scholarly journals Dimethyloxalylglycine Promotes Bone Marrow Mesenchymal Stem Cell Osteogenesis via Rho/ROCK Signaling

2016 ◽  
Vol 39 (4) ◽  
pp. 1391-1403 ◽  
Author(s):  
Lei Zhang ◽  
Guoliang Jiang ◽  
Xueling Zhao ◽  
Yuekun Gong
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Coiled Coil ◽  
Calcium Deposition ◽  
Mrna Levels ◽  
Osteogenic Induction ◽  
Calcium Deposits ◽  
Rock Activity

Background/Aims: We investigated the role of dimethyloxalylglycine (DMOG) in bone marrow mesenchymal stem cell (BMSC) osteogenesis mediated by RhoA/ROCK. Methods: BMSCs were cultured with and without DMOG and/or Y-27632 (ROCK1 inhibitor). Cell proliferation, alkaline phosphatase (ALP) levels, and calcium deposits were determined. The expression of Runx2, OSX, p-cofilin, RhoA, and GTP-bound RhoA was determined by real-time RT-PCR and Western blot. Rho-associated coiled-coil-containing protein kinase (ROCK) activity was determined by measuring the phosphorylation of myosin-binding subunit of myosin phosphatase using an ELISA kit. Actin morphology was observed by immunofluorescence. Results: After 24 h, DMOG (0.5 mM) increased the expression of GTP-bound RhoA (+141%, P < 0.001) and enhanced ROCK activity (315%, P < 0.001). DMOG (0.5 mM) enhanced ALP levels after 3, 7, and 21 days of osteogenic induction (all P < 0.001) and strengthened calcium deposition (P < 0.001). In addition, compared with controls, DMOG (0.5 mM) increased the mRNA levels of osteogenesis genes RUNX2 and OSX (all P < 0.001). Furthermore, compared with controls, DMOG increased the expression of p-cofilin (+57%, P < 0.001), which resulted in rearrangement of actin filaments. All these effects were abolished, at least in part, by Y-27632. Conclusion: DMOG promotes BMSC osteogenic differentiation via activation of RhoA/ROCK, suggesting clues for future therapies using BMSCs.

scholarly journals Role of geometrical cues in bone marrow-derived mesenchymal stem cell survival, growth and osteogenic differentiation

2017 ◽  
Vol 32 (7) ◽  
pp. 906-919 ◽  
Author(s):  
Dhanak Gupta ◽  
David M Grant ◽  
Kazi M Zakir Hossain ◽  
Ifty Ahmed ◽  
Virginie Sottile
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Cell Survival ◽  
Osteogenic Differentiation ◽  
Stem Cell Survival

Bone Marrow Mesenchymal Stem Cell (BMSC) Exosomes Inhibit Angiogenesis and Enhance Autophagy Through Decreasing miR-21 in Cervical Cancer

2021 ◽  
Vol 11 (9) ◽  
pp. 1780-1784
Author(s):  
Kewei Chen ◽  
Yiqin Ouyang ◽  
Junhua Liang ◽  
Huaifang Li ◽  
Xiaowen Tong ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Acridine Orange ◽  
Tube Formation ◽  
Fluorescent Staining ◽  
Insight Into

We aimed to explore the mechanism underlying the role of miR-21 derived from bone marrow mesenchymal stem cell exosomes (BMSC-exos) in cervical cancer (CC) and the relation between angiogenesis and autophagy. In this study, BMSC-exos were co-cultured with CC stem cells followed by analysis of miR-21 expression by RT-qPCR, autophagy after hunger-induced feeding by Acridine Orange fluorescent staining, angiogenesis by tube formation assay. Co-culture of BMSC-exos effectively reduced miR-21 expression in CC stem cells and enhanced autophagy as demonstrated by upregulated Beclin1 and LC3B with assembly of autophagosome (p < 0.05), but the autophagy restored later. Moreover, in the presence of BMSC-exos, CC stem cell angiogenesis was suppressed by 79%. In conclusion, BMSC-exos enhance autophagy and inhibit angiogenesis in CC through decreasing miR-21, which provides a novel insight into etiology of CC.

scholarly journals Bone marrow mesenchymal stem cell exosomes suppress phosphate-induced aortic calcification via SIRT6–HMGB1 deacetylation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wenqian Wei ◽  
Xiaodong Guo ◽  
Lijie Gu ◽  
Jieshuang Jia ◽  
Man Yang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Vascular Calcification ◽  
Target Genes ◽  
Elevated Serum ◽  
Aortic Calcification ◽  
In Vitro Assays ◽  
Calcium Deposition ◽  
High Phosphate

Abstract Background Vascular calcification associated with chronic kidney disease (CKD) can increase the risk of mortality. Elevated serum levels of high mobility group box 1 (HMGB1) promotes vascular calcification in CKD via the Wnt/β-catenin pathway. Sirtuin 6 (SIRT6) prevents fibrosis in CKD by blocking the expression of β-catenin target genes through deacetylation. This study aimed to investigate whether the inhibition of vascular calcification by bone marrow mesenchymal stem cell (BMSC)-derived exosomes is related to SIRT6 activity and assess the regulatory relationship between HMGB1 and SIRT6. Methods CKD characteristics, osteogenic markers, calcium deposition, and the differential expression of HMGB1 and SIRT6 have been measured in a 5/6 nephrectomized mouse CKD model fed a high-phosphate diet to induce aortic calcification. In vitro assays were also performed to validate the in vivo findings. Results High phosphate promotes the translocation of HMGB1 from the nucleus to the cytosol and induces the expression of Runx2, osteopontin, and Msx2. However, BMSC-derived exosomes were found to alleviate CKD-related fibrosis and the induction of osteogenic genes although less significantly when SIRT6 expression is suppressed. SIRT6 was found to modulate the cytosol translocation of HMGB1 by deacetylation in vascular smooth muscle cells. Conclusion Our results indicate that BMSC-derived exosomes inhibit high phosphate-induced aortic calcification and ameliorate renal function via the SIRT6–HMGB1 deacetylation pathway.

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