scholarly journals Stem Cells for Bone Regeneration: Role of Trophic Factors

Author(s):  
Yogambha Ramaswamy ◽  
Khoon S. Lim ◽  
Hala Zreiqat ◽  
Zufu Lu
Oncotarget ◽  
2017 ◽  
Vol 8 (13) ◽  
pp. 21031-21043 ◽  
Author(s):  
Deting Xue ◽  
Erman Chen ◽  
Wei Zhang ◽  
Xiang Gao ◽  
Shengdong Wang ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Muhammad Nawaz ◽  
Farah Fatima ◽  
Krishna C. Vallabhaneni ◽  
Patrice Penfornis ◽  
Hadi Valadi ◽  
...  

Stem cells are proposed to continuously secrete trophic factors that potentially serve as mediators of autocrine and paracrine activities, associated with reprogramming of the tumor microenvironment, tissue regeneration, and repair. Hitherto, significant efforts have been made to understand the level of underlying paracrine activities influenced by stem cell secreted trophic factors, as little is known about these interactions. Recent findings, however, elucidate this role by reporting the effects of stem cell derived extracellular vesicles (EVs) that mimic the phenotypes of the cells from which they originate. Exchange of genetic information utilizing persistent bidirectional communication mediated by stem cell-EVs could regulate stemness, self-renewal, and differentiation in stem cells and their subpopulations. This review therefore discusses stem cell-EVs as evolving communication factors in stem cell biology, focusing on how they regulate cell fates by inducing persistent and prolonged genetic reprogramming of resident cells in a paracrine fashion. In addition, we address the role of stem cell-secreted vesicles in shaping the tumor microenvironment and immunomodulation and in their ability to stimulate endogenous repair processes during tissue damage. Collectively, these functions ensure an enormous potential for future therapies.


2017 ◽  
Vol 3 (1) ◽  
pp. 4 ◽  
Author(s):  
Reggie Hamdy ◽  
Yasir Alabdulkarim ◽  
Bayan Ghalimah ◽  
Mohammad Al-Otaibi ◽  
HadilF Al-Jallad ◽  
...  

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Zeynep Akdeniz-Dogan ◽  
Samet Sendur ◽  
Betul Karademir-Yilmaz ◽  
Onur Bugdayci ◽  
Ozlem T. Kaya ◽  
...  

2020 ◽  
Author(s):  
Xingyun Ge ◽  
Zehan Li ◽  
Zhou Zhou ◽  
Yibo Xia ◽  
Minxia Bian ◽  
...  

Abstract Background: Bone regeneration is preferred for bone loss caused by tumors, bone defects, fractures, etc. Recently, mesenchymal stem cells are considered as optimistic tools for bone defect therapy. Dental pulp stem cells (DPSCs) are a promising candidate for regenerative medicine and bone regeneration. Our previous study showed that up-regulated circSIPA1L1 during osteogenesis of DPSCs is of significance. In this paper, the potential role of circSIPA1L1 in osteogenesis of DPSCs and its underlying mechanisms are explored.Methods: The circular structure of circSIPA1L1 was identified by Sanger sequencing and PCR. Regulatory effects of circSIPA1L1 and miR-617 on mineral deposition in DPSCs were assessed by alkaline phosphatase (ALP) and alizarin red S (ARS) staining and in vivo bone formation assay were conducted to verify the biological influences of circSIPA1L1 on DPSCs. Western blot was performed to detect the protein expression of Smad3. Localization of circSIPA1L1 and miR-617 was confirmed by FISH. Dual-luciferase reporter assay and rescue experiments were conducted to investigate the role of the circSIPA1L1/miR-617/Smad3 regulatory axis in osteogenesis of DPSCs.Results: Sanger sequencing and back-to-back primer experiments confirmed the closed loop structure of circSIPA1L1. CircSIPA1L1 could promote the committed differentiation of DPSCs. MiR-617 was predicted to be the target binding circSIPA1L1 through MiRDB, miRTarBase, and TargetScan database analyses, which was further confirmed by dual-luciferase reporter assay. FISH results showed that circSIPA1L1 and miR-617 colocalize in the cytoplasm of DPSCs. MiR-617 exerted an inhibitory effect on osteogenesis of DPSCs. Knockdown of circSIPA1L1 or upregulation of miR-617 down-regulated phosphorylated Smad3. In addition, rescue experiments showed that knockdown of miR-617 reversed the inhibitory effect of circSIPA1L1 on osteogenesis of DPSCs.Conclusion: CircRNASIPA1L1 promotes osteogenesis of DPSCs by adsorbing miR-617 and further targeting Smad3.


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