scholarly journals Combination of resveratrol and 5-azacytydine improves osteogenesis of metabolic syndrome mesenchymal stem cells

2018 ◽  
Vol 22 (10) ◽  
pp. 4771-4793 ◽  
Author(s):  
Krzysztof Marycz ◽  
Katarzyna Kornicka ◽  
Jennifer M. Irwin-Houston ◽  
Christine Weiss
2018 ◽  
Vol 22 (1) ◽  
pp. 207-211
Author(s):  
Nagwa Ahmad ◽  
Esam Abdel Raheem ◽  
Hanan Fouad ◽  
Tahia Saleem

2017 ◽  
Vol 93 (1) ◽  
pp. 93-103 ◽  
Author(s):  
Yu Meng ◽  
Alfonso Eirin ◽  
Xiang-Yang Zhu ◽  
Hui Tang ◽  
Pritha Chanana ◽  
...  

2018 ◽  
Vol 27 (10) ◽  
pp. 1495-1503 ◽  
Author(s):  
Y. Meng ◽  
A. Eirin ◽  
X.-Y. Zhu ◽  
H. Tang ◽  
L.J. Hickson ◽  
...  

Mesenchymal stem cells (MSCs) constitute an important repair system, but may be impaired by exposure to cardiovascular risk factors. Consequently, adipose tissue-derived MSCs from pigs with the metabolic syndrome (MetS) show decreased vitality. A growing number of microRNAs (miRNAs) are recognized as key modulators of senescence, but their role in regulating senescence in MSC in MetS is unclear. We tested the hypothesis that MetS upregulates in MSC expression of miRNAs that can serve as post-transcriptional regulators of senescence-associated (SA) genes. MSCs were collected from swine abdominal adipose tissue after 16 weeks of Lean or Obese diet ( n = 6 each). Next-generation miRNA sequencing (miRNA-seq) was performed to identify miRNAs up-or down-regulated in MetS-MSCs compared with Lean-MSCs. Functional pathways of SA genes targeted by miRNAs were analyzed using gene ontology. MSC senescence was evaluated by p16 and p21 immunoreactivity, H2AX protein expression, and SA-β-Galactosidase activity. In addition, gene expression of p16, p21, MAPK3 (ERK1) and MAPK14, and MSC migration were studied after inhibition of SA-miR-27b. Senescence biomarkers were significantly elevated in MetS-MSCs. We found seven upregulated miRNAs, including miR-27b, and three downregulated miRNAs in MetS-MSCs, which regulate 35 SA genes, particularly MAPK signaling. Inhibition of miR-27b in cultured MSCs downregulated p16 and MARP3 genes, and increased MSC migration. MetS modulates MSC expression of SA-miRNAs that may regulate their senescence, and the p16 pathway seems to play an important role in MetS-induced MSC senescence.


Author(s):  
WILFREDO OLIVA-OLIVERA ◽  
LETICIA COÍN-Aragüez ◽  
SAID LHAMYANI ◽  
MERCEDES CLEMENTE-POSTIGO ◽  
JUAN ALCAIDE TORRES ◽  
...  

Author(s):  
Krzysztof Marycz ◽  
Katarzyna Kornicka-Garbowska ◽  
Larry Galuppo ◽  
Lynda Bourebaba

Abstract Herein, we would like to introduce a novel concept for the prevention and treatment of metabolic syndrome, which is based on molecular relationship between liver and adipose tissue. Particularly, we believe, that unravelling the molecular crosstalk between hepatokines and adipokines will allow to better understand the pathophysiology of metabolic diseases and allow to develop novel, effective therapeutic solutions against obesity and metabolic syndrome. Graphical Abstract Inter-organ communication on the level of stem progenitor cells-hepatic stellate cells (HSTCs) and adipose-derived progenitors (ASCs) could represents a key mechanism involved in controlling glucose tolerance as well as insulin sensitivity.


2019 ◽  
Vol 9 (9) ◽  
pp. 1266-1272
Author(s):  
Yonggang Zhang ◽  
Junqi Wang ◽  
Junqi Yang ◽  
Peng Liu ◽  
Kunzheng Wang ◽  
...  

Bone marrow mesenchymal stem cells (BMSCs) can differentiate into osteogenesis. Integrin-linked kinase (ILK) regulates several biological processes. However, whether ILK affects metabolic syndrome (MS)-derived BMSCs differentiation remains unclear. SD rats were divided into control group and MS group. Diabetic rat model was prepared. BMSCs were divided into control group, MS group and ILK group, in which ILK plasmid was transfected into BMSCs from MS group followed by analysis of ILK, Bcl-2, Bax, RUNX2 and OPN expression by real time PCR, BMSCs proliferation by MTT assay, BMSCs apoptosis, expression of Beclin-3 and LC-3 by Western blot as well as secretion of IL-1β and IL-6 by ELISA. MS group showed significantly reduced BMSCs proliferation, elevated Caspase 3 activity, downregulated Bcl-2, RUNX2 and OPN expression, upregulated Bax level and increased IL-1β and IL-6 secretion as well as decreased Beclin-3 and LC-3 expression compared to control group (P < 0.05). BMSCs with ILK overexpression in high glucose presented significantly promoted BMSCs proliferation, decreased Caspase 3 activity, increased Bcl-2, RUNX2 and OPN expression, decreased Bax expression and IL-1β and IL-6 secretion as well as reduced Beclin-3 and LC-3 expression compared to MS group (P < 0.05). ILK expression in MS-derived BMSCs is decreased. ILK overexpression in BMSCs can promote autophagy, inhibit apoptosis and inflammation, and promote their differentiation into osteoblasts.


Gene ◽  
2018 ◽  
Vol 644 ◽  
pp. 101-106 ◽  
Author(s):  
Sabena M. Conley ◽  
Xiang-Yang Zhu ◽  
Alfonso Eirin ◽  
Hui Tang ◽  
Amir Lerman ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Kenichi Matsushita

Metabolic syndrome is an obesity-based, complicated clinical condition that has become a global epidemic problem with a high associated risk for cardiovascular disease and mortality. Dyslipidemia, hypertension, and diabetes or glucose dysmetabolism are the major factors constituting metabolic syndrome, and these factors are interrelated and share underlying pathophysiological mechanisms. Severe obesity predisposes individuals to metabolic syndrome, and recent data suggest that mesenchymal stem cells (MSCs) contribute significantly to adipocyte generation by increasing the number of adipocytes. Accordingly, an increasing number of studies have examined the potential roles of MSCs in managing obesity and metabolic syndrome. However, despite the growing bank of experimental and clinical data, the efficacy and the safety of MSCs in the clinical setting are still to be optimized. It is thus hoped that ongoing and future studies can elucidate the roles of MSCs in metabolic syndrome and lead to MSC-based therapeutic options for affected patients. This review discusses current understanding of the relationship between MSCs and metabolic syndrome and its potential implications for patient management.


Author(s):  
Guang-ping Ruan ◽  
Xiang Yao ◽  
Kai Wang ◽  
Jie He ◽  
Rong-qing Pang ◽  
...  

Background: Umbilical cord mesenchymal stem cell transplantation can treat metabolic syndrome, but the tracing of cells in the body after transplantation has always been a problem. Tree shrew umbilical cord mesenchymal stem cells were labeled with the dark red fluorescent dye DIR and a metabolic syndrome model in tree shrew was generated. The migration, distribution, colonization and survival of the cells were observed. Methods: Tree shrew umbilical cord mesenchymal stem cells were labeled with the dark red fluorescent dye DIR. Three days after the tree shrew model was generated, the pancreas, kidney and liver were placed in a small animal live imager to observe the distribution of the labeled cells. Result: The labeled cells showed deep red fluorescence in the live imager. After treatment with the transplanted cells, dark red fluorescent signals were observed in the liver, kidney and pancreas of the tree shrews but not in the untreated group and no dark red fluorescent signal was observed in the cell distribution.


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