free PMC Article

    03/31/2018
    TNF-alpha might mediate alveolar bone loss via inducing expression of osteocytic RANKL and sclerostin in type 1 diabetes rats with periodontitis

    Tumor necrosis factor-α antagonist diminishes osteocytic RANKL and sclerostin expression in diabetes rats with periodontitis.
    Kim JH, Kim AR, Choi YH, Jang S, Woo GH, Cha JH, Bak EJ, Yoo YJ., Free PMC Article

    12/30/2017
    Four genes are expressed significantly higher in basal bone than in alveolar bone: SOST, E-11, DMP-1, and MEPE. Three of the proteins (SOST, MEPE, and DMP-1) are associated with mature osteocytes, indicating that basal bone has more mature osteocyte phenotypes because the immature osteocyte converts to a mature osteocyte as a result of bone mineralization.

    Inherent physical characteristics and gene expression differences between alveolar and basal bones.
    Zakhary I, Alotibi F, Lewis J, ElSalanty M, Wenger K, Sharawy M, Messer RL., Free PMC Article

    08/12/2017
    These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.

    Sclerostin Promotes Bone Remodeling in the Process of Tooth Movement.
    Shu R, Bai D, Sheu T, He Y, Yang X, Xue C, He Y, Zhao M, Han X., Free PMC Article

    08/5/2017
    a direct correlation between attenuated SOST expression and an increase in the osteogenic potential of UMR-106 cells, is reported.

    Rat Osteosarcoma Cells as a Therapeutic Target Model for Osteoregeneration via Sclerostin Knockdown.
    Sedaghati B, Jahroomishirazi R, Starke A, Hacker MC, Schulz-Siegmund M.

    03/11/2017
    In conclusion, naringin could prevent progress of disuse osteoporosis in rats, which may be mediated by increased periostin expression and subsequently inhibition of sclerostin and activation of Wnt/beta-catenin signaling pathways.

    Involvement of periostin-sclerostin-Wnt/β-catenin signaling pathway in the prevention of neurectomy-induced bone loss by naringin.
    Lv J, Sun X, Ma J, Ma X, Xing G, Wang Y, Sun L, Wang J, Li F, Li Y.

    04/23/2016
    Scl-Ab increased osteoblast surface and bone formation, indicating direct bone anabolic effects, whereas TE reduced osteoclast surface with minimal effect on bone formation, indicating antiresorptive effects

    Sclerostin inhibition prevents spinal cord injury-induced cancellous bone loss.
    Beggs LA, Ye F, Ghosh P, Beck DT, Conover CF, Balaez A, Miller JR, Phillips EG, Zheng N, Williams AA, Aguirre JI, Wronski TJ, Bose PK, Borst SE, Yarrow JF., Free PMC Article

    01/16/2016
    Data indicate that sclerostin (SOST) gene expression is negatively regulated by histone deacetylase HDAC5 and positively by class I HDACs.

    Class I and IIa histone deacetylases have opposite effects on sclerostin gene regulation.
    Baertschi S, Baur N, Lueders-Lefevre V, Voshol J, Keller H., Free PMC Article

    01/31/2015
    The results suggest that Sost mRNA expression in metaphyseal bone responds to mechanical unloading in an opposite direction to that observed in diaphyseal cortical bone.

    Paradoxical Sost gene expression response to mechanical unloading in metaphyseal bone.
    Macias BR, Aspenberg P, Agholme F.

    09/7/2013
    Pharmacologic inhibition of sclerostin with Scl-Ab has no impact on articular cartilage remodeling in rats with posttraumatic osteoarthritis.

    Sclerostin is expressed in articular cartilage but loss or inhibition does not affect cartilage remodeling during aging or following mechanical injury.
    Roudier M, Li X, Niu QT, Pacheco E, Pretorius JK, Graham K, Yoon BR, Gong J, Warmington K, Ke HZ, Black RA, Hulme J, Babij P.

    04/27/2013
    Confocal immunofluorescence tiling imaging revealed the spatio-temporal distributions of osterix and sclerostin in femurs from 3-day-old, 2-week-old and 4-week-old rats to be reciprocally exclusive at the tissue level.

    Increasing participation of sclerostin in postnatal bone development, revealed by three-dimensional immunofluorescence morphometry.
    Watanabe T, Tamamura Y, Hoshino A, Makino Y, Kamioka H, Amagasa T, Yamaguchi A, Iimura T.

    12/22/2012
    The proportion of sclerostin-positive osteocytes in cortical bone was significantly higher.

    Simulated resistance training, but not alendronate, increases cortical bone formation and suppresses sclerostin during disuse.
    Macias BR, Swift JM, Nilsson MI, Hogan HA, Bouse SD, Bloomfield SA.

    09/15/2012
    Insulin-deficiency in insulin-dependent diabetes mellitus decreases osteoblastogenesis associated with inhibition of Wnt signaling through the increased expression of Sost and Dkk1 and the inhibition of Akt activation.

    Insulin-dependent diabetes mellitus decreases osteoblastogenesis associated with the inhibition of Wnt signaling through increased expression of Sost and Dkk1 and inhibition of Akt activation.
    Hie M, Iitsuka N, Otsuka T, Tsukamoto I.

    11/5/2011
    These results indicate that sclerostin inhibition by treatment with a sclerostin antibody increased bone formation, bone mass, and bone strength in aged male rats.

    Inhibition of sclerostin by monoclonal antibody increases bone formation, bone mass, and bone strength in aged male rats.
    Li X, Warmington KS, Niu QT, Asuncion FJ, Barrero M, Grisanti M, Dwyer D, Stouch B, Thway TM, Stolina M, Ominsky MS, Kostenuik PJ, Simonet WS, Paszty C, Ke HZ.

    03/5/2011
    Modulation of sclerostin levels appears to be a finely tuned mechanism by which osteocytes coordinate regional and local osteogenesis in response to increased mechanical stimulation, perhaps via releasing the local inhibition of Wnt/Lrp5 signaling

    Mechanical stimulation of bone in vivo reduces osteocyte expression of Sost/sclerostin.
    Robling AG, Niziolek PJ, Baldridge LA, Condon KW, Allen MR, Alam I, Mantila SM, Gluhak-Heinrich J, Bellido TM, Harris SE, Turner CH.

    01/21/2010
    SOST expression in osteocytes of adult bone and its inhibition by PTH is mediated by MEF2A, C, and D transcription factors controlling the SOST bone enhancer.

    Control of the SOST bone enhancer by PTH using MEF2 transcription factors.
    Leupin O, Kramer I, Collette NM, Loots GG, Natt F, Kneissel M, Keller H., Free PMC Article

    01/21/2010
    The anabolic effects of parathyroid hormone (PTH) are in line with the fall of SOST mRNA and protein in all the three bone segments examined; the rise of bone turnover supports a negative role of SOST in bone formation.

    Effects of intermittent parathyroid hormone (PTH) administration on SOST mRNA and protein in rat bone.
    Silvestrini G, Ballanti P, Leopizzi M, Sebastiani M, Berni S, Di Vito M, Bonucci E.

    01/21/2010
    SOST regulation may play a role in mediating PTH action in bone

    SOST is a target gene for PTH in bone.
    Keller H, Kneissel M.

    01/21/2010
    noggin and sclerostin form a mutually inhibitory complex that fine-tunes of BMP activity in bone homeostasis

    Noggin and sclerostin bone morphogenetic protein antagonists form a mutually inhibitory complex.
    Winkler DG, Yu C, Geoghegan JC, Ojala EW, Skonier JE, Shpektor D, Sutherland MK, Latham JA.

    01/21/2010
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