scholarly journals Diabetic Impairment of C-Kit+ Bone Marrow Stem Cells Involves the Disorders of Inflammatory Factors, Cell Adhesion and Extracellular Matrix Molecules

PLoS ONE ◽  
2011 ◽  
Vol 6 (10) ◽  
pp. e25543 ◽  
Author(s):  
Tao-Sheng Li ◽  
Satoshi Ikeda ◽  
Masayuki Kubo ◽  
Mako Ohshima ◽  
Hiroshi Kurazumi ◽  
...  
Author(s):  
Samuele Laudani ◽  
Valentina La Cognata ◽  
Rosario Iemmolo ◽  
Gabriele Bonaventura ◽  
Giusy Villaggio ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (58) ◽  
pp. 98336-98347 ◽  
Author(s):  
Xiaoyan Wang ◽  
Guanghua Chen ◽  
Chao Huang ◽  
Hualei Tu ◽  
Jilong Zou ◽  
...  

2007 ◽  
Vol 361-363 ◽  
pp. 1075-1078
Author(s):  
Michiyo Honda ◽  
Shigeki Izumi ◽  
Nobuyuki Kanzawa ◽  
Takahide Tsuchiya ◽  
Mamoru Aizawa

Appropriate culture conditions cause bone marrow stem cells to differentiate into multilineage cells such as adipocytes, chondrocytes, and osteoblasts. One key factor that regulates intercellular signaling and cell differentiation is the extracellular matrix microenvironment. The composition of the extracellular matrix influences cellular functions. In the present study, we investigated the effects of a microenvironment comprising a three-dimensional apatite-fiber scaffold (AFS) that has two kinds of pores (micro- and macro pores) on proliferation and subsequent differentiation of bone marrow stem cells. Morphologic observation revealed that osteoblastic cells in the AFS were distributed primarily in the same location on the fibrous scaffold and formed bridges within micro- and macro pores. We used molecular approaches to evaluate cell proliferation and differentiation in detail. Reverse transcription-polymerase chain reaction (RT-PCR) analysis showed that culturing bone marrow cells on AFS increases expression of osteocalcin (OC) mRNA compared with culture in a dish. Furthermore, cells cultured in AFS expressed type X collagen (Col X), which is a marker of hypertrophic cartilage. These data suggest that the three-dimensional microenvironment of AFS facilitates cell proliferation and differentiation, and promotes endochondral ossification of bone marrow cells.


Cancers ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 62
Author(s):  
Elise Aasebø ◽  
Even Birkeland ◽  
Frode Selheim ◽  
Frode Berven ◽  
Annette K. Brenner ◽  
...  

Mesenchymal stem cells (MSCs) and osteoblasts are bone marrow stromal cells that contribute to the formation of stem cell niches and support normal hematopoiesis, leukemogenesis and development of metastases from distant cancers. This support is mediated through cell–cell contact, release of soluble mediators and formation of extracellular matrix. By using a proteomic approach, we characterized the protein release by in vitro cultured human MSCs (10 donors) and osteoblasts (nine donors). We identified 1379 molecules released by these cells, including 340 proteins belonging to the GO-term Extracellular matrix. Both cell types released a wide range of functionally heterogeneous proteins including extracellular matrix molecules (especially collagens), several enzymes and especially proteases, cytokines and soluble adhesion molecules, but also several intracellular molecules including chaperones, cytoplasmic mediators, histones and non-histone nuclear molecules. The levels of most proteins did not differ between MSCs and osteoblasts, but 82 proteins were more abundant for MSC (especially extracellular matrix proteins and proteases) and 36 proteins more abundant for osteoblasts. Finally, a large number of exosomal proteins were identified. To conclude, MSCs and osteoblasts show extracellular release of a wide range of functionally diverse proteins, including several extracellular matrix molecules known to support cancer progression (e.g., metastases from distant tumors, increased relapse risk for hematological malignancies), and the large number of identified exosomal proteins suggests that exocytosis is an important mechanism of protein release.


2021 ◽  
pp. 002203452110246
Author(s):  
P.-C. Chang ◽  
Z.-J. Lin ◽  
H.-T. Luo ◽  
C.-C. Tu ◽  
W.-C. Tai ◽  
...  

To establish an ideal microenvironment for regenerating maxillofacial defects, recent research interests have concentrated on developing scaffolds with intricate configurations and manipulating the stiffness of extracellular matrix toward osteogenesis. Herein, we propose to infuse a degradable RGD-functionalized alginate matrix (RAM) with osteoid-like stiffness, as an artificial extracellular matrix, to a rigid 3D-printed hydroxyapatite scaffold for maxillofacial regeneration. The 3D-printed hydroxyapatite scaffold was produced by microextrusion technology and showed good dimensional stability with consistent microporous detail. RAM was crosslinked by calcium sulfate to manipulate the stiffness, and its degradation was accelerated by partial oxidation using sodium periodate. The results revealed that viability of bone marrow stem cells was significantly improved on the RAM and was promoted on the oxidized RAM. In addition, the migration and osteogenic differentiation of bone marrow stem cells were promoted on the RAM with osteoid-like stiffness, specifically on the oxidized RAM. The in vivo evidence revealed that nonoxidized RAM with osteoid-like stiffness upregulated osteogenic genes but prevented ingrowth of newly formed bone, leading to limited regeneration. Oxidized RAM with osteoid-like stiffness facilitated collagen synthesis, angiogenesis, and osteogenesis and induced robust bone formation, thereby significantly promoting maxillofacial regeneration. Overall, this study supported that in the stabilized microenvironment, oxidized RAM with osteoid-like stiffness offered requisite mechanical cues for osteogenesis and an appropriate degradation profile to facilitate bone formation. Combining the 3D-printed hydroxyapatite scaffold and oxidized RAM with osteoid-like stiffness may be an advantageous approach for maxillofacial regeneration.


2017 ◽  
Vol 10 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Ervina Julien Sitanggang ◽  
Radiana Dhewayani Antarianto ◽  
Sri Widia A. Jusman ◽  
Jeanne Adiwinata Pawitan ◽  
Ahmad Aulia Jusuf

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