Bone Marrow Fat and Hematopoiesis

Wang, Hong; Leng, Yamei; Gong, Yuping

doi:10.3389/fendo.2018.00694

Cited by 86 publications

(61 citation statements)

References 107 publications

(130 reference statements)

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“…37 Adiponectin has been shown to enhance the proliferation of hematopoietic stem cells and maintain their undifferentiated state. 36 The results of our study showed that the leptin-to-adiponectin ratio was significantly related to the RDW values. This relationship was relevant after adjusting for age and sex.…”

Section: Methods Subjectsmentioning

confidence: 51%

“…16,20 In this context, it is very interesting that adipocytes account for about 50% of bone marrow cells and occupy 70% of adult bone marrow volume. 15,36 Leptin is a 16-kDa peptide hormone, produced predominantly by mature adipocytes, which is involved in regulating body energy balance and body fat. 16 In adults, serum leptin levels are correlated with the percentage of body fat.…”

Section: Adipokine Imbalance and Anisocytosismentioning

confidence: 99%

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Relationship among the leptin-to-adiponectin ratio, systemic inflammation, and anisocytosis in well-controlled type 2 diabetic patients with atherosclerotic cardiovascular disease

Rostoff¹,

Siniarski²,

Haberka³

et al. 2020

Kardiol Pol

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BACKGROUND Previous studies have shown that red blood cell distribution width (RDW) is an independent predictor of poor prognosis in type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD). The mechanisms underlying increased anisocytosis in patients with T2D and confirmed ASCVD remain poorly understood. AIMS We sought to evaluate the relationship among the leptin-to-adiponectin ratio, systemic low-grade inflammation, and RDW in optimally treated patients with T2D and established ASCVD. METHODS A total of 68 patients, aged 47 to 85 years (mean [SD], 65.3 [6.8] years) and including 21 women (30.9%), were enrolled and grouped according to median RDW into those with RDW <13.5% (n = 33) and those with RDW ≥13.5% (n = 35). RESULTS Patients with RDW ≥13.5% had a significantly higher median (interquartile range [IQR]) serum leptin-to-adiponectin ratio (1.7 [0.49-2.3] ng/µg vs 0.66 [0.31-1.25] ng/µg; P = 0.04) and median (IQR) tumor necrosis factor α levels (1.58 [1.42-1.97] pg/ml vs 1.39 [1.18-1.57] pg/ml; P = 0.02). There were no significant differences in the concentrations of other inflammatory markers. The leptin-to-adiponectin ratio (r = 0.25; P = 0.04) and levels of tumor necrosis factor α (r = 0.32; P = 0.01) and soluble intercellular adhesion molecule 1 (r = 0.31; P = 0.01) were positively correlated with RDW, which was confirmed by univariate linear regression analysis. A multivariable regression model, which included demographic, clinical, and laboratory data, showed that white blood cell count (β = 0.25; 95% CI, 0.05-0.45; P = 0.01), soluble intercellular adhesion molecule 1 levels (β = 0.21; 95% CI, 0.02-0.41; P = 0.03), and mean corpuscular hemoglobin concentration (MCHC), (β =-0.48; 95% CI, 0.67 to-0.28; P <0.001) were independent predictors of RDW in our patients. CONCLUSIONS In well-controlled patients with T2D and ASCVD, the RDW values are associated with leptin-to-adiponectin imbalance and selected inflammatory markers.

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Section: Methods Subjectsmentioning

confidence: 51%

Section: Adipokine Imbalance and Anisocytosismentioning

confidence: 99%

Relationship among the leptin-to-adiponectin ratio, systemic inflammation, and anisocytosis in well-controlled type 2 diabetic patients with atherosclerotic cardiovascular disease

Rostoff¹,

Siniarski²,

Haberka³

et al. 2020

Kardiol Pol

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“…Chondrocytes originate from mesenchymal stem cells [ 71 , 72 ]. Bone-marrow-derived MSCs (BM-MSCs) have much promise in aiding articular cartilage repair due to their proximity to the joint, high differentiation capability, and ability to secrete different growth, anti-inflammatory, and immunomodulatory factors [ 73 , 74 , 75 , 76 , 77 ]. They could affect a clinically relevant improvement in joint pain and function.…”

Section: Mesenchymal Stem Cells and Tissue Regenerationmentioning

confidence: 99%

Emerging Gene-Editing Modalities for Osteoarthritis

Tanikella

Hardy

Frahs

et al. 2020

IJMS

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Osteoarthritis (OA) is a pathological degenerative condition of the joints that is widely prevalent worldwide, resulting in significant pain, disability, and impaired quality of life. The diverse etiology and pathogenesis of OA can explain the paucity of viable preventive and disease-modifying strategies to counter it. Advances in genome-editing techniques may improve disease-modifying solutions by addressing inherited predisposing risk factors and the activity of inflammatory modulators. Recent progress on technologies such as CRISPR/Cas9 and cell-based genome-editing therapies targeting the genetic and epigenetic alternations in OA offer promising avenues for early diagnosis and the development of personalized therapies. The purpose of this literature review was to concisely summarize the genome-editing options against chronic degenerative joint conditions such as OA with a focus on the more recently emerging modalities, especially CRISPR/Cas9. Future advancements in novel genome-editing therapies may improve the efficacy of such targeted treatments.

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“…They directly induce MM cell expansion through the huge amount of cytokines that they produce [6] and via the secreted exosomes [11]. They can dialogue directly with MM cells through close contact [7,12] and membrane exchange, inducing chemoresistance acquisition [13]. They also play a role in the recruitment of other microenvironment cells involved in tumor cell growth, chemoresistance acquisition, and depletion of the immune responses [14][15][16] Our own studies and that of other authors have shown that MSC from patients with newly diagnosed MM are abnormal [11,17], as they acquire pro-tumor potentialities.…”

Section: Introductionmentioning

confidence: 99%

Imprinting of Mesenchymal Stromal Cell Transcriptome Persists even after Treatment in Patients with Multiple Myeloma

Lemaître

Ferreira

Joubert

et al. 2020

IJMS

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Introduction. Multiple myeloma (MM) is a B-cell neoplasm characterized by clonal expansion of malignant plasma cells (MM cells) in the bone-marrow (BM) compartment. BM mesenchymal stromal cells (MSC) from newly diagnosed MM patients were shown to be involved in MM pathogenesis and chemoresistance. The patients displayed a distinct transcriptome and were functionally different from healthy donors’ (HD) MSC. Our aim was to determine whether MM–MSC also contributed to relapse. Methods. We obtained and characterized patients’ MSC samples at diagnosis, two years after intensive treatment, without relapse and at relapse. Results. Transcriptomic analysis revealed differences in gene expression between HD and MM-MSC, whatever the stage of the disease. An easier differentiation towards adipogenesis at the expense of osteoblatogeneis was observed, even in patients displaying a complete response to treatment. Although their transcriptome was similar, we found that MSC from relapsed patients had an increased immunosuppressive ability, compared to those from patients in remission. Conclusion. We demonstrated that imprinting of MSC transcriptome demonstrated at diagnosis of MM, persisted even after the apparent disappearance of MM cells induced by treatment, suggesting the maintenance of a local context favorable to relapse.

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Bone Marrow Fat and Hematopoiesis

Cited by 86 publications

References 107 publications

Relationship among the leptin-to-adiponectin ratio, systemic inflammation, and anisocytosis in well-controlled type 2 diabetic patients with atherosclerotic cardiovascular disease

Relationship among the leptin-to-adiponectin ratio, systemic inflammation, and anisocytosis in well-controlled type 2 diabetic patients with atherosclerotic cardiovascular disease

Emerging Gene-Editing Modalities for Osteoarthritis

Imprinting of Mesenchymal Stromal Cell Transcriptome Persists even after Treatment in Patients with Multiple Myeloma

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