scholarly journals Periocular and Intra-Articular Injection of Canine Adipose-Derived Mesenchymal Stem Cells: An In Vivo Imaging and Migration Study

2012 ◽  
Vol 28 (3) ◽  
pp. 307-317 ◽  
Author(s):  
Joshua A. Wood ◽  
Dai-Jung Chung ◽  
Shin Ae Park ◽  
Allison L. Zwingenberger ◽  
Christopher M. Reilly ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
In Vivo Imaging ◽  
Migration Study ◽  
And Migration

Overexpression of FOXQ1 enhances anti-senescence and migration effects of human umbilical cord mesenchymal stem cells in vitro and in vivo

2018 ◽  
Vol 373 (2) ◽  
pp. 379-393 ◽  
Author(s):  
Tao Zhang ◽  
Pan Wang ◽  
Yanxia Liu ◽  
Jiankang Zhou ◽  
Zhenqing Shi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Human Umbilical Cord ◽  
And Migration

scholarly journals Pharmacological Inhibition of Gal-3 in Mesenchymal Stem Cells Enhances Their Capacity to Promote Alternative Activation of Macrophages in Dextran Sulphate Sodium-Induced Colitis

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Bojana Simovic Markovic ◽  
Aleksandar Nikolic ◽  
Marina Gazdic ◽  
Jasmin Nurkovic ◽  
Irena Djordjevic ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Peritoneal Macrophages ◽  
Alternative Activation ◽  
Dextran Sulphate ◽  
Dextran Sulphate Sodium ◽  
Pharmacological Inhibition ◽  
And Migration

Transplantation of mesenchymal stem cells (MSCs) reduces the severity of dextran sulphate sodium- (DSS-) induced colitis. MSCs are able to secrete Galectin-3 (Gal-3), a protein known to affect proliferation, adhesion, and migration of immune cells. We investigate whether newly synthetized inhibitor of Gal-3 (Davanat) will affect production of Gal-3 in MSCs and enhance their potential to attenuate DSS-induced colitis. Pharmacological inhibition of Gal-3 in MSCs enhances their capacity to promote alternative activation of peritoneal macrophagesin vitroandin vivo. Injection of MSCs cultured in the presence of Davanat increased concentration of IL-10 in sera of DSS-treated animals and markedly enhanced presence of alternatively activated and IL-10 producing macrophages in the colons of DSS-treated mice. Pharmacological inhibition of Gal-3 in MSCs significantly attenuates concentration of Gal-3 in sera of DSS-treated animals, indicating that MSCs produce Gal-3 in this disease. In conclusion, our findings indicate that Davanat could be used for improvement of MSC-mediated polarization towards immunosuppressive M2 phenotype of macrophages.

Bone Marrow Mesenchymal Stem Cells (BMSC)-Derived MicroRNA-189 Inhibits Glioma Tumorigenesis Through Suppressing Tumor Necrosis Factor-α (TNF-α)-Mediated Nuclear Factor Kappa Light Chain Enhancer of Activated B Cells (NF-κB) Signaling Pathway

2022 ◽  
Vol 12 (3) ◽  
pp. 581-587
Author(s):  
Wenxu Rao ◽  
Kang Yin
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathway ◽  
Inflammatory Factors ◽  
Invasion And Migration ◽  
Marrow Mesenchymal Stem Cells ◽  
And Migration

This study aims at investigating the mechanism underlying bone marrow mesenchymal stem cells (BMSC) function in glioma. Glioma cells were administered with plasmids loading NF-κB siRNA, microRNA (miRNA)-189 inhibitor, or miR-189 mimics for transfection followed by analysis of miR-189 expression by RT-qPCR, cell apoptosis by flow cytometry, cell proliferation by MTT assay,invasion and migration by Transwell assay, inflammatory factors secretion by ELISA as well as proteins expression by western blot. A mouse model of glioma was established to detect the in vivo effect of BMSCs. miR-189 was lowly expressed in glioma cell lines but enriched in BMSCs. When miR-189 was silenced, cell proliferation, invasion and migration were potentiated and apoptosis was decreased, along with enhancement of N-cadherin, Vimentin, MMP-2 and and MMP-9, and decline in Bax, cleaved casepase-3 and cleaved PARP. Silencing of NF-κB reversed the effect of miR-189 inhibitor on cell progression, accompanied with reduction of inflammatory factors. BMSCs treatment effectively promoted miR-189 expression in glioma and inactivated TNF-α/NF-κB signaling, thereby suppressing tumor growth. In conclusion, miR-189 derived from BMSC inhibits glioma progression through regulation of TNF-α/NF-κB signaling pathway.

scholarly journals In vivo imaging of adipose-derived mesenchymal stem cells in female nude mice after simulated childbirth injury

2014 ◽  
Vol 9 (2) ◽  
pp. 372-376 ◽  
Author(s):  
MIAO DAI ◽  
PEIRONG XU ◽  
MIN HOU ◽  
YINCHENG TENG ◽  
QINGKAI WU
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Nude Mice ◽  
In Vivo Imaging ◽  
Female Nude

scholarly journals Intravenous Administration of 99mTc-HMPAO-Labeled Human Mesenchymal Stem Cells after Stroke: In Vivo Imaging and Biodistribution

2009 ◽  
Vol 18 (12) ◽  
pp. 1369-1379 ◽  
Author(s):  
Olivier Detante ◽  
Anaïck Moisan ◽  
Julien Dimastromatteo ◽  
Marie-Jeanne Richard ◽  
Laurent Riou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Intravenous Administration ◽  
In Vivo Imaging ◽  
Human Mesenchymal Stem Cells ◽  
99Mtc Hmpao

scholarly journals Curcumin Supplementation Enhances Bone Marrow Mesenchymal Stem Cells to Promote the Anabolism of Articular Chondrocytes and Cartilage Repair

2021 ◽  
Vol 30 ◽  
pp. 096368972199377
Author(s):  
Rui Zhang ◽  
Qiaoxia Zhang ◽  
Zhiyu Zou ◽  
Zheng Li ◽  
Meng Jin ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Articular Cartilage ◽  
Cartilage Repair ◽  
Articular Chondrocytes ◽  
Immunofluorescent Staining ◽  
And Migration ◽  
Proliferation And Migration

Mesenchymal stem cells derived from bone marrows (BMSCs) and curcumin derived from turmeric were used for osteoarthritis (OA) treatment, respectively. We invested the effects of curcumin supplementation for BMSC therapeutic effects. In vitro, rat BMSCs were identified by dual-immunofluorescent staining of CD44 and CD90, and flow cytometry. Primary articular chondrocytes were identified by toluidine blue staining and immunofluorescent staining of Col2a1. EdU incorporation, migration assay, real-time quantitative polymerase chain reaction, and Western blot analyses were performed to evaluate the alterations of chondrocytes cocultured with BMSCs. In vivo, the rat model of OA was established by monoiodoacetic acid. After intra-articular injection of allogeneic BMSCs, articular cartilage damage and OA progression were evaluated by histological staining, and Osteoarthritis Research Society International and Mankin score evaluation. Although curcumin alone did not improve cell viability of primary articular chondrocytes, it promoted proliferation and migration of chondrocytes when cocultured with BMSCs. Meanwhile, the expression of anabolic genes in chondrocytes was remarkably increased both at mRNA and protein levels. In OA rats, curcumin and BMSCs cooperated to greatly promote articular cartilage repair and retard OA progression. Therefore, curcumin supplementation enhanced the BMSC function for the proliferation and migration of articular chondrocytes, and anabolic gene expression of extracellular matrix in articular chondrocytes in vitro, and the generation of articular cartilage in vivo. Our study shed light on the potential clinical application of curcumin cooperated with BMSCs in cartilage repair for OA treatment.

Sotagliflozin (LX4211) Alleviates Lower Limb Ischemic Reperfusion by Inhibiting Paracrine of Bone Marrow Mesenchymal Stem Cells

2021 ◽  
Vol 11 (12) ◽  
pp. 2357-2366
Author(s):  
Xiaopeng Guo ◽  
Yingsong Liu ◽  
Mingzhu Wei
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Ischemia Reperfusion ◽  
Blood Perfusion ◽  
Lower Limbs ◽  
Marrow Mesenchymal Stem Cells ◽  
And Migration ◽  
Proliferation And Migration

We aimed to explore the mechanism by how LX4211 affects bone marrow mesenchymal stem cells (BMSCs) during ischemia-reperfusion (I/R). BMSCs were extracted and treated with LX4211 followed by analysis of cell proliferation and migration by CCK-8, Transwell assay and wound healing tests, cell apoptosis and cycle by flow cytometry, exosomes and VEGFA secretion by immunoenzyme-linked adsorption. BMSCs treated with LX4211 or DMSO were administrated into mice with blood perfusion and capillary or arteriolar density was detected. Treatment with LX4211 significantly inhibited BMSCs proliferation, increased apoptosis and activated AMPK/ACC signaling along with reduced the number of exosomes and VEGFA level and impaired physiological functions. In vivo experiments determined that LX4211 alleviated I/R of lower limbs by inhibiting the muscle retention of BMSCs and paracrine. In conclusion, LX4211 treatment can delay the blood recovery of ischemic non-diabetic mice by reducing the proliferation, migration and impairing paracrine of BMSCs.

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