See the published version of this article at Stem Cell Research & Therapy.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Short report
Ca2+-activated mitochondrial biogenesis and functions improve stem cell fate in Rg3-treated human mesenchymal stem cells
Kyu-Sang Park
Yonsei University Wonju College of Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0003-0322-9807
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published version at Stem Cell Research & Therapy.
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.
Keywords
mesenchymal stem cells, ginsenoside Rg3, cellular senescence, oxidative stress, mitochondria
Figure 1
Figure 2
Figure 3
This is a list of supplementary files associated with this preprint. Click to download.
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
Version 2
Posted 22 Sep, 2020
Published
On 04 Nov, 2020
No community comments so far
Editorial decision: Accept
On 01 Oct, 2020
Reviewer #2 agreed
On 28 Sep, 2020
Review #2 received
Received 28 Sep, 2020
Reviewers invited
Invitations sent on 25 Sep, 2020
Reviewer #1 agreed
On 25 Sep, 2020
Review #1 received
Received 25 Sep, 2020
Editor assigned
On 21 Sep, 2020
Submission checks complete
On 20 Sep, 2020
Editor invited
On 20 Sep, 2020
No comments provided
Editorial decision: Minor Revision
On 04 Sep, 2020
Review #2 received
Received 03 Sep, 2020
Reviewer #2 agreed
On 24 Aug, 2020
Review #1 received
Received 24 Aug, 2020
Reviewer #1 agreed
On 22 Aug, 2020
Reviewers invited
Invitations sent on 20 Aug, 2020
Editor assigned
On 14 Aug, 2020
Submission checks complete
On 13 Aug, 2020
Editor invited
On 13 Aug, 2020
First submitted
On 12 Aug, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Stem Cell & Developmental Cell Biology
Learn more about our company.
This preprint is under consideration at Stem Cell Research & Therapy. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Short report
Ca2+-activated mitochondrial biogenesis and functions improve stem cell fate in Rg3-treated human mesenchymal stem cells
Kyu-Sang Park
Yonsei University Wonju College of Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0003-0322-9807
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
Version 2
Posted 22 Sep, 2020
Published
On 04 Nov, 2020
No community comments so far
Editorial decision: Accept
On 01 Oct, 2020
Reviewer #2 agreed
On 28 Sep, 2020
Review #2 received
Received 28 Sep, 2020
Reviewers invited
Invitations sent on 25 Sep, 2020
Reviewer #1 agreed
On 25 Sep, 2020
Review #1 received
Received 25 Sep, 2020
Editor assigned
On 21 Sep, 2020
Submission checks complete
On 20 Sep, 2020
Editor invited
On 20 Sep, 2020
No comments provided
Editorial decision: Minor Revision
On 04 Sep, 2020
Review #2 received
Received 03 Sep, 2020
Reviewer #2 agreed
On 24 Aug, 2020
Review #1 received
Received 24 Aug, 2020
Reviewer #1 agreed
On 22 Aug, 2020
Reviewers invited
Invitations sent on 20 Aug, 2020
Editor assigned
On 14 Aug, 2020
Submission checks complete
On 13 Aug, 2020
Editor invited
On 13 Aug, 2020
First submitted
On 12 Aug, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Stem Cell & Developmental Cell Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published version at Stem Cell Research & Therapy.
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.
Figure 1
Figure 2
Figure 3