Bone marrow mesenchymal stem cells, platelet-rich plasma and nanohydroxyapatite-type I collagen beads were integral parts of biomimetic bone substitutes for bone regeneration

2012 ◽  
Vol 7 (11) ◽  
pp. 841-854 ◽  
Author(s):  
Bo-Nian Lin ◽  
Shu Wen Whu ◽  
Chih-Hwa Chen ◽  
Fu-Yin Hsu ◽  
Jyh-Cheng Chen ◽  
...  
2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Hongliang He ◽  
Xiaozhen Liu ◽  
Liang Peng ◽  
Zhiliang Gao ◽  
Yun Ye ◽  
...  

Interactions between stem cells and extracellular matrix (ECM) are requisite for inducing lineage-specific differentiation and maintaining biological functions of mesenchymal stem cells by providing a composite set of chemical and structural signals. Here we investigated if cell-deposited ECM mimickedin vivoliver's stem cell microenvironment and facilitated hepatogenic maturation. Decellularization process preserved the fibrillar microstructure and a mix of matrix proteins in cell-deposited ECM, such as type I collagen, type III collagen, fibronectin, and laminin that were identical to those found in native liver. Compared with the cells on tissue culture polystyrene (TCPS), bone marrow mesenchymal stem cells (BM-MSCs) cultured on cell-deposited ECM showed a spindle-like shape, a robust proliferative capacity, and a suppressed level of intracellular reactive oxygen species, accompanied with upregulation of two superoxide dismutases. Hepatocyte-like cells differentiated from BM-MSCs on ECM were determined with a more intensive staining of glycogen storage, an elevated level of urea biosynthesis, and higher expressions of hepatocyte-specific genes in contrast to those on TCPS. These results demonstrate that cell-deposited ECM can be an effective method to facilitate hepatic maturation of BM-MSCs and promote stem-cell-based liver regenerative medicine.


Coatings ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 840
Author(s):  
Francesca Salamanna ◽  
Nicolandrea Del Piccolo ◽  
Maria Sartori ◽  
Gianluca Giavaresi ◽  
Lucia Martini ◽  
...  

Bone regeneration remains one of the major clinical needs in orthopedics, and advanced and alternative strategies involving bone substitutes, cells, and growth factors (GFs) are mandatory. The purpose of this study was to evaluate whether the association of autologous bone marrow mesenchymal stem cells (BMSC), isolated by ‘one-step surgical procedure’, and activated platelet rich plasma (PRP) improves osseointegration and bone formation of a hydroxyapatite-coated titanium (Ti-HA) implant, already in clinical use, in a rabbit cancellous defect. The GFs present in plasma, in inactivated and activated PRP were also tested. At 2 weeks, histology and histomorphometry highlighted increased bone-to-implant contact (BIC) in Ti-HA combined with BMSC and PRP in comparison to Ti-HA alone and Ti-HA + PRP. The combined effect of BMSC and PRP peaked at 4 weeks where the BIC value was higher than all other treatments. At both experimental times, newly formed bone (Trabecular Bone Volume, BV/TV) in all tested treatments showed increased values in comparison to Ti-HA alone. At 4 weeks Ti-HA + PRP + BMSC showed the highest BV/TV and the highest osteoblasts number; additionally, a higher osteoid surface and bone formation rate were found in Ti-HA + BMSC + PRP than in all other treatments. Finally, the analyses of GFs revealed higher values in the activated PRP in comparison to plasma and to non-activated PRP. The study suggests that the combination of autologous activated PRP, as a carrier for BMSCs, is a promising regenerative strategy for bone formation, osseointegration, and mineralization of bone implants.


2020 ◽  
Vol 10 (2) ◽  
pp. 246-251
Author(s):  
Wenxiao Jiang ◽  
Yijun Zhang ◽  
Ye Huang ◽  
Yunfeng Cheng ◽  
Zhigang Liu

Hepatic kinase B1 (LKB1) is a tumor suppressor and regulates cell proliferation and apoptosis. However, whether LKB1 affects bone marrow mesenchymal stem cells (BMSCs) osteogenic differentiation of during aging remains unclear. Two BMSCs derived from Zempster24−/− (aging) and Zempster24+/+ (normal) mice were cultured in vitro followed by measurement of LKB1 expression by real-time quantitative PCR and Western blot. LKB1 siRNA was transfected into Zempster24−/−BMSCs and LKB1 expression was measured. 14 days after osteogenic induction, mineralized nodule formation was evaluated by alizarin red staining, expression of Calcin, type I collagen, RUNX2 and OPN mRNA expression was measured, together with alkaline phosphatase (ALP) activity and the PI3K/mTOR pathway activity. Compared with normal BMSCs, LKB1 expression was significantly increased, calcified nodules were decreased, with reduced expression of osteocalcin, type I collagen, RUNX2 and OPN mRNA as well as decreased ALP activity and PI3K/mTOR signaling protein expression (P < 0.05). LKB1 siRNA transfection into senescent BMSCs down-regulated LKB1 expression, increased calcification nodule formation, expression of osteocalcin, type I collagen, RUNX2 and OPN mRNA, as well as increased ALP activity and PI3K/mTOR pathway protein expression (P < 0.05). Aging can promote the increase of LKB1 expression and inhibit the osteogenic differentiation of BMSCs. Down-regulation of LKB1 expression in BMSCs during senescence can promote osteogenic differentiation through regulating PI3K/mTOR pathway.


2019 ◽  
Vol 9 (12) ◽  
pp. 1776-1782
Author(s):  
Yongyi Xu ◽  
Lei Chen

The distal low homeobox 3 (DLX3) regulates the bone marrow mesenchymal stem cells (BMSC) osteogenic differentiation. However, whether DLX3 affects osteoporosis (OP) remains unclear. An OVX-induced OP rat model was constructed and DLX3 plasmid was injected followed by analysis of bone mineral density and ALP activity. Rat BMSCs were isolated and divided into control group, OP group and DLX3 group (transfected with DLX3 plasmid) followed by analysis of chondrocytes survival rate by MTT assay, Caspase 3 activity, type I collagen and Osterix expression by Real time PCR and -catenin level by Western blot. DLX3 expression was significantly down-regulated in OP rats with deceased bone density and ALP activity compared to sham group (P < 0 05). When DLX3 was transfected into OP rats, DLX3 expression was significantly up-regulated with increased bone density and ALP activity compared with OP group (P < 0 05). BMSCs survival was significantly decreased in OP group and Caspase 3 activity was significantly increased with downregulated type I collagen, Osterix and -catenin (P < 0 05). However, transfection of DLX3 plasmid into OP group BMSCs cells can significantly reverse the above changes, compared to OP group (P < 0 05). DLX3 expression is reduced in osteoporosis. Up-regulation of DLX3 can promote osteogenic differentiation of BMSCs by regulating typical Wnt signaling, promote differentiation into osteoblasts, increase bone density increase, and then ameliorate osteoporosis.


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