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Journal articles on the topic 'Bone cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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1

Ahmed Elkammar, Hala. "Effect of human bone marrow derived mesenchymal stem cells on squamous cell carcinoma cell line." International Journal of Academic Research 6, no. 1 (January 30, 2014): 110–16. http://dx.doi.org/10.7813/2075-4124.2014/6-1/a.14.

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2

Zahran, Faten, Ahmed Abdel Zaher Ahmed Abdel.Zaher, Nermin Raafat, and Mohamed Ali Mohamed Ali. "Hepatocyte derived from Rat Bone Marrow Mesenchymal Stem Cells." Indian Journal of Applied Research 3, no. 10 (October 1, 2011): 1–5. http://dx.doi.org/10.15373/2249555x/oct2013/135.

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3

RemyaV, RemyaV, Naveen Kumar, and Kutty M. V. H. Kutty M.V.H. "A Method for Cell Culture and RNA Extraction of Rabbit Bone Marrow Derived Mesenchymal Stem Cells." International Journal of Scientific Research 3, no. 7 (June 1, 2012): 31–33. http://dx.doi.org/10.15373/22778179/july2014/11.

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4

Van Epps, Heather L. "Bone cells unite." Journal of Experimental Medicine 202, no. 3 (August 1, 2005): 335. http://dx.doi.org/10.1084/jem2023iti3.

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5

Aubin, Jane E. "Bone stem cells." Journal of Cellular Biochemistry 72, S30-31 (1998): 73–82. http://dx.doi.org/10.1002/(sici)1097-4644(1998)72:30/31+<73::aid-jcb11>3.0.co;2-l.

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6

Hashimoto, Futoshi, Kikuya Sugiura, Kyoichi Inoue, and Susumu Ikehara. "Major Histocompatibility Complex Restriction Between Hematopoietic Stem Cells and Stromal Cells In Vivo." Blood 89, no. 1 (January 1, 1997): 49–54. http://dx.doi.org/10.1182/blood.v89.1.49.

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Abstract Graft failure is a mortal complication in allogeneic bone marrow transplantation (BMT); T cells and natural killer cells are responsible for graft rejection. However, we have recently demonstrated that the recruitment of donor-derived stromal cells prevents graft failure in allogeneic BMT. This finding prompted us to examine whether a major histocompatibility complex (MHC) restriction exists between hematopoietic stem cells (HSCs) and stromal cells. We transplanted bone marrow cells (BMCs) and bones obtained from various mouse strains and analyzed the cells that accumulated in the engrafted bones. Statistically significant cell accumulation was found in the engrafted bone, which had the same H-2 phenotype as that of the BMCs, whereas only few cells were detected in the engrafted bones of the third-party H-2 phenotypes during the 4 to 6 weeks after BMT. Moreover, the BMCs obtained from the MHC-compatible bone showed significant numbers of both colony-forming units in culture (CFU-C) and spleen colony-forming units (CFU-S). These findings strongly suggest that an MHC restriction exists between HSCs and stromal cells.

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7

Hashimoto, Futoshi, Kikuya Sugiura, Kyoichi Inoue, and Susumu Ikehara. "Major Histocompatibility Complex Restriction Between Hematopoietic Stem Cells and Stromal Cells In Vivo." Blood 89, no. 1 (January 1, 1997): 49–54. http://dx.doi.org/10.1182/blood.v89.1.49.49_49_54.

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Graft failure is a mortal complication in allogeneic bone marrow transplantation (BMT); T cells and natural killer cells are responsible for graft rejection. However, we have recently demonstrated that the recruitment of donor-derived stromal cells prevents graft failure in allogeneic BMT. This finding prompted us to examine whether a major histocompatibility complex (MHC) restriction exists between hematopoietic stem cells (HSCs) and stromal cells. We transplanted bone marrow cells (BMCs) and bones obtained from various mouse strains and analyzed the cells that accumulated in the engrafted bones. Statistically significant cell accumulation was found in the engrafted bone, which had the same H-2 phenotype as that of the BMCs, whereas only few cells were detected in the engrafted bones of the third-party H-2 phenotypes during the 4 to 6 weeks after BMT. Moreover, the BMCs obtained from the MHC-compatible bone showed significant numbers of both colony-forming units in culture (CFU-C) and spleen colony-forming units (CFU-S). These findings strongly suggest that an MHC restriction exists between HSCs and stromal cells.

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8

Chambers, T. J., and K. Fuller. "Bone cells predispose bone surfaces to resorption by exposure of mineral to osteoclastic contact." Journal of Cell Science 76, no. 1 (June 1, 1985): 155–65. http://dx.doi.org/10.1242/jcs.76.1.155.

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The cell-free endocranial surface of young adult rat parietal bones was used as a substrate for osteoclastic bone resorption, either without prior treatment, or after incubation of the parietal bones with collagenase or neonatal rat calvarial cells. Untreated, the endocranial surface consisted of unmineralized organic fibres; incubation with calvarial cells or collagenase caused disruption and removal of these fibres, with extensive exposure of bone mineral on the endocranial surface, without morphologically detectable mineral dissolution. Neonatal rabbit osteoclasts resorbed bone to a greater extent from parietal bones pre-incubated with calvarial cells or collagenase than from untreated bones; mineral exposure and subsequent osteoclastic resorption were both increased if calvarial cells were incubated with parathyroid hormone; removal of bone mineral after incubation with calvarial cells removed the predisposition to osteoclastic resorption. These experiments demonstrate that calvarial cells are capable of osteoid destruction, and indicate that one mechanism by which osteoblasts induce osteoclastic bone resorption may be through digestion of the unmineralized organic material that covers bone surfaces, to expose the underlying resorption-stimulating bone mineral to osteoclastic contact.

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9

INOUE, HIROMASA. "Cells phagocytizing bone. Bone metabolism and osteoclast." Kagaku To Seibutsu 23, no. 2 (1985): 99–102. http://dx.doi.org/10.1271/kagakutoseibutsu1962.23.99.

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10

Kelder, Cindy, Cornelis J. Kleverlaan, Marjolijn Gilijamse, Astrid D. Bakker, and Teun J. de Vries. "Cells Derived from Human Long Bone Appear More Differentiated and More Actively Stimulate Osteoclastogenesis Compared to Alveolar Bone-Derived Cells." International Journal of Molecular Sciences 21, no. 14 (July 17, 2020): 5072. http://dx.doi.org/10.3390/ijms21145072.

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Osteoblasts derived from mouse skulls have increased osteoclastogenic potential compared to long bone osteoblasts when stimulated with 1,25(OH)2 vitamin D3 (vitD3). This indicates that bone cells from specific sites can react differently to biochemical signals, e.g., during inflammation or as emitted by bioactive bone tissue-engineering constructs. Given the high turn-over of alveolar bone, we hypothesized that human alveolar bone-derived osteoblasts have an increased osteogenic and osteoclastogenic potential compared to the osteoblasts derived from long bone. The osteogenic and osteoclastogenic capacity of alveolar bone cells and long bone cells were assessed in the presence and absence of osteotropic agent vitD3. Both cell types were studied in osteogenesis experiments, using an osteogenic medium, and in osteoclastogenesis experiments by co-culturing osteoblasts with peripheral blood mononuclear cells (PBMCs). Both osteogenic and osteoclastic markers were measured. At day 0, long bones seem to have a more late-osteoblastic/preosteocyte-like phenotype compared to the alveolar bone cells as shown by slower proliferation, the higher expression of the matrix molecule Osteopontin (OPN) and the osteocyte-enriched cytoskeletal component Actin alpha 1 (ACTA1). This phenotype was maintained during the osteogenesis assays, where long bone-derived cells still expressed more OPN and ACTA1. Under co-culture conditions with PBMCs, long bone cells also had a higher Tumor necrose factor-alfa (TNF-α) expression and induced the formation of osteoclasts more than alveolar bone cells. Correspondingly, the expression of osteoclast genes dendritic cell specific transmembrane protein (DC-STAMP) and Receptor activator of nuclear factor kappa-Β ligand (RankL) was higher in long bone co-cultures. Together, our results indicate that long bone-derived osteoblasts are more active in bone-remodeling processes, especially in osteoclastogenesis, than alveolar bone-derived cells. This indicates that tissue-engineering solutions need to be specifically designed for the site of application, such as defects in long bones vs. the regeneration of alveolar bone after severe periodontitis.

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11

MEHRBOD, Mehrdad, Yuta TAKAGI, Hiroshi KATSUCHI, Toshihiko SHIRAISHI, and Shin MORISHITA. "236 Development of An Overall Mechanical Model For Osteoblast Bone Cells." Proceedings of the Dynamics & Design Conference 2009 (2009): _236–1_—_236–6_. http://dx.doi.org/10.1299/jsmedmc.2009._236-1_.

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12

Marquis, Marie-Eve. "Bone cells-biomaterials interactions." Frontiers in Bioscience Volume, no. 14 (2009): 1023. http://dx.doi.org/10.2741/3293.

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13

Wong, W. "Bone-Building T Cells." Science Signaling 2, no. 87 (September 8, 2009): ec295-ec295. http://dx.doi.org/10.1126/scisignal.287ec295.

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14

SHANG, PENG, JIAN ZHANG, AIRONG QIAN, JINGBAO LI, RUI MENG, SHENGMENG DI, LIFANG HU, and ZHONGZE GU. "BONE CELLS UNDER MICROGRAVITY." Journal of Mechanics in Medicine and Biology 13, no. 05 (October 2013): 1340006. http://dx.doi.org/10.1142/s021951941340006x.

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Weightlessness environment (also microgravity) during the exploration of space is the major condition which must be faced by astronauts. One of the most serious adverse effects on astronauts is the weightlessness-induced bone loss due to the unbalanced bone remodeling. Bone remodeling of human beings has evolved during billions of years to make bone tissue adapt to the gravitational field of Earth (1g) and maintain skeleton structure to meet mechanical loading on Earth. However, under weightlessness environment the skeleton system no longer functions against the pull of gravity, so there is no necessity to keep bone strong enough to support the body's weight. Therefore, the balance of bone remodeling is disrupted and bone loss occurs, which is extremely deleterious to an astronaut's health during long-term spaceflight. Bone remodeling is mainly orchestrated by bone mesenchymal stem cells, osteoblasts, osteocytes, and osteoclasts. Here, we review how these bone cells respond to microgravity environment.

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15

Rychly, J. "Mechanobiology of bone cells." Osteologie 19, no. 03 (2010): 245–49. http://dx.doi.org/10.1055/s-0037-1619946.

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SummaryBone mass, morphology and properties of the bone material are regulated by the functions of osteoblasts, osteocytes, and osteoclasts. These cells respond directly or indirectly to mechanical forces from the environment with the expression of differentiation markers, proliferation or release of bioactive factors. Osteocytes appear to be an important regulator for the adaptation of bone to changes in the mechanical environment. Mesenchymal stem cells which are located in bone marrow can be mechanically stimulated to differentiate into osteoblasts and chondrocytes but not to adipocytes. Integrin receptors are the principal mediators of mechanical forces and induce a signal transduction. The conversion of mechanical signals into biochemical signals is facilitated by unfolding of proteins to expose binding sites. Implant materials offer the opportunity to control the mechanical stimulation of cells by modifying the rigidity, geometry of adhesion sites, and the 3D-environment.

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16

Fujita, Takuo. "Calcium, cells and bone." Journal of Bone and Mineral Metabolism 6, no. 1 (March 1988): 1–2. http://dx.doi.org/10.1007/bf02378732.

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17

Aubin, Jane E. "Bone blood stem cells." Bone 43 (October 2008): S15—S16. http://dx.doi.org/10.1016/j.bone.2008.07.018.

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18

Lu, ZuFu, Jenneke Kleine-Nulend, and Bin Li. "Bone Microenvironment, Stem Cells, and Bone Tissue Regeneration." Stem Cells International 2017 (2017): 1–2. http://dx.doi.org/10.1155/2017/1315243.

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19

Teti, Anna. "Bone Development: Overview of Bone Cells and Signaling." Current Osteoporosis Reports 9, no. 4 (September 27, 2011): 264–73. http://dx.doi.org/10.1007/s11914-011-0078-8.

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20

Rubin, Mishaela R. "Bone Cells and Bone Turnover in Diabetes Mellitus." Current Osteoporosis Reports 13, no. 3 (March 6, 2015): 186–91. http://dx.doi.org/10.1007/s11914-015-0265-0.

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21

Teti, Anna. "Bone cells and the mechanisms of bone remodelling." Frontiers in Bioscience E4, no. 6 (2012): 2302–21. http://dx.doi.org/10.2741/e543.

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22

YAMACHIKA, Eiki, Masakazu MATSUBARA, Kenichiro KITA, Kiyofumi TAKABATAKE, Yuuki FUJITA, Tatsushi MATSUMURA, Yasuhisa HIRATA, and Seiji IIDA. "Bone regeneration from mouse compact bone-derived cells." Japanese Journal of Oral and Maxillofacial Surgery 59, no. 4 (2013): 223–29. http://dx.doi.org/10.5794/jjoms.59.223.

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23

Donsante, Samantha, Biagio Palmisano, Marta Serafini, Pamela G. Robey, Alessandro Corsi, and Mara Riminucci. "From Stem Cells to Bone-Forming Cells." International Journal of Molecular Sciences 22, no. 8 (April 13, 2021): 3989. http://dx.doi.org/10.3390/ijms22083989.

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Bone formation starts near the end of the embryonic stage of development and continues throughout life during bone modeling and growth, remodeling, and when needed, regeneration. Bone-forming cells, traditionally termed osteoblasts, produce, assemble, and control the mineralization of the type I collagen-enriched bone matrix while participating in the regulation of other cell processes, such as osteoclastogenesis, and metabolic activities, such as phosphate homeostasis. Osteoblasts are generated by different cohorts of skeletal stem cells that arise from different embryonic specifications, which operate in the pre-natal and/or adult skeleton under the control of multiple regulators. In this review, we briefly define the cellular identity and function of osteoblasts and discuss the main populations of osteoprogenitor cells identified to date. We also provide examples of long-known and recently recognized regulatory pathways and mechanisms involved in the specification of the osteogenic lineage, as assessed by studies on mice models and human genetic skeletal diseases.

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24

Morinobu, Mikihiko, Tetsuya Nakamoto, Kazunori Hino, Kunikazu Tsuji, Zhong-Jian Shen, Kazuhisa Nakashima, Akira Nifuji, Haruyasu Yamamoto, Hisamaru Hirai, and Masaki Noda. "The nucleocytoplasmic shuttling protein CIZ reduces adult bone mass by inhibiting bone morphogenetic protein–induced bone formation." Journal of Experimental Medicine 201, no. 6 (March 21, 2005): 961–70. http://dx.doi.org/10.1084/jem.20041097.

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Osteoporosis is a major health problem; however, the mechanisms regulating adult bone mass are poorly understood. Cas-interacting zinc finger protein (CIZ) is a nucleocytoplasmic shuttling protein that localizes at cell adhesion plaques that form where osteoblasts attach to substrate. To investigate the potential role of CIZ in regulating adult bone mass, we examined the bones in CIZ-deficient mice. Bone volume was increased and the rates of bone formation were increased in CIZ-deficient mice, whereas bone resorption was not altered. CIZ deficiency enhanced the levels of mRNA expression of genes encoding proteins related to osteoblastic phenotypes, such as alkaline phosphatase (ALP) as well as osterix mRNA expression in whole long bones. Bone marrow cells obtained from the femora of CIZ-deficient mice revealed higher ALP activity in culture and formed more mineralized nodules than wild-type cells. CIZ deficiency enhanced bone morphogenetic protein (BMP)–induced osteoblastic differentiation in bone marrow cells in cultures, indicating that BMP is the target of CIZ action. CIZ deficiency increased newly formed bone mass after femoral bone marrow ablation in vivo. Finally, BMP-2–induced bone formation on adult mouse calvariae in vivo was enhanced by CIZ deficiency. These results establish that CIZ suppresses the levels of adult bone mass through inhibition of BMP-induced activation of osteoblasts.

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25

Wang, Quanxing, Weiping Zhang, Guoshan Ding, Lifei Sun, Guoyou Chen, and Xuetao Cao. "DENDRITIC CELLS SUPPORT HEMATOPOIESIS OF BONE MARROW CELLS1." Transplantation 72, no. 5 (September 2001): 891–99. http://dx.doi.org/10.1097/00007890-200109150-00026.

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26

Boyde, Alan, Leonora A. Wolfe, Sheila J. Jones, Pavel Vesely, and Mierek Maly. "MICROSCOPY OF BONE CELLS, BONE TISSUE, AND BONE HEALING AROUND IMPLANTS." Implant Dentistry 1, no. 2 (1992): 117–28. http://dx.doi.org/10.1097/00008505-199205000-00003.

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27

Zhu, Shi-Jiang, Byung-Ho Choi, Jin-Young Huh, Jae-Hyung Jung, Byung-Yong Kim, and Seoung-Ho Lee. "A comparative qualitative histological analysis of tissue-engineered bone using bone marrow mesenchymal stem cells, alveolar bone cells, and periosteal cells." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 101, no. 2 (February 2006): 164–69. http://dx.doi.org/10.1016/j.tripleo.2005.04.006.

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28

Henderson, J. M. "A comparative qualitative histological analysis of tissue-engineered bone using bone marrow mesenchymal stem cells, alveolar bone cells, and periosteal cells." Yearbook of Dentistry 2007 (January 2007): 139–40. http://dx.doi.org/10.1016/s0084-3717(08)70411-2.

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29

Qiang, Ya-Wei, John D. Shaughnessy, and Shmuel Yaccoby. "Wnt3a signaling within bone inhibits multiple myeloma bone disease and tumor growth." Blood 112, no. 2 (July 15, 2008): 374–82. http://dx.doi.org/10.1182/blood-2007-10-120253.

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Abstract Canonical Wnt signaling is central to normal bone homeostasis, and secretion of Wnt signaling inhibitors by multiple myeloma (MM) cells contributes to MM-related bone resorption and disease progression. The aim of this study was to test the effect of Wnt3a on bone disease and growth of MM cells in vitro and in vivo. Although Wnt3a activated canonical signaling in the majority of MM cell lines and primary cells tested, Wnt3a had no effect on MM cell growth in vitro. Moreover, forced expression of Wnt3a in H929 MM cells conferred no growth advantage over empty vector-transfected cells in vitro or importantly when grown subcutaneously in severe combined immunodeficient (SCID) mice. Importantly, although H929 cells stably expressing an empty vector injected into human bone grew rapidly and induced a marked reduction in bone mineral density, bones engrafted with Wnt3a-expressing H929 cells were preserved, exhibited increased osteoblast-to-osteoclast ratios, and reduced tumor burden. Likewise, treatment of myelomatous SCID-hu mice, carrying primary disease, with recombinant Wnt3a stimulated bone formation and attenuated MM growth. These results provide further support of the potential anabolic and anti-MM effects of enhancing Wnt signaling in the bone.

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30

Shymanskyy, I. O., O. O. Lisakovska, A. O. Mazanova, D. O. Labudzynskyi, A. V. Khomenko, and M. M. Veliky. "Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 38–47. http://dx.doi.org/10.15407/ubj88.05.038.

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31

Miyashima, S., N. Nagata, T. Nakagawa, N. Hosaka, K. Takeuchi, R. Ogawa, and S. Ikehara. "Prevention of lpr-graft-versus-host disease and transfer of autoimmune diseases in normal C57BL/6 mice by transplantation of bone marrow cells plus bones (stromal cells) from MRL/lpr mice." Journal of Immunology 156, no. 1 (January 1, 1996): 79–84. http://dx.doi.org/10.4049/jimmunol.156.1.79.

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Abstract C57BL/6 (B6) (H-2b) mice were lethally irradiated and then reconstituted with T cell-depleted MRL/Mp-lpr/lpr (MRL/lpr) (H-2k) bone marrow cells. The mice showed a short survival with splenic atrophy and fibrosis, as previously described as lpr-graft-vs-host disease (GVHD). However, when these mice received bone marrow transplantation (BMT) plus bone grafts (to recruit donor-derived stromal cells) from MRL/lpr mice, they survived for almost 1 yr without showing GVH symptoms, but showing autoimmune symptoms such as elevated serum IgG2a concentrations, autoantibody production and glomerulonephritis. When MRL/lpr bone marrow cells plus MRL/+ bones (instead of MRL/lpr bones) were transplanted into B6 mice, such improved survival was also obtained, although the MRL/+ bone grafts were less effective in prolonging survival than MRL/lpr bone grafts. H-2 typing of stromal cells in the bone marrow of the B6 mice revealed that the stromal cells had been replaced by donor(H-2k) derived stromal cells. Analyses of TCR repertoires showed that the percentage of CD4+V beta 8.1,2+ cells significantly decreased in the B6 mice that received bone marrow transplantation plus bone grafts from MRL/lpr mice. These findings suggest that stromal cells present in the bone marrow play a crucial role in the development of lpr-GVHD and autoimmune diseases.

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32

Yang, Yang, Joseph P. Ritchie, Larry J. Suva, and Ralph D. Sanderson. "Heparanase Promotes the Osteolytic Phenotype in Multiple Myeloma." Blood 112, no. 11 (November 16, 2008): 841. http://dx.doi.org/10.1182/blood.v112.11.841.841.

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Abstract Heparanase, an enzyme that cleaves the heparan sulfate chains of proteoglycans, is upregulated in many human tumors including multiple myeloma. We have shown previously using animal models that heparanase promotes robust myeloma tumor growth and spontaneous metastasis to bone. In the present study, the role of heparanase in promoting myeloma bone disease was investigated. CAG human myeloma cells expressing either high or low levels of heparanase (heparanase-high or heparanase-low cells) were directly injected into the marrow cavity of human fetal long bones implanted subcutaneously in SCID mice (SCID-hu model). A second, non-injected human fetal bone was implanted on the contralateral side. Seven weeks after injection of myeloma cells into the primary bone, mice were euthanized and the osteolytic disease of both implanted bones was evaluated. Both X-ray and microCT analysis revealed marked osteolysis in the primary bones injected with heparanase-high cells, with little osteolytic disease detected in the bones injected with heparanase-low cells. Surprisingly, the non-injected, contralateral bones of the animals bearing heparanase-high tumors were also extensively degraded. Immunohistolochemical analysis of these contralateral bones revealed that osteolysis occurred in the absence of detectable tumor cells in the bone. Consistent with this osteolytic phenotype, TRAP staining of the primary and contralateral human bones harvested from mice bearing heparanase-high tumors showed a significant increase in osteoclast numbers, as compared to bones harvested from animals bearing heparanase-low tumors. In a second approach using heparanase-high or heparanase-low cells injected into the tibia of SCID mice, heparanase again enhanced osteolysis at the site of tumor injection as well as at distal sites, in the absence of resident tumor cells. These findings parallel our previously published observation that heparanase expressing breast cancer cells implanted in the mammary fat pad induced an increase in bone resorption in the absence of tumor cells within bone. The evidence in vivo suggested the release from heparanase-high cells of factor(s) that increase osteoclast formation. To test this idea, in vitro osteoclastogenesis assays were used to test the conditioned medium from heparanase-high cells. The conditioned medium from heparanase-high cells significantly enhanced osteoclastogenesis compared to conditioned medium from heparanase-low cells. Interestingly, conditioned medium derived from CAG cells expressing heparanase mutants lacking enzymatic activity failed to enhance osteoclastogenesis. Together, these data demonstrate for the first time that expression of heparanase is a major determinant of the osteolytic phenotype in myeloma. Increased osteolysis is the result of increased osteoclastogenesis that requires active heparanase enzyme and can occur in bones distal to the primary tumor prior to any subsequent metastasis. Thus, we hypothesize that therapies designed to block heparanase function will not only inhibit tumor growth, but may also protect bone from tumor-related bone destruction and possibly disrupt the metastasis of tumor to bone.

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Zhang, J., M. Liao, X. Niu, J. Xiang, Y. Zhao, H. Chen, and S. Lu. "Cross-talking between bone marrow-derived cells and lung cancer cells." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e19068-e19068. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e19068.

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e19068 Background: Disseminated cancer cells may initially require local nutrients and growth factors to thrive and survive in bone marrow. However, data on the influence of bone marrow derived cells(BMDC, also called bone stromal cells in some publication) on lung cancer cells is largely unexplored. This study is to explore the effect from bone marrow derived cells on biological behavior of lung cancer cells. Methods: The difference among lung cancer cell lines in their abilities to bone metastasis was tested using SCID animal model. Supernatant of bone marrow aspiration(BM) and condition medium from human bone stromal cells(BSC) were used to study the activity of bone stromal factors. Affymetrix gene chip U133A 2.0 was used to study the gene expression profile of H460 cells, after exposure to secreted proteins from bone stromal cells. Results: In accordance with other literature repors, H460 was found with high bone metastasis potential, while SPC-A1 and A549 cells were low bone metastasis lung cancer cells. We found bone stromal factors significantly increased the proliferation, invasion, adhesion and expression of angiogenosis-related factors, and inhibited the apoptosis for high bone metastasis H460 lung cancer cells. These biologic effects were not seen in SPC-A1 or A549 cells, which are low bone metastasis lung cancer cells. Adhesion of H460 cells to bone stromal cells consistently up-regulated 31 genes. Ontoexpress software showed main function of 31 genes were associated with signal transduction pathways(5 genes), and adhesion molecule(5 genes), including integrin b3 and ADAMTS-1, two potential targets related with bone metastasis. Conclusions: We concluded bone marrow derived cells had a profound effect on biological behavior of lung cancers, therefore favoring the growth of lung cancer cells in bone. No significant financial relationships to disclose.

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Zahran F, Zahran F., El-Ghareb M. El-Ghareb M, and Nabil A. Nabil A. "Bone Marrow Derived Mesenchymal Stem Cells As A Therapy for Renal Injury." Indian Journal of Applied Research 4, no. 4 (October 1, 2011): 11–16. http://dx.doi.org/10.15373/2249555x/apr2014/3.

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35

Dong, Rui, Yun Bai, Jingjin Dai, Moyuan Deng, Chunrong Zhao, Zhansong Tian, Fanchun Zeng, Wanyuan Liang, Lanyi Liu, and Shiwu Dong. "Engineered scaffolds based on mesenchymal stem cells/preosteoclasts extracellular matrix promote bone regeneration." Journal of Tissue Engineering 11 (January 2020): 204173142092691. http://dx.doi.org/10.1177/2041731420926918.

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Recently, extracellular matrix-based tissue-engineered bone is a promising approach to repairing bone defects, and the seed cells are mostly mesenchymal stem cells. However, bone remodelling is a complex biological process, in which osteoclasts perform bone resorption and osteoblasts dominate bone formation. The interaction and coupling of these two kinds of cells is the key to bone repair. Therefore, the extracellular matrix secreted by the mesenchymal stem cells alone cannot mimic a complex bone regeneration microenvironment, and the addition of extracellular matrix by preosteoclasts may contribute as an effective strategy for bone regeneration. Here, we established the mesenchymal stem cell/preosteoclast extracellular matrix -based tissue-engineered bones and demonstrated that engineered-scaffolds based on mesenchymal stem cell/ preosteoclast extracellular matrix significantly enhanced osteogenesis in a 3 mm rat femur defect model compared with mesenchymal stem cell alone. The bioactive proteins released from the mesenchymal stem cell/ preosteoclast extracellular matrix based tissue-engineered bones also promoted the migration, adhesion, and osteogenic differentiation of mesenchymal stem cells in vitro. As for the mechanisms, the iTRAQ-labeled mass spectrometry was performed, and 608 differentially expressed proteins were found, including the IGFBP5 and CXCL12. Through in vitro studies, we proved that CXCL12 and IGFBP5 proteins, mainly released from the preosteoclasts, contributed to mesenchymal stem cells migration and osteogenic differentiation, respectively. Overall, our research, for the first time, introduce pre-osteoclast into the tissue engineering of bone and optimize the strategy of constructing extracellular matrix–based tissue-engineered bone using different cells to simulate the natural bone regeneration environment, which provides new sight for bone tissue engineering.

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36

Li, Bo, Yigan Wang, Yi Fan, Takehito Ouchi, Zhihe Zhao, and Longjiang Li. "Cranial Suture Mesenchymal Stem Cells: Insights and Advances." Biomolecules 11, no. 8 (July 31, 2021): 1129. http://dx.doi.org/10.3390/biom11081129.

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The cranial bones constitute the protective structures of the skull, which surround and protect the brain. Due to the limited repair capacity, the reconstruction and regeneration of skull defects are considered as an unmet clinical need and challenge. Previously, it has been proposed that the periosteum and dura mater provide reparative progenitors for cranial bones homeostasis and injury repair. In addition, it has also been speculated that the cranial mesenchymal stem cells reside in the perivascular niche of the diploe, namely, the soft spongy cancellous bone between the interior and exterior layers of cortical bone of the skull, which resembles the skeletal stem cells’ distribution pattern of the long bone within the bone marrow. Not until recent years have several studies unraveled and validated that the major mesenchymal stem cell population of the cranial region is primarily located within the suture mesenchyme of the skull, and hence, they are termed suture mesenchymal stem cells (SuSCs). Here, we summarized the characteristics of SuSCs, this newly discovered stem cell population of cranial bones, including the temporospatial distribution pattern, self-renewal, and multipotent properties, contribution to injury repair, as well as the signaling pathways and molecular mechanisms associated with the regulation of SuSCs.

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Franco, GG, BW Minto, LP Coelho, PF Malard, ER Carvalho, FYK Kawamoto, BM Alcantara, and LGGG Dias. "Autologous adipose-derived mesenchymal stem cells and hydroxyapatite for bone defect in rabbits." Veterinární Medicína 67, No. 1 (November 29, 2021): 38–45. http://dx.doi.org/10.17221/85/2020-vetmed.

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This study aims to evaluate the effect of autologous adipose-derived mesenchymal stem cells (AAD-MSC), with and without synthetic absorbable hydroxyapatite (HAP-91), on the bone regeneration in rabbits. Thirty-four female white New Zealand rabbits were submitted to a 10 mm distal diaphyseal radius ostectomy, divided into 3 experimental groups according to the treatment established. The bone gap was filled with 0.15 ml of a 0.9% saline solution containing two million AAD-MSC (G1), or AAD-MSC associated with HAP-91 (G2). The control group (CG) received only 0.15 ml of the 0.9% saline solution. Radiographs were made post-operatively, and after 15, 30, 45 and 90 days. Fifty percent of the samples were submitted to a histological examination at 45 days and the remaining ones at 90 days post-operatively. Radiographically, the periosteal reaction, bone callus volume and bone bridge quality were superior in G2 (P < 0.05). Histologically, the bone repair was faster and more efficient in G1 at 45 days (P < 0.05). In conclusion, AAD-MSC improved the regeneration on the experimentally induced bone defects in rabbits; however, the use of hydroxyapatite requires caution given the granulomatous reaction produced in the species.

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38

Compston, JE. "Bone marrow and bone: a functional unit." Journal of Endocrinology 173, no. 3 (June 1, 2002): 387–94. http://dx.doi.org/10.1677/joe.0.1730387.

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Bone and bone marrow, although often regarded as separate systems, function as a single unit. Cells in the bone marrow are the precursors of bone remodelling cells and exert an important regulatory role both on their own development and the remodelling process, acting as mediators for the effects of systemic and local factors. Other cells, such as immune cells and megakaryocytes, also contribute to the regulation of bone cell development and activity. Many diseases that affect the bone marrow have profound effects on bone, involving interactions between abnormal and normal marrow cells and those of bone. Although recent advances in bone physiology have produced new insights into the relationship between bone marrow and bone cells, much remains to be learnt about the mechanisms by which marrow and bone act in synergy to regulate bone remodelling, both in health and disease.

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39

Li, Danyang, Yiming Liu, Jinyan Qi, Xinhua Cui, Ying Guo, Dipanpan Wu, and Hui Liang. "Bone Marrow Mesenchymal Stem Cells Promote the Stemness of Hypopharyngeal Cancer Cells." Cellular Reprogramming 22, no. 5 (October 1, 2020): 269–76. http://dx.doi.org/10.1089/cell.2020.0004.

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40

Kruithof-de Julio, Marianna, Letizia Astrologo, Eugenio Zoni, Sofia Karkampouna, Peter C. Gray, Irena Klima, Joel Grosjean, et al. "Effects of ALK1Fc treatment on prostate cancer cells interacting with bone and bone cells in bone metastasis models." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e16576-e16576. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e16576.

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e16576 Background: Prostate cancer is the second most common cancer in men worldwide. Lethality is normally associated with the consequences of metastasis rather than the primary tumor. In particular, bone is the most frequent site of metastasis and once prostate tumor cells are engrafted in the skeleton, curative therapy is no longer possible. Bone morphogenetic proteins (BMPs) play a critical role in bone physiology and pathology. However, little is known about the role of BMP9 and its signaling receptors, ALK1 and ALK2, in prostate cancer and bone metastasis. In this context, we investigate the impact of BMP9 on primary prostate cancer and derived bone metastasis. Methods: The human ALK1 extracellular domain (ECD) binds BMP9 and BMP10 with high affinity. In order to study the effect of BMP9 in vitro and in vivo we use a soluble chimeric protein, consisting of ALK1 ECD fused to human Fc (ALK1Fc), for preventing the activation of endogenous signaling. ALK1Fc sequesters BMP9 and BMP10, preserving the activation of ALK1 through other ligands. Results: We show that ALK1Fc reduces BMP9-mediated signaling and decreases proliferation of highly metastatic and tumor initiating human prostate cancer cells in vitro. In line with these observations, we demonstrate that ALK1Fc reduces tumor growth in vivo in an orthotopic transplantation model. The propensity of the primary prostate cancer to metastasize to the bone is also investigated. In particular, we report how the ALK1Fc influences the prostate cancer cells in vitro and in vivo when these are probed in different bone settings (co-culture with bone cells and intraosseous transplantation in mice). Conclusions: Our study provides the first demonstration that ALK1Fc inhibits prostate cancer cells growth identifying BMP9 as a putative therapeutic target and ALK1Fc as a potential therapy. All together, these findings justify the ongoing clinical development of drugs blocking ALK1 and ALK2 receptor activity.

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41

Miura, Yasuo, Zhigang Gao, Masako Miura, Byoung-Moo Seo, Wataru Sonoyama, WanJun Chen, Stan Gronthos, Li Zhang, and Songtao Shi. "Culture-Expanded Human Bone Marrow Stromal Stem Cells Organize Functional Bone Marrow Niches In Vivo." Blood 106, no. 11 (November 16, 2005): 2314. http://dx.doi.org/10.1182/blood.v106.11.2314.2314.

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Abstract Bone marrow stromal stem cells (BMSSCs) are mesenchymal stem cells that are capable of differentiating into osteoblasts, chondrocytes, adipocytes, muscle cells and neural cells. Upon in vivo transplantation, BMSSCs form bone and associated hematopoietic marrow elements. However, the functional role of BMSSC-associated bone marrow is still unknown. In this study, we demonstrated that human BMSSCs organized ectopic bone marrow niche microarchitecture that contained hematopoietic progenitors and multiple lineages of cells including myeloid, lymphoid, erythroid and megakaryocytic cells originated from recipients. Significantly, transplantation of the ectopically generated bone marrow cells can rescue lethally irradiated mice with successful hematopoietic engraftment, suggesting a therapeutic potentiality of human BMSSC-organized hematopoietic progenitor cells. In addition, systemically administrated bone marrow cells derived from long bones of donor mice homed to BMSSC-associated ectopic bone marrow niche microenvironments. These data demonstrate that BMSSC-organized ectopic bone marrow has functional analogy to physiological bone marrow. Mechanistically, platelet-derived growth factor (PDGF)-BB was found to promote hematopoiesis in the BMSSC transplants through an up-regulated expression of β-catenin. Conversely, inhibition of PDGF signaling in BMSSCs by PDGF receptor β siRNA blocked hematopoiesis and osteogenesis in the BMSSC transplants. Moreover, the BMSSC-organized ectopic bone/marrow structure could be utilized as an organ to be re-transplanted into secondary recipient mice to deliver hematopoietic cells in the recipient’s circulation system, implying a therapeutic potential of transplanting bone/marrow organ system containing hematopoietic stem cell niches. In summary, these evidences demonstrate that regeneration of BMSSC-organized functional bone marrow niches contain hematopoietic progenitor/stem cells and therefore provide promise for clinical therapy.

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Namli, Halide, Özgür Erdogan, Gülfiliz Gönlüşen, Onur Evren Kahraman, Halil Murat Aydin, Sevil Karabag, and Ufuk Tatli. "Vertical Bone Augmentation Using Bone Marrow–Derived Stem Cells." Implant Dentistry 25, no. 1 (February 2016): 54–62. http://dx.doi.org/10.1097/id.0000000000000334.

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43

Singer, Frederick R., Barbara G. Mills, Helen E. Gruber, Jolene J. Windle, and G. David Roodman. "Ultrastructure of Bone Cells in Paget's Disease of Bone." Journal of Bone and Mineral Research 21, S2 (December 2006): P51—P54. http://dx.doi.org/10.1359/jbmr.06s209.

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Hiraga, Toru. "Bone metastasis: Interaction between cancer cells and bone microenvironment." Journal of Oral Biosciences 61, no. 2 (June 2019): 95–98. http://dx.doi.org/10.1016/j.job.2019.02.002.

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Wezeman, Frederick H., Katheryn M. Guzzino, and Beverly Waxler. "Multicellular tumor spheroid interactions with bone cells and bone." Anatomical Record 213, no. 2 (October 1985): 111–20. http://dx.doi.org/10.1002/ar.1092130202.

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46

Bravenboer⁎, N., H. W. V. Essen, P. J. Holzmann, A. C. Heijboer, and P. Lips. "Expression of klotho in bone cells and bone tissue." Bone 50 (May 2012): S103. http://dx.doi.org/10.1016/j.bone.2012.02.313.

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47

Suvannasankha, Attaya, Colin D. Crean, Douglas R. Tompkins, Jesus Delgado-Calle, Teresita M. Bellido, G. David Roodman, and John M. Chirgwin. "Regulation of Osteoblast Function in Myeloma Bone Disease By Semaphorin 4D." Blood 128, no. 22 (December 2, 2016): 4439. http://dx.doi.org/10.1182/blood.v128.22.4439.4439.

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Abstract Multiple myeloma (MM) bone disease (MMBD) is characterized by activation of osteoclasts and suppression of osteoblastic differentiation, with these changes in the bone microenvironment supporting MM cell growth and drug resistance. These complex interactions between MM cells and bone cells are incompletely understood. Current bone targeted therapy with bisphosphonates or Denosumab only blocks bone resorption but has no effect on osteoblast activity and only modest effects on MM growth. Therefore, new MMBD treatments are needed. Semaphorin-4D (Sema4D; CD100), is made by osteoclasts and inhibits osteoblasts by binding to the Plexin B receptor. Breast cancers also express Sema4d, and silencing sema4D in MDA-MB-231 breast cancer cells suppresses bone metastasis (Yang Y et al, PLoS One 2016). Since breast cancers and MM both cause osteolytic bone destruction and soluble Sema4D and Plexin B levels are increased in sera of MM patients (Terpos et al, 2012), we tested if sema4D contributed to MMBD. qPCR analysis of human MM cell lines and primary CD138+ cells showed MM cells express high levels of sema4D mRNA, comparing to the MDA-MB-231 breast cancer cells. Analysis of previously reported gene expression array data confirmed that MM cells express sema4D at a higher level compared to bone marrow plasma cells of MGUS and healthy donors (GenomicScape.com; Zhan F et al, Blood 2007; Mattiolo M et al, Oncogene, 2005). These results plus those of Terpos et al suggest that MM cells commonly express Sema4D. We next asked if the bone microenvironment increases MM expression of Sema4D. We co-cultured human MM cell lines RPMI8226 and JJN3 with mouse bones. Species -specific changes in tumor and bone were evaluated by quantitative RT-PCR. MM cells engrafted onto mouse bones, increasing markers of osteolysis similar to those seen in MM bone disease. After a week of co-culture, Sema4D expression was increased in MM cells (mean ±SD; 4.2±0.4; p=0.023), compared to MM cells grown alone. In addition, bones co-cultured with MM cells expressed higher Sema4D mRNA than bones alone (mean ±SD; 3.6±0.21; p=0.03). While co-culture increased both MM and bone Sema4D, markers of osteoblast activity, Col1a1, alkaline phosphatase and osteocalcin were suppressed. Preliminary experiments suggest that osteocytes are a major source of Sema4D expression in bone, in addition to active osteoclasts, which are much rarer cells than osteocytes. The induction of Sema4D in bone was only partially inhibited by 100nM zoledronic acid to inhibit osteoclast activity. Since osteocytes can physically interact with MM cells in vivo (Delgado Calle, Cancer Res 2016), we then tested the effect of MM cells on osteocyte sema4D expression in co-cultures of RPMI 8226 and JJN3 MM cells with MOL-Y4 osteocytic cells, separated by transwells. Both MM cell lines increased the Sema4D mRNA content of MLO-Y4 cells (mean ±SD; 3.1±0.4; p=0.036), suggesting that myeloma-secreted factors regulate osteocyte Sema4D expression. Since Sema4D is a potent osteoblast inhibitor, our data suggest that osteocyte -derived Sema4D may be a major contributor to MMBD, and that neutralization of Sema4D activity should improve the suppressed bone formation in MM. Disclosures Roodman: Amgen: Consultancy.

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Liu, Yanan, Haifeng Wang, Huixin Dou, Bin Tian, Le Li, Luyuan Jin, Zhenting Zhang, and Lei Hu. "Bone regeneration capacities of alveolar bone mesenchymal stem cells sheet in rabbit calvarial bone defect." Journal of Tissue Engineering 11 (January 2020): 204173142093037. http://dx.doi.org/10.1177/2041731420930379.

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Mesenchymal stem cells sheets have been verified as a promising non-scaffold strategy for bone regeneration. Alveolar bone marrow mesenchymal stem cells, derived from neural crest, have the character of easily obtained and strong multi-differential potential. However, the bone regenerative features of alveolar bone marrow mesenchymal stem cells sheets in the craniofacial region remain unclear. The purpose of the present study was to compare the osteogenic differentiation and bone defect repairment characteristics of bone marrow mesenchymal stem cells sheets derived from alveolar bone (alveolar bone marrow mesenchymal stem cells) and iliac bone (Lon-bone marrow mesenchymal stem cells) in vitro and in vivo. Histology character, osteogenic differentiation, and osteogenic gene expression of human alveolar bone marrow mesenchymal stem cells and Lon-bone marrow mesenchymal stem cells were compared in vitro. The cell sheets were implanted in rabbit calvarial defects to evaluate tissue regeneration characteristics. Integrated bioinformatics analysis was used to reveal the specific gene and pathways expression profile of alveolar bone marrow mesenchymal stem cells. Our results showed that alveolar bone marrow mesenchymal stem cells had higher osteogenic differentiation than Lon-bone marrow mesenchymal stem cells. Although no obvious differences were found in the histological structure, fibronectin and integrin β1 expression between them, alveolar-bone marrow mesenchymal stem cells sheet exhibited higher mineral deposition and expression levels of osteogenic marker genes. After being transplanted in the rabbit calvarial defects area, the results showed that greater bone volume and trabecular thickness regeneration were found in bone marrow mesenchymal stem cells sheet group compared to Lon-bone marrow mesenchymal stem cells group at both 4 weeks and 8 weeks. Finally, datasets of bone marrow mesenchymal stem cells versus Lon-bone marrow mesenchymal stem cells, and periodontal ligament mesenchymal stem cells (another neural crest derived mesenchymal stem cells) versus umbilical cord mesenchymal stem cells were analyzed. Total 71 differential genes were identified by overlap between the 2 datasets. Homeobox genes, such as LHX8, MKX, PAX9, MSX, and HOX, were identified as the most significantly changed and would be potential specific genes in neural crest mesenchymal stem cells. In conclusion, the Al-bone marrow mesenchymal stem cells sheet-based tissue regeneration appears to be a promising strategy for craniofacial defect repair in future clinical applications.

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Luby, Alexandra O., Kavitha Ranganathan, Jeremy V. Lynn, Noah S. Nelson, Alexis Donneys, and Steven R. Buchman. "Stem Cells for Bone Regeneration." Journal of Craniofacial Surgery 30, no. 3 (May 2019): 730–35. http://dx.doi.org/10.1097/scs.0000000000005250.

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Mankani, Mahesh H., and Pamela Gehron Robey. "Transplantation of Bone-Forming Cells." Endocrinologist 8, no. 6 (November 1998): 459–68. http://dx.doi.org/10.1097/00019616-199811000-00009.

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