scholarly journals Sustained delivery of bioactive TGF-β1 from self-assembling peptide hydrogels induces chondrogenesis of encapsulated bone marrow stromal cells

2013 ◽  
Vol 102 (5) ◽  
pp. 1275-1285 ◽  
Author(s):  
Paul W. Kopesky ◽  
Sangwon Byun ◽  
Eric J. Vanderploeg ◽  
John D. Kisiday ◽  
David D. Frisbie ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Sustained Delivery ◽  
Self Assembling ◽  
Peptide Hydrogels ◽  
Tgf Β1

scholarly journals Self-Assembling Peptide Hydrogels Modulate In Vitro Chondrogenesis of Bovine Bone Marrow Stromal Cells

2010 ◽  
Vol 16 (2) ◽  
pp. 465-477 ◽  
Author(s):  
Paul W. Kopesky ◽  
Eric J. Vanderploeg ◽  
John S. Sandy ◽  
Bodo Kurz ◽  
Alan J. Grodzinsky
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Bovine Bone ◽  
Self Assembling ◽  
Peptide Hydrogels

Associations between TGF-β1 receptors in human bone marrow stromal cells

1998 ◽  
Vol 102 (3) ◽  
pp. 804-811 ◽  
Author(s):  
Mar M. Robledo ◽  
Ma Angeles Ursa ◽  
Francisco Sánchez-Madrid ◽  
JoaquÍn TeixidÓ
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Tgf Β1

scholarly journals Exendin-4 Induces Bone Marrow Stromal Cells Migration Through Bone Marrow-Derived Macrophages Polarization via PKA-STAT3 Signaling Pathway

2017 ◽  
Vol 44 (5) ◽  
pp. 1696-1714 ◽  
Author(s):  
Ning Wang ◽  
Jian Gao ◽  
Min Jia ◽  
Xue Ma ◽  
Zhanxiang Lei ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Formation ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Macrophage Polarization ◽  
Marrow Stromal Cells ◽  
Bone Surface ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Tgf Β1

Background/Aims: The synthesis and degradation processes involved in bone remodeling are critically regulated by osteoblasts and osteoclasts. The GLP-1 receptor agonist Exendin-4 is beneficial for osteoblast differentiation and increases the number of osteoblasts. Methods: We constructed an ovariectomized model to evaluate the impact of Exendin-4 on bone formation in osteoporosis. A macrophage-depleted model was also created to investigate the effect of macrophages on bone formation. Thirty-two female WT C57BL/6 mice (aged 3 months) were randomly assigned to a normal control group and four ovariectomized (OVX) subgroups: OVX + vehicle group, OVX + Exendin-4 (4.2 µg/kg/day) group, OVX + chloride phosphate liposome group and OVX + chloride phosphate liposome + Exendin-4 group. Results: In this study, we found that Exendin-4 not only increased the number of osteoblasts and decreased the number of osteoclasts, but also increased the number of bone marrow stromal cells (BMSCs) at the bone surface. Moreover, we found that OVX mice treated with Exendin-4 increased TGF-β1 levels at the bone surface compared with that in OVX mice. Besides, Exendin-4 promoted the polarization of bone marrow-derived macrophages into M2 subtype and increased TGF-β1 secretion by the M2 subtype. Finally, we found that Exendin-4 induced macrophage polarization via the cAMP-PKA-STAT3 signaling pathway. Conclusion: Exendin-4 promotes bone marrow-derived macrophage polarization to the M2 subtype and induces BMSC migration to the bone surface via PKA-STAT3 signaling.

scholarly journals Differential response of human bone marrow stromal cells to either TGF-β1 or rhGDF-5

2010 ◽  
Vol 20 (6) ◽  
pp. 962-971 ◽  
Author(s):  
Benjamin Gantenbein-Ritter ◽  
Lorin M. Benneker ◽  
Mauro Alini ◽  
Sibylle Grad
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Differential Response ◽  
Marrow Stromal Cells ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Tgf Β1

scholarly journals Bone marrow stromal cells induce an ALDH+ stem cell-like phenotype in AML cells through TGF-β-p38-ALDH2 pathway

2020 ◽  
Author(s):  
Bin Yuan ◽  
Fouad El Dana ◽  
Stanley Ly ◽  
Yuanqing Yan ◽  
Vivian Ruvolo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Myeloid Leukemia ◽  
Chemotherapy Resistance ◽  
Marrow Stromal Cells ◽  
Mechanistic Studies ◽  
Aldh Activity ◽  
Pathway Inhibition ◽  
Tgf Β1

AbstractMesenchymal stromal cells (MSCs) in the bone marrow (BM) microenvironment have been shown to induce chemotherapy resistance in acute myeloid leukemia (AML) cells, but the mechanism is not clear. We hypothesized that stromal cells induce a stem-like phenotype in AML cells, thereby promoting tumorigenicity and chemotherapy resistance. We found that aldehyde dehydrogenase (ALDH), an enzyme that is highly expressed in hematopoietic as well as leukemic stem cells was dramatically activated in AML cells co-cultured with BM-MSCs mainly through upregulation of a specific isoform, ALDH2. Mechanistic studies revealed that stroma-derived TGF-β1 induced an ALDH+ phenotype in AML cells via the non-canonical TGF-β pathway through p38 activation. Inhibition of ALDH2 using specific inhibitors significantly inhibited BM-MSC-induced ALDH activity and sensitized AML cells to chemotherapy. Collectively, our data indicate that BM stroma induces a stem-like phenotype in AML cells through the non-canonical TGF-β pathway. Inhibition of ALDH2 sensitizes AML cells to chemotherapy.Impact StatementCurrently there is no standard therapy for AML. In this study we identified the mechanism of chemotherapy resistance in AML cells and discovered TGF-β-p38-ALDH2 signaling pathway as a therapeutic target.

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