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Artykuły w czasopismach na temat „Osteoblast”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Kim, Jung Ha, Kabsun Kim, Inyoung Kim, Semun Seong, Jeong-Tae Koh, and Nacksung Kim. "The ATF3–OPG Axis Contributes to Bone Formation by Regulating the Differentiation of Osteoclasts, Osteoblasts, and Adipocytes." International Journal of Molecular Sciences 23, no. 7 (2022): 3500. http://dx.doi.org/10.3390/ijms23073500.

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Activating transcription factor 3 (ATF3) has been identified as a negative regulator of osteoblast differentiation in in vitro study. However, it was not associated with osteoblast differentiation in in vivo study. To provide an understanding of the discrepancy between the in vivo and in vitro findings regarding the function of ATF3 in osteoblasts, we investigated the unidentified roles of ATF3 in osteoblast biology. ATF3 enhanced osteoprotegerin (OPG) production, not only in osteoblast precursor cells, but also during osteoblast differentiation and osteoblastic adipocyte differentiation. In a

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2

Giuliani, Nicola, Francesca Morandi, Sara Tagliaferri, et al. "The proteasome inhibitor bortezomib affects osteoblast differentiation in vitro and in vivo in multiple myeloma patients." Blood 110, no. 1 (2007): 334–38. http://dx.doi.org/10.1182/blood-2006-11-059188.

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The proteasome inhibitor bortezomib may increase osteoblast-related markers in multiple myeloma (MM) patients; however, its potential osteoblastic stimulatory effect is not known. In this study, we show that bortezomib significantly induced a stimulatory effect on osteoblast markers in human mesenchymal cells without affecting the number of osteoblast progenitors in bone marrow cultures or the viability of mature osteoblasts. Consistently we found that bortezomib significantly increased the transcription factor Runx2/Cbfa1 activity in human osteoblast progenitors and osteoblasts without affect

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Bauer, Omri, Amnon Sharir, Ayako Kimura, Shay Hantisteanu, Shu Takeda, and Yoram Groner. "Loss of Osteoblast Runx3 Produces Severe Congenital Osteopenia." Molecular and Cellular Biology 35, no. 7 (2015): 1097–109. http://dx.doi.org/10.1128/mcb.01106-14.

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Congenital osteopenia is a bone demineralization condition that is associated with elevated fracture risk in human infants. Here we show thatRunx3, likeRunx2, is expressed in precommitted embryonic osteoblasts and that Runx3-deficient mice develop severe congenital osteopenia. Runx3-deficient osteoblast-specific (Runx3fl/fl/Col1α1-cre), but not chondrocyte-specific (Runx3fl/fl/Col1α2-cre), mice are osteopenic. This demonstrates that an osteoblastic cell-autonomous function of Runx3 is required for proper osteogenesis. Bone histomorphometry revealed that decreased osteoblast numbers and reduced

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4

Ducy, P., and G. Karsenty. "Two distinct osteoblast-specific cis-acting elements control expression of a mouse osteocalcin gene." Molecular and Cellular Biology 15, no. 4 (1995): 1858–69. http://dx.doi.org/10.1128/mcb.15.4.1858.

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Osteoblasts are cells of mesodermal origin that play a pivotal role during bone growth and mineralization. The mechanisms governing osteoblast-specific gene expression are still unknown. To understand these mechanisms, we analyzed the cis-acting elements of mouse osteocalcin gene 2 (mOG2), the best-characterized osteoblast-specific gene, by DNA transfection experiments in osteoblastic and nonosteoblastic cell lines and by DNA-binding assays. 5' deletion analysis of an mOG2 promoter-luciferase chimeric gene showed that a region located between -147 and -34 contained most if not all of the regul

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5

Sutton, Amelia L. M., Xiaoxue Zhang, Diane R. Dowd, Yogendra P. Kharode, Barry S. Komm, and Paul N. MacDonald. "Semaphorin 3B Is a 1,25-Dihydroxyvitamin D3-Induced Gene in Osteoblasts that Promotes Osteoclastogenesis and Induces Osteopenia in Mice." Molecular Endocrinology 22, no. 6 (2008): 1370–81. http://dx.doi.org/10.1210/me.2007-0363.

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Abstract The vitamin D endocrine system is important for skeletal homeostasis. 1,25-Dihydroxyvitamin D3 [1,25(OH)2D3] impacts bone indirectly by promoting intestinal absorption of calcium and phosphate and directly by acting on osteoblasts and osteoclasts. Despite the direct actions of 1,25(OH)2D3 in bone, relatively little is known of the mechanisms or target genes that are regulated by 1,25(OH)2D3 in skeletal cells. Here, we identify semaphorin 3B (SEMA3B) as a 1,25(OH)2D3-stimulated gene in osteoblastic cells. Northern analysis revealed strong induction of SEMA3B mRNA by 1,25(OH)2D3 in MG-6

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6

Park, Yu-Seong, Hyun-Woo Kim, Jin-Hyeon Hwang, et al. "Plum-Derived Exosome-like Nanovesicles Induce Differentiation of Osteoblasts and Reduction of Osteoclast Activation." Nutrients 15, no. 9 (2023): 2107. http://dx.doi.org/10.3390/nu15092107.

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Osteoblasts and osteoclasts play crucial roles in bone formation and bone resorption. We found that plum-derived exosome-like nanovesicles (PENVs) suppressed osteoclast activation and modulated osteoblast differentiation. PENVs increased the proliferation, differentiation, and mineralization of osteoblastic MC3T3-E1 cells and osteoblasts from mouse bone marrow cultures. Notably, PENVs elevated the expression of osteoblastic transcription factors and osteoblast differentiation marker proteins in MC3T3-E1 cells. Higher levels of phosphorylated BMP-2, p38, JNK, and smad1 proteins were detected in

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7

Skillington, Jeremy, Lisa Choy, and Rik Derynck. "Bone morphogenetic protein and retinoic acid signaling cooperate to induce osteoblast differentiation of preadipocytes." Journal of Cell Biology 159, no. 1 (2002): 135–46. http://dx.doi.org/10.1083/jcb.200204060.

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Mesenchymal cells can differentiate into osteoblasts, adipocytes, myoblasts, or chondroblasts. Whether mesenchymal cells that have initiated differentiation along one lineage can transdifferentiate into another is largely unknown. Using 3T3-F442A preadipocytes, we explored whether extracellular signals could redirect their differentiation from adipocyte into osteoblast. 3T3-F442A cells expressed receptors and Smads required for bone morphogenetic protein (BMP) signaling. BMP-2 increased proliferation and induced the early osteoblast differentiation marker alkaline phosphatase, yet only mildly

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8

Hernández-Tapia, Laura G., Zdenka Fohlerová, Jan Žídek, et al. "Effects of Cryopreservation on Cell Metabolic Activity and Function of Biofabricated Structures Laden with Osteoblasts." Materials 13, no. 8 (2020): 1966. http://dx.doi.org/10.3390/ma13081966.

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Biofabrication and maturation of bone constructs is a long-term task that requires a high degree of specialization. This specialization falls onto the hierarchy complexity of the bone tissue that limits the transfer of this technology to the clinic. This work studied the effects of the short-term cryopreservation on biofabricated osteoblast-containing structures, with the final aim to make them steadily available in biobanks. The biological responses studied include the osteoblast post-thawing metabolic activity and the recovery of the osteoblastic function of 3D-bioprinted osteoblastic struct

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9

Kim, Jung Ha, Kabsun Kim, Inyoung Kim, et al. "Bifunctional Role of CrkL during Bone Remodeling." International Journal of Molecular Sciences 22, no. 13 (2021): 7007. http://dx.doi.org/10.3390/ijms22137007.

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Coupled signaling between bone-forming osteoblasts and bone-resorbing osteoclasts is crucial to the maintenance of bone homeostasis. We previously reported that v-crk avian sarcoma virus CT10 oncogene homolog-like (CrkL), which belongs to the Crk family of adaptors, inhibits bone morphogenetic protein 2 (BMP2)-mediated osteoblast differentiation, while enhancing receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast differentiation. In this study, we investigated whether CrkL can also regulate the coupling signals between osteoblasts and osteoclasts, facilitating bone h

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10

Moriishi, Takeshi, Yosuke Kawai, Ryo Fukuyama, et al. "Bcl2l1 Deficiency in Osteoblasts Reduces the Trabecular Bone Due to Enhanced Osteoclastogenesis Likely through Osteoblast Apoptosis." International Journal of Molecular Sciences 24, no. 24 (2023): 17319. http://dx.doi.org/10.3390/ijms242417319.

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Bcl2l1 (Bcl-XL) belongs to the Bcl-2 family, Bcl2 and Bcl2-XL are major anti-apoptotic proteins, and the apoptosis of osteoblasts is a key event for bone homeostasis. As the functions of Bcl2l1 in osteoblasts and bone homeostasis remain unclear, we generated osteoblast-specific Bcl2l1-deficient (Bcl2l1fl/flCre) mice using 2.3-kb Col1a1 Cre. Trabecular bone volume and the trabecular number were lower in Bcl2l1fl/flCre mice of both sexes than in Bcl2l1fl/fl mice. In bone histomorphometric analysis, osteoclast parameters were increased in Bcl2l1fl/flCre mice, whereas osteoblast parameters and the

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11

Yu, Vionnie W. C., Gourgen Ambartsoumian, Lieve Verlinden, et al. "FIAT represses ATF4-mediated transcription to regulate bone mass in transgenic mice." Journal of Cell Biology 169, no. 4 (2005): 591–601. http://dx.doi.org/10.1083/jcb.200412139.

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We report the characterization of factor inhibiting activating transcription factor 4 (ATF4)–mediated transcription (FIAT), a leucine zipper nuclear protein. FIAT interacted with ATF4 to inhibit binding of ATF4 to DNA and block ATF4-mediated transcription of the osteocalcin gene in vitro. Transgenic mice overexpressing FIAT in osteoblasts also had reduced osteocalcin gene expression and decreased bone mineral density, bone volume, mineralized volume, trabecular thickness, trabecular number, and decreased rigidity of long bones. Mineral homeostasis, osteoclast number and activity, and osteoblas

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12

Giuliani, Nicola, Francesca Morandi, Sara Tagliaferri, et al. "The Proteasome Inhibitor Bortezomib Affects Osteoblastogenesis and Bone Formation In Vitro and In Vivo in Multiple Myeloma Patients." Blood 108, no. 11 (2006): 508. http://dx.doi.org/10.1182/blood.v108.11.508.508.

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Abstract It is well established that osteoblast formation and function are profoundly impaired in multiple myeloma (MM) patients. Osteoblastic cells also regulate myeloma cell growth and increasing bone formation result in a reduction of tumoral burden in mice. Recent data suggest that ubiquitin-proteasome pathway, the major cellular degradative system and therapeutic target in myeloma cells, also regulates osteoblast differentiation. Further it has been demonstrated that different proteasome inhibitors may stimulate bone formation in mice. Finally, preliminary observations obtained in MM pati

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13

Weivoda, Megan M., and Raymond J. Hohl. "Effects of Farnesyl Pyrophosphate Accumulation on Calvarial Osteoblast Differentiation." Endocrinology 152, no. 8 (2011): 3113–22. http://dx.doi.org/10.1210/en.2011-0016.

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Statins, drugs commonly used to lower serum cholesterol, have been shown to stimulate osteoblast differentiation and bone formation. Statins inhibit 3-hydroxy-3-methylglutaryl (HMG)-coenzyme A reductase (HMGCR), the first step of the isoprenoid biosynthetic pathway, leading to the depletion of the isoprenoids farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP). The effects of statins on bone have previously been attributed to the depletion of GGPP, because the addition of exogenous GGPP prevented statin-stimulated osteoblast differentiation in vitro. However, in a recent repor

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14

Di Benedetto, Adriana, Francesca Posa, Claudia Carbone, et al. "NURR1 Downregulation Favors Osteoblastic Differentiation of MSCs." Stem Cells International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/7617048.

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Mesenchymal stem cells (MSCs) have been identified in human dental tissues. Dental pulp stem cells (DPSCs) were classified within MSC family, are multipotent, can be isolated from adult teeth, and have been shown to differentiate, under particular conditions, into various cell types including osteoblasts. In this work, we investigated how the differentiation process of DPSCs toward osteoblasts is controlled. Recent literature data attributed to the nuclear receptor related 1 (NURR1), a still unclarified role in osteoblast differentiation, while NURR1 is primarily involved in dopaminergic neuro

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15

Grey, Andrew, Qi Chen, Xin Xu, Karen Callon, and Jill Cornish. "Parallel Phosphatidylinositol-3 Kinase and p42/44 Mitogen-Activated Protein Kinase Signaling Pathways Subserve the Mitogenic and Antiapoptotic Actions of Insulin-Like Growth Factor I in Osteoblastic Cells." Endocrinology 144, no. 11 (2003): 4886–93. http://dx.doi.org/10.1210/en.2003-0350.

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Abstract IGF-I is an endocrine and paracrine regulator of skeletal homeostasis, principally by virtue of its anabolic effects on osteoblastic cells. In the current study, we examined the intracellular signaling pathways by which IGF-I promotes proliferation and survival in SaOS-2 human osteoblastic cells. Inhibition of each of the phosphatidylinositol-3 kinase (PI-3 kinase), p42/44 MAPK, and p70s6 kinase pathways partially inhibited the ability of IGF-I to stimulate osteoblast proliferation and survival. Because activation of p70s6 kinase is downstream of both PI-3 kinase and p42/44 MAPK activ

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16

Ogata, Naoshi, Hiroshi Kawaguchi, Ung-il Chung, Sanford I. Roth та Gino V. Segre. "Continuous Activation of Gαq in Osteoblasts Results in Osteopenia through Impaired Osteoblast Differentiation". Journal of Biological Chemistry 282, № 49 (2007): 35757–64. http://dx.doi.org/10.1074/jbc.m611902200.

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We explored the role of Gαq-mediated signaling on skeletal homeostasis by selectively expressing a constitutively active Gαq (mutation of Q209L) in osteoblasts. Continuous signaling via Gαq in mouse osteoblastic MC3T3-E1 cells impaired differentiation. Mice that expressed the constitutively active Gαq transgene in cells of the osteoblast lineage exhibited severe osteopenia in cortical and trabecular bones. Osteoblast number, bone volume, and trabecular thickness were reduced in transgenic mice, but the osteoclasts were unaffected. Osteoblasts from transgenic mice showed impaired differentiatio

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17

Ponzetti, Marco, and Nadia Rucci. "Osteoblast Differentiation and Signaling: Established Concepts and Emerging Topics." International Journal of Molecular Sciences 22, no. 13 (2021): 6651. http://dx.doi.org/10.3390/ijms22136651.

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Osteoblasts, the cells that build up our skeleton, are remarkably versatile and important cells that need tight regulation in all the phases of their differentiation to guarantee proper skeletal development and homeostasis. Although we know many of the key pathways involved in osteoblast differentiation and signaling, it is becoming clearer and clearer that this is just the tip of the iceberg, and we are constantly discovering novel concepts in osteoblast physiology. In this review, we discuss well-established pathways of osteoblastic differentiation, i.e., the classical ones committing mesenc

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18

Taichman, Russell S. "Blood and bone: two tissues whose fates are intertwined to create the hematopoietic stem-cell niche." Blood 105, no. 7 (2005): 2631–39. http://dx.doi.org/10.1182/blood-2004-06-2480.

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AbstractThe mechanisms of bone and blood formation have traditionally been viewed as distinct, unrelated processes, but compelling evidence suggests that they are intertwined. Based on observations that hematopoietic precursors reside close to endosteal surfaces, it was hypothesized that osteoblasts play a central role in hematopoiesis, and it has been shown that osteoblasts produce many factors essential for the survival, renewal, and maturation of hematopoietic stem cells (HSCs). Preceding these observations are studies demonstrating that the disruption or perturbation of normal osteoblastic

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Giardullo, Liberato, Alberto Altomare, Cinzia Rotondo, Addolorata Corrado, and Francesco Paolo Cantatore. "Osteoblast Dysfunction in Non-Hereditary Sclerosing Bone Diseases." International Journal of Molecular Sciences 22, no. 15 (2021): 7980. http://dx.doi.org/10.3390/ijms22157980.

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A review of the available literature was performed in order to summarize the existing evidence between osteoblast dysfunction and clinical features in non-hereditary sclerosing bone diseases. It has been known that proliferation and migration of osteoblasts are concerted by soluble factors such as fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), transforming growth factor (TGF), bone morphogenetic protein (BMP) but also by signal transduction cascades such as Wnt signaling pathway. Protein kinases play also a leading role in triggering the activation of osteoblasts in thi

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Troka, Ildi, Gabriele Griffanti, Lucie Canaff, Geoffrey Hendy, David Goltzman, and Showan Nazhat. "Effect of Menin Deletion in Early Osteoblast Lineage on the Mineralization of an In Vitro 3D Osteoid-like Dense Collagen Gel Matrix." Biomimetics 7, no. 3 (2022): 101. http://dx.doi.org/10.3390/biomimetics7030101.

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Bone has a complex microenvironment formed by an extracellular matrix (ECM) composed mainly of mineralized type I collagen fibres. Bone ECM regulates signaling pathways important in the differentiation of osteoblast-lineage cells, necessary for bone mineralization and in preserving tissue architecture. Compared to conventional 2D cell cultures, 3D in vitro models may better mimic bone ECM and provide an environment to support osteoblastic differentiation. In this study, a biomimetic 3D osteoid-like dense collagen gel model was used to investigate the role of the nuclear protein menin plays in

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21

Park, Jin-Ho, Su A. Park, Young-Hoon Kang, et al. "Zinc Sulfate Stimulates Osteogenic Phenotypes in Periosteum-Derived Cells and Co-Cultures of Periosteum-Derived Cells and THP-1 Cells." Life 11, no. 5 (2021): 410. http://dx.doi.org/10.3390/life11050410.

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Coupling between osteoblast-mediated bone formation and osteoclast-mediated bone resorption maintains both mechanical integrity and mineral homeostasis. Zinc is required for the formation, mineralization, growth, and maintenance of bones. We examined the effects of zinc sulfate on osteoblastic differentiation of human periosteum-derived cells (hPDCs) and osteoclastic differentiation of THP-1 cells. Zinc sulfate enhanced the osteoblastic differentiation of hPDCs; however, it did not affect the osteoclastic differentiation of THP-1 cells. The levels of extracellular signaling-related kinase (ERK

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22

Zhang, K., X. Liu, Y. Tang, et al. "Fluid Shear Stress Promotes Osteoblast Proliferation and Suppresses Mitochondrial-Mediated Osteoblast Apoptosis Through the miR-214-3p-ATF4 Signaling Axis." Physiological Research 71, no. 4 (2022): 527–38. http://dx.doi.org/10.33549/physiolres.934917.

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MicroRNAs (miRNAs) play vital roles in bone metabolism and participate in the mechanically induced bone alterations. The underlying molecular mechanisms by which fluid shear stress (FSS) regulate the proliferative and apoptotic phenotypic changes of osteoblasts remain elusive. The study aimed to investigate the regulatory effects of FSS on osteoblast proliferative and apoptotic phenotypes and the roles of miR-214-3p-ATF4 (activating transcription factor 4) signaling axis in the mechanomodulation processes. FSS promoted the proliferative activity of osteoblasts and suppressed mitochondrial-medi

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Enríquez, Juana, Ana Elena Lemus, Jesús Chimal-Monroy, et al. "The effects of synthetic 19-norprogestins on osteoblastic cell function are mediated by their non-phenolic reduced metabolites." Journal of Endocrinology 193, no. 3 (2007): 493–504. http://dx.doi.org/10.1677/joe-06-0038.

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The key role of estrogens on osteoblastic cell function is well documented; however, the role of progesterone (P) and synthetic progestins remains controversial. While several reports indicate that P has no significant effects on bone cells, a number of clinical studies have shown that 19-norprogestins restore postmenopausal bone loss. The mechanisms by which 19-norprogestins induce estrogen-like effects on bone cells are not fully understood. To assess whether the actions of 19-norprogestins on osteoblasts are mediated by their non-phenolic metabolites, we studied the effects of norethisteron

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Mackie, E. J., and R. P. Tucker. "Tenascin in bone morphogenesis: expression by osteoblasts and cell type-specific expression of splice variants." Journal of Cell Science 103, no. 3 (1992): 765–71. http://dx.doi.org/10.1242/jcs.103.3.765.

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The extracellular matrix glycoprotein, tenascin, is associated in vivo with mesenchyme undergoing osteogenesis and chondrogenesis, but is absent from mature bone and cartilage matrix. The expression of tenascin by osteoblastic cells in vitro has been investigated by immunoblotting and immunocytochemistry. Tenascin was secreted into the medium and deposited in the matrix by human and rat osteoblast-like cell lines, as well as by primary osteoblast-enriched cultures from chick embryo calvarial bones. In primary osteoblast-enriched cultures, extracellular tenascin was found only in cell aggregate

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Kanazawa, Ippei, Ayumu Takeno, Ken-ichiro Tanaka, Masakazu Notsu, and Toshitsugu Sugimoto. "Osteoblast AMP-Activated Protein Kinase Regulates Postnatal Skeletal Development in Male Mice." Endocrinology 159, no. 2 (2017): 597–608. http://dx.doi.org/10.1210/en.2017-00357.

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Abstract Studies have shown that AMP-activated protein kinase (AMPK), a crucial regulator of energy homeostasis, plays important roles in osteoblast differentiation and mineralization. However, little is known about in vivo roles of osteoblastic AMPK in bone development. Thus, to investigate in vivo roles of osteoblast AMPK, we conditionally inactivated Ampk in osterix (Osx)–expressing cells by crossing Osx-Cre mice with floxed AMPKα1 to generate mice lacking AMPKα1 in osteoblasts (Ampk−/− mice). Compared with wild-type and Ampk+/− mice, Ampk−/− mice displayed retardation of postnatal bone dev

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Weinstein, Robert S., Robert L. Jilka, Maria Almeida, Paula K. Roberson, and Stavros C. Manolagas. "Intermittent Parathyroid Hormone Administration Counteracts the Adverse Effects of Glucocorticoids on Osteoblast and Osteocyte Viability, Bone Formation, and Strength in Mice." Endocrinology 151, no. 6 (2010): 2641–49. http://dx.doi.org/10.1210/en.2009-1488.

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Glucocorticoids act directly on bone cells to decrease production of osteoblasts and osteoclasts, increase osteoblast and osteocyte apoptosis, and prolong osteoclast life span. Conversely, daily injections of PTH decrease osteoblast and osteocyte apoptosis and increase bone formation and strength. Using a mouse model, we investigated whether the recently demonstrated efficacy of PTH in glucocorticoid-induced bone disease results from the ability of this therapeutic modality to counteract at least some of the direct effects of glucocorticoids on bone cells. Glucocorticoid administration to 5- t

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Kassem, Moustapha, Leif Mosekilde, and Erik F. Eriksen. "Effects of fluoride on human bone cells in vitro: differences in responsiveness between stromal osteoblast precursors and mature osteoblasts." European Journal of Endocrinology 130, no. 4 (1994): 381–86. http://dx.doi.org/10.1530/eje.0.1300381.

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Kassem M, Mosekilde L, Eriksen EF. Effects of fluoride on human bone cells in vitro: differences in responsiveness between stromal osteoblast precursors and mature osteoblasts. Eur J Endocrinol 1994;130:381–6. ISSN 0804–4643 The cellular effects of sodium fluoride (NaF) on human bone cells in vitro have been variable and dependent on the culture system used. Variability could be attributed to differences in responsiveness to NaF among different populations of cells at various stages of differentiation in the osteoblastic lineage. In this study we compared the effects of NaF in serum-free mediu

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Funato, Noriko, Kiyoshi Ohtani, Kimie Ohyama, Takayuki Kuroda, and Masataka Nakamura. "Common Regulation of Growth Arrest and Differentiation of Osteoblasts by Helix-Loop-Helix Factors." Molecular and Cellular Biology 21, no. 21 (2001): 7416–28. http://dx.doi.org/10.1128/mcb.21.21.7416-7428.2001.

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ABSTRACT Cellular differentiation entails the coordination of cell cycle arrest and tissue-specific gene expression. We investigated the involvement of basic helix-loop-helix (bHLH) factors in differentiation of osteoblasts using the human osteoblastic cell line MG63. Serum starvation induced growth arrest at G1 phase, accompanied by expression of cyclin-dependent kinase inhibitor p21WAF1/Cip1. Reporter assays with the p21 gene promoter demonstrated that the combination of E2A (E12 or E47) and coactivator CBP was responsible for p21 induction independent of p53. Twist inhibited E2A-CBP-depende

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Guo, Ying, Nicole Pischon, Amitha H. Palamakumbura, and Philip C. Trackman. "Intracellular distribution of the lysyl oxidase propeptide in osteoblastic cells." American Journal of Physiology-Cell Physiology 292, no. 6 (2007): C2095—C2102. http://dx.doi.org/10.1152/ajpcell.00613.2006.

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Lysyl oxidase plays a critical role in the formation of the extracellular matrix, and its activity is required for the normal maturation and cross-linking of collagen and elastin. An 18-kDa lysyl oxidase propeptide (LOPP) is generated from 50-kDa prolysyl oxidase by extracellular proteolytic cleavage during the biosynthesis of active 30-kDa lysyl oxidase enzyme. The fate and the functions of the LOPP are largely unknown, although intact LOPP was previously observed in osteoblast cultures. We investigated the spatial localization of molecular forms of lysyl oxidase, including LOPP in proliferat

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Bassett, J. H. Duncan, Anne van der Spek, John G. Logan, et al. "Thyrostimulin Regulates Osteoblastic Bone Formation During Early Skeletal Development." Endocrinology 156, no. 9 (2015): 3098–113. http://dx.doi.org/10.1210/en.2014-1943.

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The ancestral glycoprotein hormone thyrostimulin is a heterodimer of unique glycoprotein hormone subunit alpha (GPA)2 and glycoprotein hormone subunit beta (GPB)5 subunits with high affinity for the TSH receptor. Transgenic overexpression of GPB5 in mice results in cranial abnormalities, but the role of thyrostimulin in bone remains unknown. We hypothesized that thyrostimulin exerts paracrine actions in bone and determined: 1) GPA2 and GPB5 expression in osteoblasts and osteoclasts, 2) the skeletal consequences of thyrostimulin deficiency in GPB5 knockout (KO) mice, and 3) osteoblast and osteo

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Lemus, Ana E., Juana Enríquez, Ángeles Hernández, René Santillán, and Gregorio Pérez-Palacios. "Bioconversion of norethisterone, a progesterone receptor agonist into estrogen receptor agonists in osteoblastic cells." Journal of Endocrinology 200, no. 2 (2008): 199–206. http://dx.doi.org/10.1677/joe-08-0166.

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A number of clinical studies have demonstrated that norethisterone (NET), a potent synthetic progestin, restores postmenopausal bone loss, although its mode of action on bone cells is not fully understood, while the effect of naturally occurring progesterone in bone has remained controversial. A recent report claims that the potent effects of NET on osteoblastic cell proliferation and differentiation, mimicking the action of estrogens, are mediated by non-phenolic NET derivatives. To determine whether osteoblasts possess the enzymes required to bioconvert a progesterone receptor (PR) agonist i

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Yamaguchi, Akira, Toshihisa Komori, and Tatsuo Suda. "Regulation of Osteoblast Differentiation Mediated by Bone Morphogenetic Proteins, Hedgehogs, and Cbfa1." Endocrine Reviews 21, no. 4 (2000): 393–411. http://dx.doi.org/10.1210/edrv.21.4.0403.

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Abstract Osteoblasts arise from common progenitors with chondrocytes, muscle and adipocytes, and various hormones and local factors regulate their differentiation. We review here regulation of osteoblast differentiation mediated by the local factors such as bone morphogenetic proteins (BMPs) and hedgehogs and the transcription factor, core-binding factor α-1 (Cbfa1). BMPs are the most potent regulators of osteoblast differentiation among the local factors. Sonic and Indian hedgehogs are involved in osteoblast differentiation by interacting with BMPs. Cbfa1, a member of the runt domain gene fam

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Aubin, Jane E. "Advances in the osteoblast lineage." Biochemistry and Cell Biology 76, no. 6 (1998): 899–910. http://dx.doi.org/10.1139/o99-005.

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Osteoblasts are the skeletal cells responsible for synthesis, deposition and mineralization of the extracellular matrix of bone. By mechanisms that are only beginning to be understood, stem and primitive osteoprogenitors and related mesenchymal precursors arise in the embryo and at least some appear to persist in the adult organism, where they contribute to replacement of osteoblasts in bone turnover and in fracture healing. In this review, we describe the morphological, molecular, and biochemical criteria by which osteoblasts are defined and cell culture approaches that have helped to clarify

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Morandi, Francesca, Sara Tagliaferri, Sabrina Bonomini, et al. "Beta-Catenin Depended and Independent Effects Induced by Myeloma Cells in Human and Murine Osteoblasts and Osteoblast Progenitors." Blood 108, no. 11 (2006): 3433. http://dx.doi.org/10.1182/blood.v108.11.3433.3433.

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Abstract Osteoblast impairment occurs within myeloma (MM) cell infiltration into the bone marrow (BM). Wnt signaling is involved in the regulation of osteoblast formation. Canonical Wnt signaling pathway is activated by Wnt 1/3a that induce the activation of GSK3/Axin complex leading to the stabilization and nuclear translocation of beta-catenin that in turn activates the transcription system Lef1/TCF. Recently it has been reported that MM cells produce the Wnt inhibitors DKK-1 demonstrating a correlation between its expression and the presence of bone lesions in MM patients. However the effec

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Zhu, Haitao, Hua Chen, Degang Ding, Shui Wang, Xiaofeng Dai, and Yulong Zhu. "Overexpression of PIK3R1 Promotes Bone Formation by Regulating Osteoblast Differentiation and Osteoclast Formation." Computational and Mathematical Methods in Medicine 2021 (October 14, 2021): 1–13. http://dx.doi.org/10.1155/2021/2909454.

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In an effort to bolster our understanding of regulation of bone formation in the context of osteoporosis, we screened out differentially expressed genes in osteoporosis patients with high and low bone mineral density by bioinformatics analysis. PIK3R1 is increasingly being nominated as a pivotal mediator in the differentiation of osteoblasts and osteoclasts that is closely related to bone formation. However, the specific mechanisms underlying the way that PIK3R1 affects bone metabolism are not fully elucidated. We intended to examine the potential mechanism by which PIK3R1 regulates osteoblast

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Wang, Xueying, Hui-Yi Kua, Yuanyu Hu, et al. "p53 functions as a negative regulator of osteoblastogenesis, osteoblast-dependent osteoclastogenesis, and bone remodeling." Journal of Cell Biology 172, no. 1 (2005): 115–25. http://dx.doi.org/10.1083/jcb.200507106.

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p53 is a well known tumor suppressor. We show that p53 also regulates osteoblast differentiation, bone formation, and osteoblast-dependent osteoclast differentiation. Indeed, p53−/− mice display a high bone mass phenotype, and p53−/− osteoblasts show accelerated differentiation, secondary to an increase in expression of the osteoblast differentiation factor osterix, as a result. Reporter assays indicate that p53 represses osterix transcription by the minimal promoter in a DNA-binding–independent manner. In addition, p53−/− osteoblasts have an enhanced ability to favor osteoclast differentiatio

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Billiard, Julia, Deana S. Way, Laura M. Seestaller-Wehr, Robert A. Moran, Annamarie Mangine, and Peter V. N. Bodine. "The Orphan Receptor Tyrosine Kinase Ror2 Modulates Canonical Wnt Signaling in Osteoblastic Cells." Molecular Endocrinology 19, no. 1 (2005): 90–101. http://dx.doi.org/10.1210/me.2004-0153.

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Abstract Ror2 is an orphan receptor tyrosine kinase that plays crucial roles in developmental morphogenesis, particularly of the skeleton. We have identified human Ror2 as a novel regulator of canonical Wnt signaling in osteoblastic (bone-forming) cells with selective activities, enhancing Wnt1 but antagonizing Wnt3. Immunoprecipitation studies demonstrated physical interactions between human Ror2 and mammalian Wnt1 and Wnt3. Functionally, Ror2 antagonized Wnt1- and Wnt3-mediated stabilization of cytosolic β-catenin in osteoblastic cells. However, Ror2 had opposing effects on a more distal ste

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Zhu, Jiang, Yi Zhang, Nacksung Kim, et al. "Osteoblasts Support Early B Lymphoiesis as well as Stem Cell Proliferation and Myelopoiesis: Identification of the Mammalian Cellular Analog of the Bursa of Fabricius." Blood 104, no. 11 (2004): 508. http://dx.doi.org/10.1182/blood.v104.11.508.508.

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Abstract The self-renewal, survival and differentiation of hematopoietic stem cells (HSC) are greatly influenced by the activities of neighboring osteoblasts and non-osteogenic bone marrow (BM) stromal cells such as fibroblasts, endothelial cells and adipocytes. Previously, we showed that osteoblasts from human long bones support the in vitro self-renewal as well as myeloid differentiation of human CD34+ cord blood cells. Recently, Li’s and Scadden’s groups provided in vivo evidence indicating a primary role of trabecular osteoblasts as a major component of HSC niche and of stromal osteoblasti

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Alonso-Pérez, Ana, María Guillán-Fresco, Eloi Franco-Trepat, et al. "Improved Protocol to Study Osteoblast and Adipocyte Differentiation Balance." Biomedicines 11, no. 1 (2022): 31. http://dx.doi.org/10.3390/biomedicines11010031.

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Adipogenesis-osteoblastogenesis balance-rupture is relevant in multiple diseases. Current human mesenchymal stem cells (hMSCs) in vitro differentiation models are expensive, and are hardly reproducible. Their scarcity and variability make an affordable and reliable method to study adipocyte-osteoblast-equilibrium difficult. Moreover, media composition has been inconstant throughout the literature. Our aims were to compare improved differentiation lab-made media with consensus/commercial media, and to identify a cell-line to simultaneously evaluate both MSCs differentiations. Lab-made media wer

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Choi, J. Y., A. J. van Wijnen, F. Aslam, et al. "Developmental association of the beta-galactoside-binding protein galectin-1 with the nuclear matrix of rat calvarial osteoblasts." Journal of Cell Science 111, no. 20 (1998): 3035–43. http://dx.doi.org/10.1242/jcs.111.20.3035.

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The protein composition of the nuclear matrix changes significantly as the osteoblast matures from a proliferating pre-osteoblast to an osteocyte embedded in a mineralized matrix. These matrix protein are the result of developmental stage-specific gene expression during osteoblast differentiation. To isolate nuclear matrix proteins unique to the bone phenotype we analyzed nuclear matrix preparations from cultures of rat calvarial osteoblasts by high resolution two-dimensional gel electrophoresis at two different stages: proliferation (day 3) and differentiation (day 18, mineralized). We charac

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Yano, Shozo, Romuald Mentaverri, Deepthi Kanuparthi та ін. "Functional Expression of β-Chemokine Receptors in Osteoblasts: Role of Regulated upon Activation, Normal T Cell Expressed and Secreted (RANTES) in Osteoblasts and Regulation of Its Secretion by Osteoblasts and Osteoclasts". Endocrinology 146, № 5 (2005): 2324–35. http://dx.doi.org/10.1210/en.2005-0065.

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Abstract The expression and functions of receptors for the β-chemokine, regulated upon activation, normal T cell expressed, and secreted (RANTES)/CCL5, were investigated in osteoblasts. Both primary osteoblasts and the MC3T3-E1 osteoblast cell line express the RANTES receptors, CCR1, 3, 4, and 5 (by RT-PCR), which encode functional receptors in osteoblasts as shown by [125I]-RANTES binding followed by Scatchard analysis. Expression of all four RANTES receptor mRNAs in osteoblast is in contrast to the reports of expression of CCR1 being the only RANTES receptor expressed by osteoclasts. Exogeno

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Choi, Je-Yong, André J. van Wijnen, Fauzia Aslam та ін. "Developmental association of the β-galactoside-binding protein galectin-1 with the nuclear matrix of rat calvarial osteoblasts". Journal of Cell Science 111, № 20 (1998): 3035–43. http://dx.doi.org/10.1242/jcs.20.111.3035.

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ABSTRACT The protein composition of the nuclear matrix changes significantly as the osteoblast matures from a proliferating pre-osteoblast to an osteocyte embedded in a mineralized matrix. These matrix protein are the result of developmental stage-specific gene expression during osteoblast differentiation. To isolate nuclear matrix proteins unique to the bone phenotype we analyzed nuclear matrix preparations from cultures of rat calvarial osteoblasts by high resolution two-dimensional gel electrophoresis at two different stages: proliferation (day 3) and differentiation (day 18, mineralized).

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Borsotti, Chiara, Paolo E. Di Simone, Vakhtang Kalandadze, and Antonia Follenzi. "Extracoagulative Role of FVIII: Impact on in Vitro and In Vivo Murine Bone Cell Differentiation and Function." Blood 144, Supplement 1 (2024): 2571. https://doi.org/10.1182/blood-2024-193877.

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Introduction: The complex interplay between hemophilia A (HA) and skeletal health has been demonstrated in several pre-clinical and clinical studies. Patients with HA exhibit low bone mineral density (BMD) and heightened fracture risk, and osteopenia and osteoporosis have been reported as early as 12 years of age. Deficiency of factor VIII (FVIII) could be contributing to an imbalance in bone metabolism, leading to reduced BMD. The reduction in BMD may be caused by altered signaling between cells responsible for bone remodeling: osteoblasts for building and osteoclasts for resorption. However,

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Bonnelye, E., L. Merdad, V. Kung та J. E. Aubin. "The Orphan Nuclear Estrogen Receptor–Related Receptor α (Errα) Is Expressed Throughout Osteoblast Differentiation and Regulates Bone Formation in Vitro". Journal of Cell Biology 153, № 5 (2001): 971–84. http://dx.doi.org/10.1083/jcb.153.5.971.

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The orphan nuclear estrogen receptor–related receptor α (ERRα), is expressed by many cell types, but is very highly expressed by osteoblastic cells in which it transactivates at least one osteoblast-associated gene, osteopontin. To study the putative involvement of ERRα in bone, we first assessed its expression in rat calvaria (RC) in vivo and in RC cells in vitro. ERRα mRNA and protein were expressed at all developmental stages from early osteoprogenitors to bone-forming osteoblasts, but protein was most abundant in mature cuboidal osteoblasts. To assess a functional role for ERRα in osteobla

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Park, Kyung-Ran, Hanna Lee, MyoungLae Cho, and Hyung-Mun Yun. "A Phytochemical Constituent, (E)-Methyl-Cinnamate Isolated from Alpinia katsumadai Hayata Suppresses Cell Survival, Migration, and Differentiation in Pre-Osteoblasts." International Journal of Molecular Sciences 21, no. 10 (2020): 3700. http://dx.doi.org/10.3390/ijms21103700.

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Background: (E)-methyl-cinnamate (EMC), a phytochemical constituent isolated from Alpinia katsumadai Hayata, is a natural flavor compound with anti-inflammatory properties, which is widely used in the food and commodity industry. However, the pharmacological effects of methyl-cinnamate on pre-osteoblasts remain unknown. This study aimed to investigate the pharmacological effects and mechanisms of EMC in pre-osteoblast MC3T3-E1 cells (pre-osteoblasts). Methods: Cell viability and apoptosis were evaluated using the MTT assay and TUNEL staining. Cell migration and osteoblast differentiation were

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Bozec, Aline, Latifa Bakiri, Maria Jimenez, Thorsten Schinke, Michael Amling, and Erwin F. Wagner. "Fra-2/AP-1 controls bone formation by regulating osteoblast differentiation and collagen production." Journal of Cell Biology 190, no. 6 (2010): 1093–106. http://dx.doi.org/10.1083/jcb.201002111.

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The activator protein-1 (AP-1) transcription factor complex, in particular the Fos proteins, is an important regulator of bone homeostasis. Fra-2 (Fosl2), a Fos-related protein of the AP-1 family, is expressed in bone cells, and newborn mice lacking Fra-2 exhibit defects in chondrocytes and osteoclasts. Here we show that Fra-2–deficient osteoblasts display a differentiation defect both in vivo and in vitro. Moreover, Fra-2–overexpressing mice are osteosclerotic because of increased differentiation of osteoblasts, which appears to be cell autonomous. Importantly, the osteoblast-specific osteoca

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Komori, Toshihisa. "Regulation of Proliferation, Differentiation and Functions of Osteoblasts by Runx2." International Journal of Molecular Sciences 20, no. 7 (2019): 1694. http://dx.doi.org/10.3390/ijms20071694.

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Runx2 is essential for osteoblast differentiation and chondrocyte maturation. During osteoblast differentiation, Runx2 is weakly expressed in uncommitted mesenchymal cells, and its expression is upregulated in preosteoblasts, reaches the maximal level in immature osteoblasts, and is down-regulated in mature osteoblasts. Runx2 enhances the proliferation of osteoblast progenitors by directly regulating Fgfr2 and Fgfr3. Runx2 enhances the proliferation of suture mesenchymal cells and induces their commitment into osteoblast lineage cells through the direct regulation of hedgehog (Ihh, Gli1, and P

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Zou, Zihao, Ranran Dai, Nan Deng, Wei Su, and Ping Liu. "Exosomal miR-1275 Secreted by Prostate Cancer Cells Modulates Osteoblast Proliferation and Activity by Targeting the SIRT2/RUNX2 Cascade." Cell Transplantation 30 (January 1, 2021): 096368972110529. http://dx.doi.org/10.1177/09636897211052977.

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Prostate cancer (PCa) is one of the most frequently diagnosed malignancies and the second leading cause of cancer mortality among men worldwide. Modulation of osteoblast activity is involved in PCa metastasis, and miR-1275 is also reported to regulate PCa metastasis; however, the association between cancer-derived exosomal miR-1275 and osteoblast activity is unclear. Here, we isolated exosomes from PC3-derived conditioned medium by ultracentrifugation. We found that miR-1275 could be transferred from PCa cells to osteoblasts via exosomes. Exosomal miR-1275 significantly accelerated the prolife

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Filvaroff, E., A. Erlebacher, J. Ye, et al. "Inhibition of TGF-beta receptor signaling in osteoblasts leads to decreased bone remodeling and increased trabecular bone mass." Development 126, no. 19 (1999): 4267–79. http://dx.doi.org/10.1242/dev.126.19.4267.

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Transforming growth factor-beta (TGF-beta) is abundant in bone matrix and has been shown to regulate the activity of osteoblasts and osteoclasts in vitro. To explore the role of endogenous TGF-(beta) in osteoblast function in vivo, we have inhibited osteoblastic responsiveness to TGF-beta in transgenic mice by expressing a cytoplasmically truncated type II TGF-beta receptor from the osteocalcin promoter. These transgenic mice develop an age-dependent increase in trabecular bone mass, which progresses up to the age of 6 months, due to an imbalance between bone formation and resorption during bo

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Suwannasing, Chanyatip, Ausanai Prapan, Piyaporn Surinlert, Chanyarak Sombutkayasith, and Wattana Weerachatyanukul. "The Osteoinductive Effect of Water-Soluble Matrix from Nano-Nacre Particles of Haliotis diversicolor (H. diversicolor) Abalone on MC3T3-E1 Osteoblasts." Applied Sciences 15, no. 6 (2025): 2907. https://doi.org/10.3390/app15062907.

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Osteoporosis is characterized by an imbalance between osteoblastic bone formation and osteoclastic bone resorption, leading to an increased risk of fractures. The water-soluble matrix (WSM) of nacre exhibits osteoinductive properties in osteoblastic cells, both in vitro and in vivo. However, its release from natural nacre remains challenging due to its solid and compact surface. This study aimed to prepare nano-nacre particles with smaller diameters than intact aragonite crystals to enhance WSM release and to investigate its effects on osteoblast differentiation. Size analysis and SEM imaging

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