Strategies to improve homing of mesenchymal stem cells for greater efficacy in stem cell therapy

2014 ◽  
Vol 39 (1) ◽  
pp. 23-34 ◽  
Author(s):  
Hojjat Naderi-Meshkin ◽  
Ahmad Reza Bahrami ◽  
Hamid Reza Bidkhori ◽  
Mahdi Mirahmadi ◽  
Naghmeh Ahmadiankia
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Cell Therapy ◽  
Stem Cell Therapy

Mesenchymal stem cells: Stem cell therapy perspectives for type 1 diabetes

2009 ◽  
Vol 35 (2) ◽  
pp. 85-93 ◽  
Author(s):  
L. Vija ◽  
D. Farge ◽  
J.-F. Gautier ◽  
P. Vexiau ◽  
C. Dumitrache ◽  
...  
Keyword(s):  
Stem Cells ◽  
Type 1 Diabetes ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Cell Therapy ◽  
Stem Cell Therapy

scholarly journals Journey of Mesenchymal Stem Cells for Homing: Strategies to Enhance Efficacy and Safety of Stem Cell Therapy

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Sung Keun Kang ◽  
Il Seob Shin ◽  
Myung Soon Ko ◽  
Jung Youn Jo ◽  
Jeong Chan Ra
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Cell Therapy ◽  
Stem Cell Therapy ◽  
Human Mesenchymal Stem Cells ◽  
Cellular Damage ◽  
Efficacy And Safety ◽  
Clinical Benefits

Human mesenchymal stem cells (MSCs) communicate with other cells in the human body and appear to “home” to areas of injury in response to signals of cellular damage, known as homing signals. This review of the state of current research on homing of MSCs suggests that favorable cellular conditions and thein vivoenvironment facilitate and are required for the migration of MSCs to the site of insult or injuryin vivo. We review the current understanding of MSC migration and discuss strategies for enhancing both the environmental and cellular conditions that give rise to effective homing of MSCs. This may allow MSCs to quickly find and migrate to injured tissues, where they may best exert clinical benefits resulting from improved homing and the presence of increased numbers of MSCs.

scholarly journals Human amnion-derived mesenchymal stem cells are a potential source for uterine stem cell therapy

2008 ◽  
Vol 41 (5) ◽  
pp. 709-725 ◽  
Author(s):  
K. Han ◽  
J. E. Lee ◽  
S. J. Kwon ◽  
S. Y. Park ◽  
S. H. Shim ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Cell Therapy ◽  
Stem Cell Therapy ◽  
Human Amnion ◽  
Potential Source

Fetal bone marrow homing of donor mesenchymal stem cells after transamniotic stem cell therapy (TRASCET)

2018 ◽  
Vol 53 (1) ◽  
pp. 174-177 ◽  
Author(s):  
Hester F. Shieh ◽  
Azra Ahmed ◽  
Sarah A. Tracy ◽  
David Zurakowski ◽  
Dario O. Fauza
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Cell Therapy ◽  
Stem Cell Therapy ◽  
Fetal Bone

Human Umbilical Cord Mesenchymal Stem Cells: A New Era for Stem Cell Therapy

2015 ◽  
Vol 24 (3) ◽  
pp. 339-347 ◽  
Author(s):  
Dah-Ching Ding ◽  
Yu-Hsun Chang ◽  
Woei-Cherng Shyu ◽  
Shinn-Zong Lin
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Cell Therapy ◽  
Umbilical Cord ◽  
Stem Cell Therapy ◽  
Human Umbilical Cord ◽  
New Era

scholarly journals Fetal liver mesenchymal stem cells restore ovarian function in premature ovarian insufficiency by targeting MT1

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Boxian Huang ◽  
Chunfeng Qian ◽  
Chenyue Ding ◽  
Qingxia Meng ◽  
Qinyan Zou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Cell Therapy ◽  
Stem Cell Therapy ◽  
Ovarian Function ◽  
Ovarian Insufficiency ◽  
Apoptotic Genes

Abstract Background With the development of regenerative medicine and tissue engineering technology, almost all stem cell therapy is efficacious for the treatment of premature ovarian failure (POF) or premature ovarian insufficiency (POI) animal models, whereas little stem cell therapy has been practiced in clinical settings. The underlying molecular mechanism and safety of stem cell treatment in POI are not fully understood. In this study, we explored whether fetal mesenchymal stem cells (fMSCs) from the liver restore ovarian function and whether melatonin membrane receptor 1 (MT1) acts as a regulator for treating POI disease. Methods We designed an in vivo model (chemotherapy-induced ovary damage) and an in vitro model (human ovarian granulosa cells (hGCs)) to understand the efficacy and molecular cues of fMSC treatment of POI. Follicle development was observed by H&E staining. The concentration of sex hormones in serum (E2, AMH, and FSH) and the concentration of oxidative and antioxidative metabolites and the enzymes MDA, SOD, CAT, LDH, GR, and GPx were measured by ELISA. Flow cytometry (FACS) was employed to detect the percentages of ROS and proliferation rates. mRNA and protein expression of antiapoptotic genes (SURVIVIN and BCL2), apoptotic genes (CASPASE-3 and CASPASE-9), and MT1 and its downstream genes (JNK1, PCNA, AMPK) were tested by qPCR and western blotting. MT1 siRNA and related antagonists were used to assess the mechanism. Results fMSC treatment prevented cyclophosphamide (CTX)-induced follicle loss and recovered sex hormone levels. Additionally, fMSCs significantly decreased oxidative damage, increased oxidative protection, improved antiapoptotic effects, and inhibited apoptotic genes in vivo and in vitro. Furthermore, fMSCs also upregulated MT1, JNK1, PCNA, and AMPK at the mRNA and protein levels. With MT1 knockdown or antagonist treatment in normal hGCs, the protein expression of JNK1, PCNA, and AMPK and the percentage of proliferation were impaired. Conclusions fMSCs might play a crucial role in mediating follicular development in the POI mouse model and stimulating the activity of POI hGCs by targeting MT1.

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