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Artículos de revistas sobre el tema "Bone marrow adipocytes"

Autor: Grafiati

Publicado: 1 de febrero de 2025

Última modificación: 31 de julio de 2025

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1

Naveiras, Olaia, Valentina Nardi, and George Q. Daley. "Bone Marrow Adipocytes Prevent Hematopoietic Expansion in Homeostasis and in Bone Marrow Transplantation." Blood 112, no. 11 (2008): 551. http://dx.doi.org/10.1182/blood.v112.11.551.551.

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Abstract In mammalian bone marrow (BM), osteoblasts and endothelium constitute functional niches that support hematopoietic stem cells (HSC). Adult BM also contains numerous adipocytes, whose numbers correlate inversely with the hematopoietic activity of the marrow. As described by Neumann’s law in 1882, distal skeletal regions are adipocytic and thus non-hematopoietic in the adult. Fatty infiltration of the hematopoietic red marrow also occurs following irradiation or chemotherapy and is a diagnostic feature in biopsies from patients with marrow aplasia. However, whether adipocytes participat

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2

Yang, S., W. Lu, C. Zhao, et al. "PF457 MECHANISM OF MORPHOLOGICAL REMODELING OF BONE MARROW ADIPOCYTES IN ACUTE MYELOID LEUKEMIA." HemaSphere 3, S1 (2019): 180. http://dx.doi.org/10.1002/j.2572-9241.2019.tb00056.x.

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Background:We have previously found that morphological remodeling of bone marrow adipocytes in acute myeloid leukemia (AML) patients is closely related to poor prognosis, and growth differentiation factor 15 (GDF15) may be a key factor in this pathological phenomenon.Aims:In this study, we further explored the mechanism of GDF15 regulating the bone marrow adipocyte remodeling from the perspective of calcium channel TRPV4.Methods:GDF15‐induced adipocytes were analyzed using gene expression profiling, and gene knockdown cells were generated by lentiviral‐mediated shRNA. Chip‐qPCR was used to eva

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3

Kwak, Jun-Goo, and Jungwoo Lee. "Bone Marrow Adipocytes Contribute to Tumor Microenvironment-Driven Chemoresistance via Sequestration of Doxorubicin." Cancers 15, no. 10 (2023): 2737. http://dx.doi.org/10.3390/cancers15102737.

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Chemoresistance is a significant problem in the effective treatment of bone metastasis. Adipocytes are a major stromal cell type in the bone marrow and may play a crucial role in developing microenvironment-driven chemoresistance. However, detailed investigation remains challenging due to the anatomical inaccessibility and intrinsic tissue complexity of the bone marrow microenvironment. In this study, we developed 2D and 3D in vitro models of bone marrow adipocytes to examine the mechanisms underlying adipocyte-induced chemoresistance. We first established a protocol for the rapid and robust d

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4

Lecka-Czernik, Beata, та Larry J. Suva. "Resolving the Two “Bony” Faces of PPAR-γ". PPAR Research 2006 (2006): 1–9. http://dx.doi.org/10.1155/ppar/2006/27489.

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Bone loss with aging results from attenuated and unbalanced bone turnover that has been associated with a decreased number of bone forming osteoblasts, an increased number of bone resorbing osteoclasts, and an increased number of adipocytes (fat cells) in the bone marrow. Osteoblasts and adipocytes are derived from marrow mesenchymal stroma/stem cells (MSC). The milieu of intracellular and extracellular signals that controls MSC lineage allocation is diverse. The adipocyte-specific transcription factor peroxisome proliferator-activated receptor-gamma (PPAR-γ) acts as a critical positive regula

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5

Liu, Huan, Jin He, Su Pin Koh, et al. "Reprogrammed marrow adipocytes contribute to myeloma-induced bone disease." Science Translational Medicine 11, no. 494 (2019): eaau9087. http://dx.doi.org/10.1126/scitranslmed.aau9087.

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Osteolytic lesions in multiple myeloma are caused by osteoclast-mediated bone resorption and reduced bone formation. A unique feature of myeloma is a failure of bone healing after successful treatment. We observed adipocytes on trabecular bone near the resorbed area in successfully treated patients. Normal marrow adipocytes, when cocultured with myeloma cells, were reprogrammed and produced adipokines that activate osteoclastogenesis and suppress osteoblastogenesis. These adipocytes have reduced expression of peroxisome proliferator–activated receptor γ (PPARγ) mediated by recruitment of polyc

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6

Jin, Linhua, Marina Konopleva, Yixin Zhou, et al. "Pro-Apoptotic and Proliferative Effects of Bone Marrow Adipocytes on Myeloid Leukemia Cells." Blood 114, no. 22 (2009): 4572. http://dx.doi.org/10.1182/blood.v114.22.4572.4572.

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Abstract Abstract 4572 Bone marrow stromal cells (MSCs) from elderly subjects have a reduced capacity to differentiate into osteoblasts and an increased capacity to differentiate into adipocytes, which leads to progressive accumulation of fat in the bone marrow space with increasing age. Adipocytes are the prevalent stromal cell type in adult BM that play an important role in the leukemic bone marrow microenvironment (Tabe et al., Blood 2004 103:1815-22). In this study, we examined the role of BM-derived adipocytes at different stages of differentiation on proliferation and apoptosis of AML ce

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7

Naveiras, Olaia, Valentina Nardi, Parul Sharma, Peter Hauschka, and George Q. Daley. "Bone Marrow Adipocytes: A Novel Negative Regulator of the Hematopoietic Microenvironment." Blood 110, no. 11 (2007): 1405. http://dx.doi.org/10.1182/blood.v110.11.1405.1405.

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Abstract In the bone marrow (BM), osteoblasts and endothelium constitute functional niches providing positive or negative signals for hematopoietic stem cell (HSC) self-renewal. In addition to hematopoietic cells, endothelial cells, and osteoblasts, adult BM contains numerous adipocytes. Interestingly, the number of adipocytes correlates inversely with the gross hematopoietic activity of the marrow. Whether adipocytes have a direct effect on hematopoietic progenitors or whether they act as mere space-fillers in this context remains unclear. To determine the potential role of bone marrow adipoc

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8

Horowitz, Mark C., Ryan Berry, Brandon Holtrup, et al. "Bone marrow adipocytes." Adipocyte 6, no. 3 (2017): 193–204. http://dx.doi.org/10.1080/21623945.2017.1367881.

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9

Kastrenopoulou, Afroditi, Kyriakos E. Kypreos, Nicholaos I. Papachristou, et al. "ApoA1 Deficiency Reshapes the Phenotypic and Molecular Characteristics of Bone Marrow Adipocytes in Mice." International Journal of Molecular Sciences 23, no. 9 (2022): 4834. http://dx.doi.org/10.3390/ijms23094834.

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In the present study, we studied the effect of apolipoprotein A-1 (APOA1) on the spatial and molecular characteristics of bone marrow adipocytes, using well-characterized ApoA1 knockout mice. APOA1 is a central regulator of high-density lipoprotein cholesterol (HDL-C) metabolism, and thus HDL; our recent work showed that deficiency of APOA1 increases bone marrow adiposity in mice. We found that ApoA1 deficient mice have greatly elevated adipocytes within their bone marrow compared to wild type counterparts. Morphologically, the increased adipocytes were similar to white adipocytes, and display

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10

Trotter, Timothy N., Tshering D. Lama-Sherpa, Deniz Peker, Amjad Javed, Larry J. Suva, and Yang Yang. "The Role of Adipocyte Lineage Cells in Myeloma Growth and Dissemination in Bone." Blood 126, no. 23 (2015): 1797. http://dx.doi.org/10.1182/blood.v126.23.1797.1797.

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Abstract Background: Multiple myeloma (MM) is hematologic malignancy of plasma cells that thrives in and progresses throughout the bone marrow microenvironment. The bone marrow is host to a variety of cell types, including bone marrow stromal cells and hematopoietic cells, as well as osteoblasts, osteoclasts and adipocytes. We and others have shown that MM cells not only alter the local bone microenvironment to support MM progression, but also modify distant bone sites through secretion of soluble factors before arrival of tumor cells. One critical alteration in bone is the shift of osteoblast

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11

Zhang, Lili, Mengmeng Liu, Xiaokang Zhou, et al. "Role of Osteoprotegerin (OPG) in Bone Marrow Adipogenesis." Cellular Physiology and Biochemistry 40, no. 3-4 (2016): 681–92. http://dx.doi.org/10.1159/000452580.

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Background/Aims: Bone marrow adipogenesis is one of the major characteristics of aged bone. Bone marrow mesenchymal stem cells (BMMSCs) prefer to differentiate into adipocytes instead of osteoblasts in the bone marrow cavity in aged hosts. The mechanism of formation and function of adipocytes in aged bone marrow needs further investigation. Osteoprotegerin (OPG) is a member of the tumor necrosis factor receptor (TNFR) super family, and it can inhibit the activities of osteoclasts. We found that adipocyte numbers increased in the bone marrow of Opg knockout mice. In this study, we investigated

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12

Tencerova, Michaela, Meshail Okla, and Moustapha Kassem. "Insulin Signaling in Bone Marrow Adipocytes." Current Osteoporosis Reports 17, no. 6 (2019): 446–54. http://dx.doi.org/10.1007/s11914-019-00552-8.

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Abstract Purpose of Review The goal of this review is to discuss the role of insulin signaling in bone marrow adipocyte formation, metabolic function, and its contribution to cellular senescence in relation to metabolic bone diseases. Recent Findings Insulin signaling is an evolutionally conserved signaling pathway that plays a critical role in the regulation of metabolism and longevity. Bone is an insulin-responsive organ that plays a role in whole body energy metabolism. Metabolic disturbances associated with obesity and type 2 diabetes increase a risk of fragility fractures along with incre

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13

Philchenkov, A. A. "Bone marrow adipocytes and multiple myeloma." Oncohematology 14, no. 1 (2019): 60–75. http://dx.doi.org/10.17650/1818-8346-2019-14-1-60-75.

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Multiple myeloma originating from clonal proliferation of plasma cells in the bone marrow is one of the most prevalent hematological malignancies worldwide. The pathogenetic mechanisms of multiple myeloma are far from being elucidated. Nevertheless, it is known that the adipocytes as the prevalent cellular component of bone marrow microenvironment contribute significantly to multiple myeloma growth and progression. The review discloses the recent data on the interactions between bone marrow adipocytes and myeloma cells, hematopoietic stemcells, hematopoietic progenitor cells, mesenchimal stem

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14

Starling, Shimona. "Characterizing bone marrow adipocytes." Nature Reviews Endocrinology 16, no. 4 (2020): 196. http://dx.doi.org/10.1038/s41574-020-0333-0.

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15

Lu, Wei, and Jun Shi. "Bone Marrow Small Adipocytes in Acute Myeloid Leukemia Correlate with Prognosis." Blood 128, no. 22 (2016): 2874. http://dx.doi.org/10.1182/blood.v128.22.2874.2874.

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Abstract Introduction: Adipocytes have a substantial effect on the outcome and progression of certain solid tumors. However, little attention has been paid to the role of bone marrow (BM) adipocytes in acute myeloid leukemia (AML) because it is difficult to observe adipocytes through clinical BM aspiration. Although it was reported that adipocytes affected the behavior of leukemia cells in vitro, there is still no direct in vivo evidence. In the present study, we investigated the influence of adipocytes by focusing on their changing size in BM from primary AML patients. Methods: We retrospecti

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16

Beekman, Kerensa M., Marleen Zwaagstra, Annegreet G. Veldhuis-Vlug, et al. "Ovariectomy increases RANKL protein expression in bone marrow adipocytes of C3H/HeJ mice." American Journal of Physiology-Endocrinology and Metabolism 317, no. 6 (2019): E1050—E1054. http://dx.doi.org/10.1152/ajpendo.00142.2019.

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Estrogen deficiency induces bone loss by increasing bone resorption, in part through upregulation of receptor activator of nuclear factor-κB ligand (RANKL). RANKL is secreted by osteoblasts and osteocytes, but more recently bone marrow (pre)adipocytes have also been shown to express RANKL. Estrogen deficiency increases bone marrow adipose tissue (BMAT). The aim of this study was to determine the effect of ovariectomy (OVX) on RANKL protein expression by bone marrow adipocytes in C3H/HeJ mice. Fourteen-week-old female C3H/HeJ mice ( n = 20) were randomized to sham surgery (Sham) or OVX. After 4

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17

Appiagyei-Dankah, Yaw, Carmen D. Tapiador, Jodi F. Evans, Mariano Castro-Magana, John F. Aloia, and James K. Yeh. "Influence of growth hormone on bone marrow adipogenesis in hypophysectomized rats." American Journal of Physiology-Endocrinology and Metabolism 284, no. 3 (2003): E566—E573. http://dx.doi.org/10.1152/ajpendo.00213.2002.

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The hypophysectomized rat has been used as a model to study the effects of growth hormone deficiency on bone. Here, we have investigated the influence of growth hormone administration to hypophysectomized rats (HX) for 6 wk on accumulation of triglycerides in bone marrow and on the differentiation of primary marrow stromal cells into adipocytes under in vitro conditions. We found that hypophysectomy significantly increased triglyceride concentration in bone marrow, which was attenuated by growth hormone administration. Primary bone marrow stromal cells derived from HX rats also had more adipoc

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18

Zhou, Haodong, Guy Trudel, Konstantin Alexeev, Justin Thomas, and Odette Laneuville. "Hyperplasia and accelerated hypertrophy of marrow adipocytes with knee immobilization were sustained despite remobilization." Journal of Applied Physiology 129, no. 4 (2020): 701–8. http://dx.doi.org/10.1152/japplphysiol.00539.2020.

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This longitudinal study elucidates the response of marrow adipose tissue adipocytes in weight-bearing joints to changes in different mechanical environments, and we provide insight on the malleability of the changes over time. In a rat animal model, knee immobilization induced hyperplasia and accelerated the age-dependent hypertrophy of adipocytes. Changes in adipocyte number and size were sustained despite unassisted remobilization. Multimodal distributions of cell size were characteristic of bone marrow adipocytes.

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19

de Paula, Francisco J. A., and Clifford J. Rosen. "Marrow Adipocytes: Origin, Structure, and Function." Annual Review of Physiology 82, no. 1 (2020): 461–84. http://dx.doi.org/10.1146/annurev-physiol-021119-034513.

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The skeleton harbors an array of lineage cells that have an essential role in whole body homeostasis. Adipocytes start the colonization of marrow space early in postnatal life, expanding progressively and influencing other components of the bone marrow through paracrine signaling. In this unique, closed, and hypoxic environment close to the endosteal surface and adjacent to the microvascular space the marrow adipocyte can store or provide energy, secrete adipokines, and target neighboring bone cells. Adipocyte progenitors can also migrate from the bone marrow to populate white adipose tissue,

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20

Jin, Linhua, Marina Konopleva, Masato Shikami, et al. "Molecular Mechanisms of Pro-Survival and Differentiating Function of Bone Marrow-Derived Adipocytes On Acute Monoblastic Leukemia Cells." Blood 120, no. 21 (2012): 2582. http://dx.doi.org/10.1182/blood.v120.21.2582.2582.

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Abstract Abstract 2582 Survival of adult patients with acute monocytic leukemia remains dismal. We proposed the hypothesis that bone marrow (BM) adipocytes abundant in aging marrow microenvironment play a role in chemoresistance of AML cells. We have reported that BM adipocytes promote monocytic differentiation, activation, and survival of monoblastic leukemia cells (ASH, 2012).In this study, we examined the molecular mechanism of BM adipocytes causing survival and differentiation of monoblastic leukemia cells. Monoblastic leukemia cell line U937 and primary samples from acute monoblastic leuk

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21

Yang, Xiaoyu, Jing Li, Liting Zhao, et al. "Targeting adipocytic discoidin domain receptor 2 impedes fat gain while increasing bone mass." Cell Death & Differentiation 29, no. 4 (2021): 737–49. http://dx.doi.org/10.1038/s41418-021-00887-9.

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AbstractObesity is closely associated with low-bone-mass disorder. Discoidin domain receptor 2 (DDR2) plays essential roles in skeletal metabolism, and is probably involved in fat metabolism. To test the potential role of DDR2 in fat and fat-bone crosstalk, Ddr2 conditional knockout mice (Ddr2Adipo) were generated in which Ddr2 gene is exclusively deleted in adipocytes by Adipoq Cre. We found that Ddr2Adipo mice are protected from fat gain on high-fat diet, with significantly decreased adipocyte size. Ddr2Adipo mice exhibit significantly increased bone mass and mechanical properties, with enha

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22

Rozman, C., JC Reverter, E. Feliu, L. Berga, M. Rozman, and C. Climent. "Variations of fat tissue fraction in abnormal human bone marrow depend both on size and number of adipocytes: a stereologic study." Blood 76, no. 5 (1990): 892–95. http://dx.doi.org/10.1182/blood.v76.5.892.892.

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Abstract Studies dealing with the number or size of individual adipose cells in abnormal human bone marrow are lacking. To ascertain whether variations in fat tissue fraction depend on the size of individual adipocytes or their number or both, a stereologic study of 30 human bone marrow specimens (10 with aplasia, 10 with hyperplasia, and 10 with dysplasia) was performed. A total of 23,435 adipocyte profiles were measured and two stereologic parameters were obtained in each specimen: mean diameter and number of cells per mm3 of bone marrow. The fat tissue fraction correlated positively with th

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23

Rozman, C., JC Reverter, E. Feliu, L. Berga, M. Rozman, and C. Climent. "Variations of fat tissue fraction in abnormal human bone marrow depend both on size and number of adipocytes: a stereologic study." Blood 76, no. 5 (1990): 892–95. http://dx.doi.org/10.1182/blood.v76.5.892.bloodjournal765892.

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Studies dealing with the number or size of individual adipose cells in abnormal human bone marrow are lacking. To ascertain whether variations in fat tissue fraction depend on the size of individual adipocytes or their number or both, a stereologic study of 30 human bone marrow specimens (10 with aplasia, 10 with hyperplasia, and 10 with dysplasia) was performed. A total of 23,435 adipocyte profiles were measured and two stereologic parameters were obtained in each specimen: mean diameter and number of cells per mm3 of bone marrow. The fat tissue fraction correlated positively with the size (r

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24

Shafat, Manar S., Thomas Oellerich, Sebastian Mohr, et al. "Leukemic blasts program bone marrow adipocytes to generate a protumoral microenvironment." Blood 129, no. 10 (2017): 1320–32. http://dx.doi.org/10.1182/blood-2016-08-734798.

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25

Diedrich, Jonathan D., Craig E. Cole, Matthew J. Pianko, Justin A. Colacino, and Jamie J. Bernard. "Non-Toxicological Role of Aryl Hydrocarbon Receptor in Obesity-Associated Multiple Myeloma Cell Growth and Survival." Cancers 15, no. 21 (2023): 5255. http://dx.doi.org/10.3390/cancers15215255.

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Obesity is not only a risk factor for multiple myeloma (MM) incidence, but it is also associated with an increased risk of progression from myeloma precursors—monoclonal gammopathy of undetermined significance—and smoldering myeloma. Adipocytes in the bone marrow (BMAs) microenvironment have been shown to facilitate MM cell growth via secreted factors, but the nature of these secreted factors and their mechanism of action have not been fully elucidated. The elevated expression of aryl hydrocarbon receptor (AhR) is associated with a variety of different cancers, including MM; however, the role

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26

Lewis, Kenneth T., and Ormond A. MacDougald. "Bone marrow adipocytes in 3D." Nature Reviews Endocrinology 14, no. 5 (2018): 254–55. http://dx.doi.org/10.1038/nrendo.2018.31.

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27

Sebo, Zachary L., Elizabeth Rendina-Ruedy, Gene P. Ables, et al. "Bone Marrow Adiposity: Basic and Clinical Implications." Endocrine Reviews 40, no. 5 (2019): 1187–206. http://dx.doi.org/10.1210/er.2018-00138.

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AbstractThe presence of adipocytes in mammalian bone marrow (BM) has been recognized histologically for decades, yet, until recently, these cells have received little attention from the research community. Advancements in mouse transgenics and imaging methods, particularly in the last 10 years, have permitted more detailed examinations of marrow adipocytes than ever before and yielded data that show these cells are critical regulators of the BM microenvironment and whole-body metabolism. Indeed, marrow adipocytes are anatomically and functionally separate from brown, beige, and classic white a

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28

Shu, Ling-Ling, Shuzhao Chen, Jinyuan Li, et al. "Bone Marrow Adipocyte Promotes Epithelial-Mesenchymal-Transition-like Activation in Multiple Myeloma Via CXCL-12/CXCR4 Axis." Blood 138, Supplement 1 (2021): 1584. http://dx.doi.org/10.1182/blood-2021-152400.

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Abstract Extra-medullary disease (EMD) in multiple myeloma (MM) is associated with poor prognosis and resistance to chemotherapy. The bone marrow microenvironment is a key regulator of myeloma metastatic progression through the secretion of growth factors that activate epithelial-mesenchymal transition (EMT)-like characters. Bone marrow adipocyte (BMA) accumulates in obese patients and displays distinct immune regulatory properties rather than provides energy substrates, forming a bulk portion of the bone marrow microenvironment. Emerging evidence indicates the potential for adipocytes to infl

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29

Shaoxin Yang, Wei Lu, Chong Zhao, et al. "Leukemia cells remodel marrow adipocytes via TRPV4-dependent lipolysis." Haematologica 105, no. 11 (2019): 2572–83. http://dx.doi.org/10.3324/haematol.2019.225763.

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Remodeling of adipocyte morphology and function plays a critical role in prostate cancer development. We previously reported that leukemia cells secrete growth differentiation factor 15 (GDF15)，which remodels the residual bone marrow (BM) adipocytes into small adipocytes and is associated with a poor prognosis in acute myeloid leukemia (AML) patients. However, little is known about how GDF15 drives BM adipocyte remodeling. In this study, we examined the role of the transient receptor potential vanilloid (TRPV) channels in the remodeling of BM adipocytes exposed to GDF15. We found that TRPV4 ne

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30

Wang, Feng-Sheng, Yu-Shan Chen, Jih-Yang Ko, et al. "Bromodomain Protein BRD4 Accelerates Glucocorticoid Dysregulation of Bone Mass and Marrow Adiposis by Modulating H3K9 and Foxp1." Cells 9, no. 6 (2020): 1500. http://dx.doi.org/10.3390/cells9061500.

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Glucocorticoid provokes bone mass loss and fatty marrow, accelerating osteoporosis development. Bromodomain protein BRD4, an acetyl–histone-binding chromatin reader, regulates stem cell and tissue homeostasis. We uncovered that glucocorticoid inhibited acetyl Lys-9 at the histone 3 (H3K9ac)-binding Runx2 promoter and decreased osteogenic differentiation, whereas bromodomain protein 4 (BRD4) and adipocyte formation were upregulated in bone-marrow mesenchymal progenitor cells. BRD4 knockdown improved H3K9ac occupation at the Runx2 promoter and osteogenesis, but attenuated glucocorticoid-mediated

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31

Kennedy, Domenick Edward, and Katherine L. Knight. "Bone marrow fat induces inflammation that inhibits B lymphopoiesis." Journal of Immunology 196, no. 1_Supplement (2016): 122.11. http://dx.doi.org/10.4049/jimmunol.196.supp.122.11.

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Abstract Adipocytes accumulate in the bone marrow (BM) during aging and obesity, correlating with decreased B lymphopoiesis. We previously found that adipocyte factors induce MDSCs, which in turn inhibit B lymphopoiesis via IL-1 production. In this study, we asked what adipocyte factor(s) promotes MDSC accumulation. By cytokine array, we found that adipocyte conditioned medium (ACM) contains inflammatory cytokines known to induce MDSCs (ex. IL-6, G-CSF, C3a). These and other adipocyte factors can activate the NLRP3 inflammasome, leading us to test if blocking NLRP3 activation would prevent MDS

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32

Tabe, Yoko, Linhua Jin, Saiko Kazuno, et al. "A Plant Triterpenoid Avicin D Stimulates Adipocytic Differentiation of Bone Marrow Stromal Cells and Promotes Their Pro-Survival Effects On Acute Monoblastic Leukemia Cells." Blood 120, no. 21 (2012): 4315. http://dx.doi.org/10.1182/blood.v120.21.4315.4315.

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Abstract Abstract 4315 A natural triterpene Avicin D induces apoptosis in various tumor cells and regulates cellular metabolism via Glucocorticoid receptor (GR) signalling, known to be involved in adipocyte differentiation (Tang, Annu Rev Biochem. 2012;81:715). Since adipocytes represent an essential component of the aging bone marrow (BM) microenvironment (Tabe, Blood 2004;103:1815), and promote monocytic differentiation and survival of monoblastic leukemia cells (Tabe, ASH, 2011), we examined the potential of Avicin D to modulate BM adipocytes and its effects on the survival of the leukemic

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33

Yang, Jing, Zhiqiang Liu, Huan Liu, et al. "Myeloma Cells Switch Osteoblastogenesis to Adipogenesis and Suppress Bone Formation." Blood 124, no. 21 (2014): 3386. http://dx.doi.org/10.1182/blood.v124.21.3386.3386.

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Abstract Bone destruction is a hallmark of myeloma, and has a severe impact on patients’ quality of life and survival. Unfortunately, current treatment only offers moderate palliative effects, and this disease remains incurable. The bone changes in myeloma patients results from increased osteoclast-mediated bone resorption and decreased osteoblast-mediated bone formation. In particular, new bone formation that usually occurs at sites of previously resorbed bones is deeply suppressed; as a result, areas of bone destruction rarely heal. Previous studies have shown that myeloma cells inhibit oste

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34

Vashum, Yaongamphi, and Zenith Khashim. "Obesity and Cathepsin K: A Complex Pathophysiological Relationship in Breast Cancer Metastases." Endocrine, Metabolic & Immune Disorders - Drug Targets 20, no. 8 (2020): 1227–31. http://dx.doi.org/10.2174/1871530320666200505115132.

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Background: Breast cancer appears in a strong inclination to metastasize in bone tissue. Several strategies are discussed in combating bone metastasis in breast cancer. However, therapy is only palliative and does not provide any improvement in survival to the majority of patients with advanced cancer. Obese and overweight women with breast cancer are three times more likely to develop metastatic disease compared to normal-weight women with the same treatment regimen. Overweight greatly intensify adipocytes formation in the bone marrow affecting bone metabolism by decreasing osteoblast differe

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35

Li, Jingyuan, Xiaoyu Lai, and Huang He. "Study on Telomerase Activity of Human Bone Marrow Mesenchymal Stem Cells." Blood 104, no. 11 (2004): 4255. http://dx.doi.org/10.1182/blood.v104.11.4255.4255.

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Abstract Human mesenchymal stem cells(hMSCs) have multiple differentiate potential, and it can differentiate into adipocytes, osteogenic cells, chondrocyte and neural cells et al. It has been reported that telomerase activity in hMSCs is negative, but it is still controversial and telomerase activity in hMSCs-derived adipocytes has not been reported. We investigate the telomerase activity in hMSCs before and after their committed differentiation into adipocytes in vitro and cryopreservation. hMSCs were isolated from normal human bone marrow fellowed by cell culture in DMEM with low glucose con

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36

Frączak, Ewa, Mateusz Olbromski, Aleksandra Piotrowska, et al. "Bone marrow adipocytes in haematological malignancies." Acta Histochemica 120, no. 1 (2018): 22–27. http://dx.doi.org/10.1016/j.acthis.2017.10.010.

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37

Okla, Meshail, and Moustapha Kassem. "Thermogenic potentials of bone marrow adipocytes." Bone 143 (February 2021): 115658. http://dx.doi.org/10.1016/j.bone.2020.115658.

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38

Higos, Romane, Kevin Saitoski, Mathieu Hautefeuille, et al. "The Critical Role of Adipocytes in Leukemia." Biology 14, no. 6 (2025): 624. https://doi.org/10.3390/biology14060624.

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The bone marrow microenvironment is a dynamic and complex niche that plays a central role in the development, progression, and therapeutic resistance of leukemia. Among the various stromal and immune cells that compose this microenvironment, adipocytes are increasingly recognized as active participants rather than passive bystanders. These cells contribute to leukemia pathophysiology by supplying leukemic cells with vital metabolic fuels such as free fatty acids and glutamine, which support cellular bioenergetics and biosynthesis. Furthermore, adipocytes secrete adipokines—including leptin, ad

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Liu, Haiyan, Yuanmei Zhai, Wenli Zhao, et al. "Consolidation Chemotherapy Prevents Relapse by Indirectly Regulating Bone Marrow Adipogenesis in Patients with Acute Myeloid Leukemia." Cellular Physiology and Biochemistry 45, no. 6 (2018): 2389–400. http://dx.doi.org/10.1159/000488225.

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Background/Aims: Chemotherapy is still the main strategy used to prevent the relapse of acute myeloid leukaemia (AML). As the most abundant stromal component in bone marrow (BM), marrow adipocytes have been previously shown to promote leukaemogenesis. The present study was designed to further validate whether marrow adipocytes exert synergistic effects on strengthening chemotherapeutic efficacy and evaluate the underlying mechanism. Methods: A retrospective study of BM biopsies from 80 patients with AML in remission and 71 control subjects was applied to quantitatively analyse the marrow adipo

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Gimble, J. M., M. A. Dorheim, Q. Cheng, et al. "Response of bone marrow stromal cells to adipogenic antagonists." Molecular and Cellular Biology 9, no. 11 (1989): 4587–95. http://dx.doi.org/10.1128/mcb.9.11.4587-4595.1989.

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Adipocytes constitute a major part of the bone marrow stroma in vivo and may play an active role in lymphohematopoiesis. Earlier studies had shown that the bone marrow stromal cell clone BMS2 was capable of adipocyte differentiation in vitro, in addition to its well-defined ability to support B lymphopoiesis. We now demonstrate that the process of adipogenesis in this functional bone marrow stromal cell clone can be inhibited by the cytokines interleukin-1 alpha, tumor necrosis factor, and transforming growth factor beta. Exposure of preadipocyte BMS2 cells to these agents blocked the inductio

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41

Gimble, J. M., M. A. Dorheim, Q. Cheng, et al. "Response of bone marrow stromal cells to adipogenic antagonists." Molecular and Cellular Biology 9, no. 11 (1989): 4587–95. http://dx.doi.org/10.1128/mcb.9.11.4587.

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Adipocytes constitute a major part of the bone marrow stroma in vivo and may play an active role in lymphohematopoiesis. Earlier studies had shown that the bone marrow stromal cell clone BMS2 was capable of adipocyte differentiation in vitro, in addition to its well-defined ability to support B lymphopoiesis. We now demonstrate that the process of adipogenesis in this functional bone marrow stromal cell clone can be inhibited by the cytokines interleukin-1 alpha, tumor necrosis factor, and transforming growth factor beta. Exposure of preadipocyte BMS2 cells to these agents blocked the inductio

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42

Caers, Jo, Zakia Belaid, Sarah Deleu, Marie Paule Defresne, and Karin Vanderkerken. "Bone Marrow Adipocytes Influence Multiple Myeloma Development by Secretion of Different Growth Factors and Chemokines." Blood 108, no. 11 (2006): 5030. http://dx.doi.org/10.1182/blood.v108.11.5030.5030.

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Abstract In multiple myeloma (MM) monoclonal plasma cells accumulate in the bone marrow (BM) where they interact with neighboring cells to receive supportive signals. Since BM adipocytes are known to participate in normal and malignant hematopoiesis, we presumed interactions between BM adipocytes and myeloma cells. Using an adipocytic cell line and primary isolated BM adipocytes, we performed functional assays indicating that adipocytes support MM cell development by affecting proliferation, apoptosis, cell migration and adhesion. We subsequently analyzed the secretion of different cytokines b

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Shu, Lingling, Jinyuan Li, Weida Wang, et al. "Adipocyte Fatty Acid Binding Protein Promotes Multiple Myeloma through Regulating Bone Marrow Microenvironment." Blood 136, Supplement 1 (2020): 31–32. http://dx.doi.org/10.1182/blood-2020-140732.

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Multiple myeloma (MM) is a plasma cell malignancy in bone marrow, which often occurs in middle-aged and elderly people and also obese patients. Aging and obesity can lead to the ectopic accumulation of adipocytes in bone marrow, which can cause the change of bone marrow microenvironment. Bone marrow adipocyte (BMA) displays distinct immune regulatory properties rather than provides energy substrates. Despite BMA accounts for 70% of the entire volume of bone marrow microenvironment, while the mechanisms still remain elusive. The present study aims to investigate the precise mechanism of BMA pro

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Wilson, Alexis, Mackenzie Herroon, Shane Mecca, Laimar Garmo, and Izabela Podgorski. "Abstract B039: Adipocyte regulation of ER stress and mTOR signaling in bone-metastatic PCa: The role of stearoyl-CoA desaturase." Cancer Research 83, no. 2_Supplement_2 (2023): B039. http://dx.doi.org/10.1158/1538-7445.metastasis22-b039.

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Abstract Bone metastatic disease is correlated with increased morbidity and mortality in prostate cancer (PCa) patients. Current treatments for bone-metastatic PCa are palliative, and new targets for therapy are desperately needed for this presently incurable disease. Various studies have determined that the supportive nature of the bone marrow (BM) niche and crosstalk between the bone-resident cells and the tumor lead to increased tumor cell survival and escape from therapy. Specifically, studies from our lab highlighted the critical role of bone marrow adipose tissue and its expansion due to

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Cohen, Adi, David W. Dempster, Emily M. Stein, et al. "Increased Marrow Adiposity in Premenopausal Women with Idiopathic Osteoporosis." Journal of Clinical Endocrinology & Metabolism 97, no. 8 (2012): 2782–91. http://dx.doi.org/10.1210/jc.2012-1477.

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Abstract Context: We have previously reported that premenopausal women with idiopathic osteoporosis based on fractures (IOP) or idiopathic low bone mineral density (ILBMD) exhibit markedly reduced bone mass, profoundly abnormal trabecular microstructure, and significant deficits in trabecular bone stiffness. Bone remodeling was heterogeneous. Those with low bone turnover had evidence of osteoblast dysfunction and the most marked deficits in microstructure and stiffness. Objective: Because osteoblasts and marrow adipocytes derive from a common mesenchymal precursor and excess marrow fat has bee

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Kokabu, Shoichiro, Jonathan W. Lowery, and Eijiro Jimi. "Cell Fate and Differentiation of Bone Marrow Mesenchymal Stem Cells." Stem Cells International 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/3753581.

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Osteoblasts and bone marrow adipocytes originate from bone marrow mesenchymal stem cells (BMMSCs) and there appears to be a reciprocal relationship between adipogenesis and osteoblastogenesis. Alterations in the balance between adipogenesis and osteoblastogenesis in BMMSCs wherein adipogenesis is increased relative to osteoblastogenesis are associated with decreased bone quality and quantity. Several proteins have been reported to regulate this reciprocal relationship but the exact nature of the signals regulating the balance between osteoblast and adipocyte formation within the bone marrow sp

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Li, Guan-Wu, Zheng Xu, Shi-Xin Chang, et al. "Influence of Early Zoledronic Acid Administration on Bone Marrow Fat in Ovariectomized Rats." Endocrinology 155, no. 12 (2014): 4731–38. http://dx.doi.org/10.1210/en.2014-1359.

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Although the primary target cell of bisphosphonates is the osteoclast, increasing attention is being given to other effector cells influenced by bisphosphonates, such as osteoblasts and marrow adipocytes. Early zoledronic acid (ZA) treatment to ovariectomized (OVX) rats has been found to fully preserve bone microarchitecture over time. However, little is known regarding the influence of ZA on marrow adipogenesis. The purpose of this study was to monitor the ability of early administration of ZA in restoring marrow adiposity in an estrogen-deficient rat model. Thirty female Sprague-Dawley rats

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Miyajima, Yurina, Kafi N. Ealey, Yasutaka Motomura, et al. "Effects of BMP7 produced by group 2 innate lymphoid cells on adipogenesis." International Immunology 32, no. 6 (2020): 407–19. http://dx.doi.org/10.1093/intimm/dxaa013.

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Abstract Group 2 innate lymphoid cells (ILC2s) are type 2 cytokine-producing cells that have important roles in helminth infection and allergic inflammation. ILC2s are tissue-resident cells, and their phenotypes and roles are regulated by tissue-specific environmental factors. While the role of ILC2s in the lung, intestine and bone marrow has been elucidated in many studies, their role in adipose tissues is still unclear. Here, we report on the role of ILC2-derived bone morphogenetic protein 7 (BMP7) in adipocyte differentiation and lipid accumulation. Co-culture of fat-derived ILC2s with plur

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Švajger, Urban, Patrik Milić, and Primož J. Rožman. "Bone Marrow Niche Aging: Are Adipocytes Detrimental Cells in the Bone Marrow?" Cells 14, no. 11 (2025): 814. https://doi.org/10.3390/cells14110814.

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Aging disrupts the bone marrow (BM) niche, a complex microenvironment crucial for hematopoietic stem cell (HSC) maintenance. A key, yet debated, hallmark of this aging process is the accumulation of bone marrow adipocytes (BMAds). This review explores the evolving role of BMAds in the aging BM, particularly their influence on HSC regulation via metabolic, endocrine, and inflammatory pathways. Aging BMAds exhibit altered secretory profiles, including reduced leptin and adiponectin and increased pro-inflammatory signals, which skew hematopoiesis toward myeloid over lymphoid lineage production. A

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James, Sophie C., Samantha Atkinson, Richard Burt, Cristina Lo Celso, and Paolo Gallipoli. "Specific Bone Marrow Niche Components Determine Degree of Protection from Gilteritinib Induced Differentiation Response in FLT3-ITD AML." Blood 144, Supplement 1 (2024): 4152. https://doi.org/10.1182/blood-2024-205582.

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Background:the FLT3 tyrosine kinase inhibitor (TKI) gilteritinib relieves the differentiation blockade in around 50% of acute myeloid leukaemia (AML) patients carrying FLT3 internal tandem duplication (ITD) mutations. However, differentiation responses are often incomplete and are poorly understood. This limited understanding is partly due to the strong cytotoxic effects seen with gilteritinib in cellular in vitro models and suggests that the in vivo bone marrow microenvironment (BMM) plays roles in modulating the differentiation response. Recent evidence suggests that the BMM induces changes

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