Magnetic field assisted stem cell differentiation – role of substrate magnetization in osteogenesis

2015 ◽  
Vol 3 (16) ◽  
pp. 3150-3168 ◽  
Author(s):  
Sunil Kumar Boda ◽  
Greeshma Thrivikraman ◽  
Bikramjit Basu

Substrate magnetization as a tool for modulating the osteogenesis of human mesenchymal stem cells for bone tissue engineering applications.

2014 ◽  
Vol 50 (62) ◽  
pp. 8484-8487 ◽  
Author(s):  
Rameshwar Tatavarty ◽  
Hao Ding ◽  
Guijin Lu ◽  
Robert J. Taylor ◽  
Xiaohong Bi

Nanocomposites consisting of oblong ultrathin plate shaped calcium phosphate nanoparticles and graphene oxide microflakes were synthesized and have demonstrated markedly synergistic effect in accelerating stem cell differentiation to osteoblasts.


2015 ◽  
Vol 35 (10) ◽  
pp. 1700-1711 ◽  
Author(s):  
Fenfang Chen ◽  
Xia Lin ◽  
Pinglong Xu ◽  
Zhengmao Zhang ◽  
Yanzhen Chen ◽  
...  

Bone morphogenetic proteins (BMPs) play vital roles in regulating stem cell maintenance and differentiation. BMPs can induce osteogenesis and inhibit myogenesis of mesenchymal stem cells. Canonical BMP signaling is stringently controlled through reversible phosphorylation and nucleocytoplasmic shuttling of Smad1, Smad5, and Smad8 (Smad1/5/8). However, how the nuclear export of Smad1/5/8 is regulated remains unclear. Here we report that the Ran-binding protein RanBP3L acts as a nuclear export factor for Smad1/5/8. RanBP3L directly recognizes dephosphorylated Smad1/5/8 and mediates their nuclear export in a Ran-dependent manner. Increased expression of RanBP3L blocks BMP-induced osteogenesis of mouse bone marrow-derived mesenchymal stem cells and promotes myogenic induction of C2C12 mouse myoblasts, whereas depletion of RanBP3L expression enhances BMP-dependent stem cell differentiation activity and transcriptional responses. In conclusion, our results demonstrate that RanBP3L, as a nuclear exporter for BMP-specific Smads, plays a critical role in terminating BMP signaling and regulating mesenchymal stem cell differentiation.


2019 ◽  
Vol 7 (16) ◽  
pp. 2703-2713 ◽  
Author(s):  
Na Li ◽  
Alex P. Rickel ◽  
Hanna J. Sanyour ◽  
Zhongkui Hong

Stem cell differentiation on a decellularized native blood vessel scaffold under mechanical stimulation for vascular tissue engineering.


2016 ◽  
Vol 8 (41) ◽  
pp. 7437-7444 ◽  
Author(s):  
Hongjun Song ◽  
Jenna M. Rosano ◽  
Yi Wang ◽  
Charles J. Garson ◽  
Balabhaskar Prabhakarpandian ◽  
...  

A dual-micropore-based microfluidic electrical impedance flow cytometer for non-invasive identification of the differentiation state of mesenchymal stem cells.


Small ◽  
2016 ◽  
Vol 12 (13) ◽  
pp. 1770-1778 ◽  
Author(s):  
Jichuan Qiu ◽  
Jianhua Li ◽  
Shu Wang ◽  
Baojin Ma ◽  
Shan Zhang ◽  
...  

2016 ◽  
Vol 215 (3) ◽  
pp. 345-355 ◽  
Author(s):  
Bryne Ulmschneider ◽  
Bree K. Grillo-Hill ◽  
Marimar Benitez ◽  
Dinara R. Azimova ◽  
Diane L. Barber ◽  
...  

Despite extensive knowledge about the transcriptional regulation of stem cell differentiation, less is known about the role of dynamic cytosolic cues. We report that an increase in intracellular pH (pHi) is necessary for the efficient differentiation of Drosophila adult follicle stem cells (FSCs) and mouse embryonic stem cells (mESCs). We show that pHi increases with differentiation from FSCs to prefollicle cells (pFCs) and follicle cells. Loss of the Drosophila Na+–H+ exchanger DNhe2 lowers pHi in differentiating cells, impairs pFC differentiation, disrupts germarium morphology, and decreases fecundity. In contrast, increasing pHi promotes excess pFC cell differentiation toward a polar/stalk cell fate through suppressing Hedgehog pathway activity. Increased pHi also occurs with mESC differentiation and, when prevented, attenuates spontaneous differentiation of naive cells, as determined by expression of microRNA clusters and stage-specific markers. Our findings reveal a previously unrecognized role of pHi dynamics for the differentiation of two distinct types of stem cell lineages, which opens new directions for understanding conserved regulatory mechanisms.


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