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Chicken model of steroid-induced bone marrow adipogenesis using proteome analysis: a preliminary study.

ABSTRACT: BACKGROUND:Steroid-induced adipogenesis increases fat-cell volume and pressure in bone marrow. This may be a contributing factor in some forms of osteonecrosis. In this observational study, we aimed to determine the protein expression relating to steroid-induced adipogenesis of femoral bone marrow with use of a chicken model. We compared the histologic features of the femoral marrow of eight methylprednisolone (MP)-treated chickens with those of three control chickens and assessed differential proteins with 2-dimensional gel electrophoresis and differential proteins were identified by MALDI-TOF MS. RESULTS:One MP-induced chicken died of overdose anesthesia. Methylprednisolone-induced proliferation of adipose tissue and new bone formation were found on histologic examination. In our study, 13 proteins in the control and MP-induced groups were differently expressed and nine protein spots showed marked threefold downregulation after 19 weeks of MP treatment. These were serum amyloid P-component precursor, zinc finger protein 28, endothelial zinc finger protein 71, T-box transcription factor 3, cyclin-dependent kinase inhibitor 1, myosin 1D, dimethylaniline monooxygenase, and two uncharacterized proteins. CONCLUSIONS:Proteomic profiling can be a useful dynamic approach for detecting protein expression in MP-induced adipogenesis of the femur in chickens.

SUBMITTER: Li SC

PROVIDER: S-EPMC2949814 | biostudies-literature | 2010 Sep

REPOSITORIES: biostudies-literature

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Chicken model of steroid-induced bone marrow adipogenesis using proteome analysis: a preliminary study.

Li Sing Chung SC Lin Ching Yu CY Kuo Tzong Fu TF Lin Yun Ho YH Chen Chia Chun CC Lin Way Neng WN Chan Wing P WP

Proteome science 20100914

<h4>Background</h4>Steroid-induced adipogenesis increases fat-cell volume and pressure in bone marrow. This may be a contributing factor in some forms of osteonecrosis. In this observational study, we aimed to determine the protein expression relating to steroid-induced adipogenesis of femoral bone marrow with use of a chicken model. We compared the histologic features of the femoral marrow of eight methylprednisolone (MP)-treated chickens with those of three control chickens and assessed differ ...[more]

PMID: 20840762

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Project description:Cell-extracellular matrix (ECM) interactions play major roles in controlling progenitor cell fate and differentiation. The receptor tyrosine kinase, discoidin domain receptor 2 (DDR2), is an important mediator of interactions between cells and fibrillar collagens. DDR2 signals through both ERK1/2 and p38 MAP kinase, which stimulate osteoblast differentiation and bone formation. Here we show that DDR2 is critical for skeletal development and differentiation of marrow progenitor cells to osteoblasts while suppressing marrow adipogenesis. Smallie mice (Ddr2slie/slie ), which contain a nonfunctional Ddr2 allele, have multiple skeletal defects. A progressive decrease in tibial trabecular bone volume/total volume (BV/TV) was observed when wild-type (WT), Ddr2wt/slie , and Ddr2slie/slie mice were compared. These changes were associated with reduced trabecular number (Tb.N) and trabecular thickness (Tb.Th) and increased trabecular spacing (Tb.Sp) in both males and females, but reduced cortical thickness only in Ddr2slie/slie females. Bone changes were attributed to decreased bone formation rather than increased osteoclast activity. Significantly, marrow fat and adipocyte-specific mRNA expression were significantly elevated in Ddr2slie/slie animals. Additional skeletal defects include widened calvarial sutures and reduced vertebral trabecular bone. To examine the role of DDR2 signaling in cell differentiation, bone marrow stromal cells (BMSCs) were grown under osteogenic and adipogenic conditions. Ddr2slie/slie cells exhibited defective osteoblast differentiation and accelerated adipogenesis. Changes in differentiation were related to activity of runt-related transcription factor 2 (RUNX2) and PPARγ, transcription factors that are both controlled by MAPK-dependent phosphorylation. Specifically, the defective osteoblast differentiation in calvarial cells from Ddr2slie/slie mice was associated with reduced ERK/MAP kinase and RUNX2-S319 phosphorylation and could be rescued with a constitutively active phosphomimetic RUNX2 mutant. Also, DDR2 was shown to increase RUNX2-S319 phosphorylation and transcriptional activity while also increasing PPARγ-S112 phosphorylation, but reducing its activity. DDR2 is, therefore, important for maintenance of osteoblast activity and suppression of marrow adipogenesis in vivo and these actions are related to changes in MAPK-dependent RUNX2 and PPARγ phosphorylation. © 2016 American Society for Bone and Mineral Research.

Project description:BackgroundThere is a need for therapies that can mitigate bone marrow dysfunction and organ toxicity that occur following myeloablative injury and reduced intensity conditioning regimens used in patients undergoing bone marrow transplantation (BMT). The pathogenesis of adverse effects from BMT conditioning has been linked to injury to the vascular endothelium, bone marrow (BM), and other organs.ObjectiveTo evaluate the impact of the thrombopoietin mimetic drug JNJ-26366821 (TPOm) on BM vascular recovery in mice undergoing myeloablative radiation conditioning followed by BMT.Study designTPOm (doses: 0 µg, 300 µg, 1000 µg per Kg body weight) was administered on Days 0 and 7 after BMT, in mice receiving a total body irradiation (TBI) conditioning regimen (5.5 Gy x 2) before congenic BMT. BM donner cell engraftment was analyzed using flow cytometry on Days 7, 14, and 30 post-BMT. The morphological and biophysical properties of the BM vasculature were evaluated by intravital multiphoton microscopy (MPM) and immunofluorescence confocal imaging. Herein, morphological properties involve microvascular density (MVD), vessel diameter, and vascular area, while biophysical properties include transfer rate (Ktrans) of contrast within the BM vascular niche, as well as the fractional volume (vec ) of extracellular extravascular tissue (EES).ResultsNo significant difference in donor chimerism was observed at days 7, 14, and 30 post-BMT, between TPOm and PBS-treated mice. TPOm intervention improved BM vasculature regeneration in transplanted mice. The MVD, Ktrans, and BM vasculature as well as vascular endothelial growth factor receptor-2 (VEGFR2) in the BM, showed a dose dependent improvement in mice treated with TPOm. On day 14 post-BMT, the group receiving 1000 µg/Kg TPOm showed significant shifts (p-value < 0.05) in MVD, Ktrans, and VEGFR2 expression from their corresponding control types (TPOm dose 0 µg) towards levels comparable to healthy controls.ConclusionTPOm intervention augments BM vascular structure and function, which may be important for hematopoietic recovery and bone marrow function in radiation conditioned hematopoietic stem cell transplant patients, in addition to enhancing platelet recovery.

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Chicken model of steroid-induced bone marrow adipogenesis using proteome analysis: a preliminary study.

Publications

Chicken model of steroid-induced bone marrow adipogenesis using proteome analysis: a preliminary study.

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