scholarly journals The impact of bone marrow adipocytes on osteoblast and osteoclast differentiation

IUBMB Life ◽  
2014 ◽  
Vol 66 (3) ◽  
pp. 147-155 ◽  
Author(s):  
Shanmugam Muruganandan ◽  
Christopher J. Sinal
Keyword(s):  
Bone Marrow ◽  
Osteoclast Differentiation ◽  
Bone Marrow Adipocytes ◽  
The Impact

Bone marrow adipocytes support dexamethasone-induced osteoclast differentiation

2009 ◽  
Vol 382 (4) ◽  
pp. 780-784 ◽  
Author(s):  
Akira Hozumi ◽  
Makoto Osaki ◽  
Hisataka Goto ◽  
Kazutaka Sakamoto ◽  
Shigeru Inokuchi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Osteoclast Differentiation ◽  
Bone Marrow Adipocytes

scholarly journals Human bone marrow adipocytes support dexamethasone-induced osteoclast differentiation and function through RANKL expression

2011 ◽  
Vol 32 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Hisataka Goto ◽  
Makoto Osaki ◽  
Tatsuya Fukushima ◽  
Kazutaka Sakamoto ◽  
Akira Hozumi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Osteoclast Differentiation ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Rankl Expression ◽  
Bone Marrow Adipocytes ◽  
And Function

Primary human bone marrow adipocytes support TNF-α-induced osteoclast differentiation and function through RANKL expression

Cytokine ◽  
2011 ◽  
Vol 56 (3) ◽  
pp. 662-668 ◽  
Author(s):  
Hisataka Goto ◽  
Akira Hozumi ◽  
Makoto Osaki ◽  
Tatsuya Fukushima ◽  
Kazutaka Sakamoto ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Osteoclast Differentiation ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Rankl Expression ◽  
Bone Marrow Adipocytes ◽  
Tnf Α ◽  
And Function

scholarly journals At the Crossroads of the Adipocyte and Osteoclast Differentiation Programs: Future Therapeutic Perspectives

2020 ◽  
Vol 21 (7) ◽  
pp. 2277 ◽  
Author(s):  
Shanmugam Muruganandan ◽  
Andreia M. Ionescu ◽  
Christopher J. Sinal
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Transcription Factors ◽  
Bone Loss ◽  
Osteoclast Differentiation ◽  
Signaling Molecules ◽  
Osteogenic Potential ◽  
Bone Homeostasis ◽  
Hematopoietic Stem ◽  
Bone Marrow Adipocytes

The coordinated development and function of bone-forming (osteoblasts) and bone-resorbing (osteoclasts) cells is critical for the maintenance of skeletal integrity and calcium homeostasis. An enhanced adipogenic versus osteogenic potential of bone marrow mesenchymal stem cells (MSCs) has been linked to bone loss associated with diseases such as diabetes mellitus, as well as aging and postmenopause. In addition to an inherent decrease in bone formation due to reduced osteoblast numbers, recent experimental evidence indicates that an increase in bone marrow adipocytes contributes to a disproportionate increase in osteoclast formation. Therefore, a potential strategy for therapeutic intervention in chronic bone loss disorders such as osteoporosis is to interfere with the pro-osteoclastogenic influence of marrow adipocytes. However, application of this approach is limited by the extremely complex regulatory processes in the osteoclastogenic program. For example, key regulators of osteoclastogenesis such as the receptor activator of nuclear factor-kappaB ligand (RANKL) and the soluble decoy receptor osteoprotegerin (OPG) are not only secreted by both osteoblasts and adipocytes, but are also regulated through several cytokines produced by these cell types. In this context, biologically active signaling molecules secreted from bone marrow adipocytes, such as chemerin, adiponectin, leptin, visfatin and resistin, can have a profound influence on the osteoclast differentiation program of hematopoietic stem cells (HSCs), and thus, hold therapeutic potential under disease conditions. In addition to these paracrine signals, adipogenic transcription factors including CCAAT/enhancer binding protein alpha (C/EBPα), C/EBP beta (C/EBPβ) and peroxisome proliferator-associated receptor gamma (PPARγ) are also expressed by osteoclastogenic cells. However, in contrast to MSCs, activation of these adipogenic transcription factors in HSCs promotes the differentiation of osteoclast precursors into mature osteoclasts. Herein, we discuss the molecular mechanisms that link adipogenic signaling molecules and transcription factors to the osteoclast differentiation program and highlight therapeutic strategies targeting these mechanisms for promoting bone homeostasis.

scholarly journals Bone Marrow Adipocytes and Hematology: A Literature Review

2021 ◽  
Vol 11 (2) ◽  
pp. 123-130
Author(s):  
Nataliia Kriventsova ◽  
Alexander Shestopalov ◽  
Galina Tereshchenko
Keyword(s):  
Bone Marrow ◽  
Marrow Fat ◽  
Hematological Diseases ◽  
Active Involvement ◽  
Bone Marrow Fat ◽  
Cytokines And Chemokines ◽  
Bone Marrow Adipocytes ◽  
Number Of Publications ◽  
The Impact

This review focuses on the impact of bone marrow adipocytes on hematopoiesis and the development of hematological diseases. Bone marrow fat is a metabolically active organ capable of accumulating energy required for active hematopoiesis as well as of performing endocrine functions and participating in bone formation. Adipocytes can interact with the surrounding cells both directly and indirectly via cytokines and chemokines. Apart from their active involvement in the normal hematopoiesis, BMA have also been shown to play an important role in such diseases as leukemia, multiple myeloma and aplastic anemia. The role of fat cells in hematopoiesis is still unclear and not well studied, yet it is undoubtedly important, as demonstrated by the ever increasing number of publications supporting this conclusion.

The Impact of Proinflammatory Cytokynes of Rheumatoid Polyarthritis on the Generalized Loss of Bone Mass

2018 ◽  
Vol 69 (9) ◽  
pp. 2541-2545
Author(s):  
Raluca Barzoi ◽  
Elena Rezus ◽  
Codruta Badescu ◽  
Razan Al Namat ◽  
Manuela Ciocoiu
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune Cells ◽  
Osteoclast Differentiation ◽  
Bone Destruction ◽  
Nuclear Factor ◽  
Receptor Activator ◽  
Level Function ◽  
Rheumatoid Polyarthritis ◽  
The Impact ◽  
Nuclear Factor Kb

There is a bidirectional interaction between most immune cells and osteoblasts, osteoclasts and their precursor cells. The receptor activator of nuclear factor-kB ligand (RANKL)/RANK/osteoprotegerin (OPG) system plays an essential role in the formation of osteoblasts, but it also has implications in osteoclast biology and implicitly on the diseases characterized by bone loss. Proinflammatory cytokines existing at synovial level function as direct or indirect stimulators of osteoclast differentiation, but also of its survival or activity, although some cytokines may also play an antiosteocastogenic role. The fate of bone destruction is determined by the balance between osteoclastogenic and antiosteoclastogenic mediators. Our study has shown that the early initiation of the therapy with anti-TNF and anti-IL6 biological agents, in patients with rheumatoid arthritis, inhibits bone destruction, regardless of the anti-inflammatory activity in patients with rheumatoid arthritis.

scholarly journals Titanium Dioxide Presents a Different Profile in Dextran Sodium Sulphate-Induced Experimental Colitis in Mice Lacking the IBD Risk Gene Ptpn2 in Myeloid Cells

2021 ◽  
Vol 22 (2) ◽  
pp. 772
Author(s):  
Javier Conde ◽  
Marlene Schwarzfischer ◽  
Egle Katkeviciute ◽  
Janine Häfliger ◽  
Anna Niechcial ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Titanium Dioxide ◽  
Genetic Risk ◽  
Intestinal Inflammation ◽  
Sodium Sulphate ◽  
Food Additive ◽  
Wild Type ◽  
Dextran Sodium Sulphate ◽  
Risk Gene ◽  
The Impact

Environmental and genetic factors have been demonstrated to contribute to the development of inflammatory bowel disease (IBD). Recent studies suggested that the food additive; titanium dioxide (TiO2) might play a causative role in the disease. Therefore, in the present study we aimed to explore the interaction between the food additive TiO2 and the well-characterized IBD risk gene protein tyrosine phosphatase non-receptor type 2 (Ptpn2) and their role in the development of intestinal inflammation. Dextran sodium sulphate (DSS)-induced acute colitis was performed in mice lacking the expression of Ptpn2 in myeloid cells (Ptpn2LysMCre) or their wild type littermates (Ptpn2fl/fl) and exposed to the microparticle TiO2. The impact of Ptpn2 on TiO2 signalling pathways and TiO2-induced IL-1β and IL-10 levels were studied using bone marrow-derived macrophages (BMDMs). Ptpn2LysMCre exposed to TiO2 exhibited more severe intestinal inflammation than their wild type counterparts. This effect was likely due to the impact of TiO2 on the differentiation of intestinal macrophages, suppressing the number of anti-inflammatory macrophages in Ptpn2 deficient mice. Moreover, we also found that TiO2 was able to induce the secretion of IL-1β via mitogen-activated proteins kinases (MAPKs) and to repress the expression of IL-10 in bone marrow-derived macrophages via MAPK-independent pathways. This is the first evidence of the cooperation between the genetic risk factor Ptpn2 and the environmental factor TiO2 in the regulation of intestinal inflammation. The results presented here suggest that the ingestion of certain industrial compounds should be taken into account, especially in individuals with increased genetic risk

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