Human Mesenchymal Stem Cells Signals Regulate Neural Stem Cell Fate

2006 ◽  
Vol 32 (2) ◽  
pp. 353-362 ◽  
Author(s):  
Lianhua Bai ◽  
Arnold Caplan ◽  
Donald Lennon ◽  
Robert H. Miller
2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Taeui Hong ◽  
Moon Young Kim ◽  
Dat Da Ly ◽  
Su Jung Park ◽  
Young Woo Eom ◽  
...  

Abstract Although mitochondrial functions are essential for cell survival, their critical roles in stem cell fate, including proliferation, differentiation, and senescence, remain elusive. Ginsenoside Rg3 exhibits various biological activities and reportedly increases mitochondrial biogenesis and respiration. Herein, we observed that Rg3 increased proliferation and suppressed senescence of human bone marrow-derived mesenchymal stem cells. Osteogenic, but not adipogenic, differentiation was facilitated by Rg3 treatment. Rg3 suppressed reactive oxygen species production and upregulated mitochondrial biogenesis and antioxidant enzymes, including superoxide dismutase. Consistently, Rg3 strongly augmented basal and ATP synthesis-linked respiration with high spare respiratory capacity. Rg3 treatment elevated cytosolic Ca2+ concentration contributing to mitochondrial activation. Reduction of intracellular or extracellular Ca2+ levels strongly inhibited Rg3-induced activation of mitochondrial respiration and biogenesis. Taken together, Rg3 enhances capabilities of mitochondrial and antioxidant functions mainly through a Ca2+-dependent pathway, which improves the proliferation and differentiation potentials and prevents the senescence of human mesenchymal stem cells.


2020 ◽  
Author(s):  
Taeui Hong ◽  
Moon Young Kim ◽  
Dat Da Ly ◽  
Su Jung Park ◽  
Young Woo Eom ◽  
...  

Abstract Although mitochondrial functions are essential for cell survival, their critical roles in stem cell fate, including proliferation, differentiation, and senescence, remain elusive. Ginsenoside Rg3 exhibits various biological activities and reportedly increases mitochondrial biogenesis and respiration. Herein, we observed that Rg3 increased proliferation and suppressed senescence of human bone marrow-derived mesenchymal stem cells. Osteogenic, but not adipogenic, differentiation was facilitated by Rg3 treatment. Rg3 suppressed reactive oxygen species production and upregulated mitochondrial biogenesis and antioxidant enzymes, including superoxide dismutase. Consistently, Rg3 strongly augmented basal and ATP synthesis-linked respiration with high spare respiratory capacity. Rg3 treatment elevated cytosolic Ca2+ concentration contributing to mitochondrial activation. Reduction of intracellular or extracellular Ca2+ levels strongly inhibited Rg3-induced activation of mitochondrial respiration and biogenesis. Taken together, Rg3 enhances capabilities of mitochondrial and antioxidant functions mainly through a Ca2+-dependent pathway, which improves the proliferation and differentiation potentials and prevents the senescence of human mesenchymal stem cells.


2020 ◽  
Author(s):  
Taeui Hong ◽  
Moon Young Kim ◽  
Dat Da Ly ◽  
Su Jung Park ◽  
Young Woo Eom ◽  
...  

Abstract Although mitochondrial functions are essential for cell survival, their critical roles in stem cell fate, including proliferation, differentiation, and senescence, remain elusive. Ginsenoside Rg3 exhibits various biological activities and reportedly increases mitochondrial biogenesis and respiration. Herein, we observed that Rg3 increased proliferation and suppressed senescence of human bone marrow-derived mesenchymal stem cells. Osteogenic, but not adipogenic, differentiation was facilitated by Rg3 treatment. Rg3 suppressed reactive oxygen species production and upregulated mitochondrial biogenesis and antioxidant enzymes, including superoxide dismutase. Consistently, Rg3 strongly augmented basal and ATP synthesis-linked respiration with high spare respiratory capacity. Rg3 treatment elevated cytosolic Ca2+ concentration contributing to mitochondrial activation. Reduction of intracellular or extracellular Ca2+ levels strongly inhibited Rg3-induced activation of mitochondrial respiration and biogenesis. Taken together, Rg3 enhances capabilities of mitochondrial and antioxidant functions mainly through a Ca2+-dependent pathway, which improves the proliferation and differentiation potentials and prevents the senescence of human mesenchymal stem cells.


2010 ◽  
Vol 30 (5) ◽  
pp. 403-408 ◽  
Author(s):  
Hyo-Jung Park ◽  
Jun-Kyum Kim ◽  
Hye-Min Jeon ◽  
Se-Yeong Oh ◽  
Sung-Hak Kim ◽  
...  

2011 ◽  
Vol 31 (2) ◽  
pp. 199-199 ◽  
Author(s):  
Hyo-Jung Park ◽  
Jun-Kyum Kim ◽  
Hye-Min Jeon ◽  
Se-Yeong Oh ◽  
Sung-Hak Kim ◽  
...  

2014 ◽  
Vol 2 (11) ◽  
pp. 1661-1671 ◽  
Author(s):  
Yujie Ma ◽  
Martin P. Neubauer ◽  
Julian Thiele ◽  
Andreas Fery ◽  
W. T. S. Huck

Mesenchymal stem cells are encapsulated in a 3D fibrinogen–hyaluronic acid culture through droplet microfluidics, whose morphology, multipotency and differentiation are studied.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Louis N. Manganas ◽  
Irene Durá ◽  
Sivan Osenberg ◽  
Faith Semerci ◽  
Mehmet Tosun ◽  
...  

AbstractThe mechanisms responsible for determining neural stem cell fate are numerous and complex. To begin to identify the specific components involved in these processes, we generated several mouse neural stem cell (NSC) antibodies against cultured mouse embryonic neurospheres. Our immunohistochemical data showed that the NSC-6 antibody recognized NSCs in the developing and postnatal murine brains as well as in human brain organoids. Mass spectrometry revealed the identity of the NSC-6 epitope as brain abundant, membrane-attached signal protein 1 (BASP1), a signaling protein that plays a key role in neurite outgrowth and plasticity. Western blot analysis using the NSC-6 antibody demonstrated multiple BASP1 isoforms with varying degrees of expression and correlating with distinct developmental stages. Herein, we describe the expression of BASP1 in NSCs in the developing and postnatal mammalian brains and human brain organoids, and demonstrate that the NSC-6 antibody may be a useful marker of these cells.


2011 ◽  
Vol 33 (10) ◽  
pp. 1083-1093 ◽  
Author(s):  
K Ma ◽  
L Fox ◽  
G Shi ◽  
J Shen ◽  
Q Liu ◽  
...  

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