scholarly journals Native Adipose Stromal Cells Egress from Adipose Tissue In Vivo: Evidence During Lymph Node Activation

Stem Cells ◽  
2013 ◽  
Vol 31 (7) ◽  
pp. 1309-1320 ◽  
Author(s):  
Marta Gil-Ortega ◽  
Lucile Garidou ◽  
Corinne Barreau ◽  
Marie Maumus ◽  
Ludovic Breasson ◽  
...  
2005 ◽  
Vol 328 (1) ◽  
pp. 258-264 ◽  
Author(s):  
Min Jeong Seo ◽  
Su Young Suh ◽  
Yong Chan Bae ◽  
Jin Sup Jung

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Dmitry O Traktuev ◽  
Daniel N Prater ◽  
Aravind R Sanjeevaiah ◽  
Stephanie Merfeld-Clauss ◽  
Brian H Johnstone ◽  
...  

Introduction Both Endothelial progenitor cells (EPC) and adipose stromal cells (ASC) are under investigation as therapies for cardiovascular diseases. Both cell types are capable of modulating vascular assembly and are, thereby, capable of directly promoting revascularization of ischemic tissues. We have shown that EPC differentiate into endothelial cells to form small vessels, whereas ASC have pericytic properties and naturally stabilize vessels. In this study we tested the possibility that ASC would interact with EPC to assemble de novo vessels in collagen in an in vivo chimeric implant. Methods and Results Collagen implants embedded with either umbilical cord blood EPC or adult ASC or a 4:1 mixture of both (2x10 6 cells/ml) were implanted subcutaneously into NOD/SCID mice. After 14 d implants were harvested and evaluated by immunohistochemistry. There was a pronounced difference among the groups in vascular network assembly. The majority of vessels formed in the EPC and ASC monocultures were small capillaries bounded by a single endothelial layer. Conversely, 100% of the plugs embedded with both cell types were highly invaded with multilayered arteriolar vessels. The density of the CD31 + vessels in the EPC and co-culture plugs was 26.6 ± 5.8 and 122.4 ± 9.8 per mm 2 , respectively. No CD31 + cells of human origin were detected in the ASC monocultures, indicating that ASC, which do not express this EC-specific marker, engage murine EC or form pseudovessels in this system. The density of α-SMA + vessels with lumens per mm 2 was 13.1 ± 3.6 (EPC), 10.2 ± 3.5 (ASC) and 124.7 ± 19.7 (co-culture). The total overlap of CD31 + and SMA + vessels demonstrates that mature, multilayered conduits were formed with the co-culture. Moreover, the majority of these vessels were filled with erythrocytes (92.5 ± 16.2 per mm 2 ), indicating inosculation with the native vasculature, which was confirmed by ultrasound with echogenic microbubbles and persisted to at least 4 months. Conclusion This study is the first to demonstrate that non-transformed human EPC and ASC cooperatively form mature and stable vasculature with subsequent functional integration into a host vasculature system.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J Dulak ◽  
J Stepniewski ◽  
M Tomczyk ◽  
K Andrysiak ◽  
I Kraszewska ◽  
...  

Abstract Introduction Despite progress in pharmacological treatment of myocardial infarction (MI), there is still an immense need for novel therapies for this life-threatening condition. Accordingly, cell-based therapies have been extensively investigated with most studies focusing on mesenchymal stromal cells. However due to their inability to differentiate into cardiomyocytes as well as limited survival upon in vivo administration, no effective treatment of MI has been developed. In contrast, application of hiPSC-derived cardiomyocytes (hiPSC-CM) represent biologically rational approach with pre-clinical studies confirming their therapeutic potential in various models of MI. However further optimization is required due to limited survival of hiPSC-CM upon in vivo administration. Therefore, we evaluated the therapeutic potential of genetically modified hiPSC-CM in murine model of acute MI and compared it to the effect of adipose tissue-derived stromal cells (ADSC). Methods In the first step hiPSC overexpressing GFP, luciferase (Luc) and pro-angiogenic and cardioprotective factors: heme oxygenase-1 (HO-1, heme degrading enzyme) or stromal cell-derived factor-1 (SDF-1, pro-angiogenic chemokine) were subjected to cardiac differentiation which yielded in each group 70–90% cardiac troponin T-positive contracting cells. hiPSC-CM (5x105 in 10 μl) were administered into NOD-SCID mice which underwent permanent ligation of left anterior descending (LAD) coronary artery. The cells were injected into the peri-infarct zone. Mice subjected to sham operation as well as injected with saline after MI were used as controls. The ultrasonography of hearts was performed on day 7, 14, 28 and 42 whereas the presence of hiPSC-CM was monitored using IVIS Spectrum system upon administration of luciferin and analysed in sections of collected hearts. The same experimental scheme was used to assess therapeutic potential of ADSC (CD105+CD73+CD90+CD44+CD146-CD34-) overexpressing luciferase and GFP. Results Ultrasonography demonstrated that upon delivery of hiPSC-CM the left ventricle ejection fraction (LVEF) was very significantly higher in comparison to control group injected with saline after induction of MI. In contrast, no improvement of LVEF was observed after administration of ADSC. Interestingly, measurements of luciferase activity revealed the strongest bioluminescent signal in the hearts of mice transplanted with iPSC-CM-HO1 42 days after MI. Importantly, the survival of hiPSC-CM in murine myocardium six weeks upon administration was further confirmed with immunofluorescent analysis of heart sections using human specific anti-Ku80 antibody. Again, luciferase activity was not observed upon delivery of ADSC. Conclusion These results strongly indicate that administration of hiPSC-CM, unlike ADSC, preserve murine heart function in acute MI model. Additionally, overexpression of HO-1 may positively influence their survival upon in vivo delivery into infarcted tissue. Acknowledgement/Funding The National Centre for Research and Development (STRATEGMED 2/269415/11/NCBR/2015), National Science Centre of Poland (HARMONIA 2014/14/M/NZ1/00010)


2020 ◽  
Vol 21 (3) ◽  
pp. 799 ◽  
Author(s):  
Joanna Lelek ◽  
Ewa K. Zuba-Surma

Mesenchymal stem/ stromal cells (MSCs) represent progenitor cells of various origin with multiple differentiation potential, representing the most studied population of stem cells in both in vivo pre-clinical and clinical studies. MSCs may be found in many tissue sources including extensively studied adipose tissue (ADSCs) and umbilical cord Wharton’s jelly (UC-MSCs). Most of sanative effects of MSCs are due to their paracrine activity, which includes also release of extracellular vesicles (EVs). EVs are small, round cellular derivatives carrying lipids, proteins, and nucleic acids including various classes of RNAs. Due to several advantages of EVs when compare to their parental cells, MSC-derived EVs are currently drawing attention of several laboratories as potential new tools in tissue repair. This review focuses on pro-regenerative properties of EVs derived from ADSCs and UC-MSCs. We provide a synthetic summary of research conducted in vitro and in vivo by employing animal models and within initial clinical trials focusing on neurological, cardiovascular, liver, kidney, and skin diseases. The summarized studies provide encouraging evidence about MSC-EVs pro-regenerative capacity in various models of diseases, mediated by several mechanisms. Although, direct molecular mechanisms of MSC-EV action are still under investigation, the current growing data strongly indicates their potential future usefulness for tissue repair.


2011 ◽  
Vol 56 (9) ◽  
pp. 2545-2552 ◽  
Author(s):  
Simone Coghetto Acedo ◽  
Érica Martins Ferreira Gotardo ◽  
Janilda Martins Lacerda ◽  
Caroline Candida de Oliveira ◽  
Patrícia de Oliveira Carvalho ◽  
...  

Endocrinology ◽  
2007 ◽  
Vol 148 (5) ◽  
pp. 1996-2005 ◽  
Author(s):  
Julien Tirard ◽  
Johann Gout ◽  
Anne Marie Lefrançois-Martinez ◽  
Antoine Martinez ◽  
Martine Begeot ◽  
...  

The aldo-keto reductase 1B7 (AKR1B7) encodes an aldose-reductase that has been reported as a detoxification enzyme until now. We have demonstrated that AKR1B7 is differently expressed in various mouse white adipose tissues depending on their location. Its expression is associated with a higher ratio of preadipocytes vs. adipocytes. The cells that express AKR1B7 did not contain lipid droplets, and the expression level of akr1b7 was very low in mature adipocytes. We have defined the role of AKR1B7 in adipogenesis using either primary cultures of adipose stromal cells (containing adipocyte precursors) or the 3T3-L1 cell line. Under the same differentiation conditions, adipose stromal cells from tissues that expressed AKR1B7 had a decreased capacity to accumulate lipids compared with those that did not express it. Moreover, the overexpression of sense or antisense AKR1B7 in 3T3-L1 preadipocytes inhibited or accelerated, respectively, their rate of differentiation into adipocytes. In vivo experiments demonstrated that AKR1B7-encoding mRNA expression decreased in adipose tissues from mice where obesity was induced by a high-fat diet. All these results attributed for the first time a novel role to AKR1B7, which is the inhibition of adipogenesis in some adipose tissues.


2007 ◽  
Vol 292 (1) ◽  
pp. E246-E252 ◽  
Author(s):  
Sagar Ghosh ◽  
Yunzhe Lu ◽  
Adam Katz ◽  
Yanfen Hu ◽  
Rong Li

Adipose tissue provides an important extragonadal source of estrogen. Obesity-associated elevation of estrogen production increases risk of breast cancer in postmenopausal women. Aromatase ( CYP19), which converts androgen to estrogen, is a key enzyme in estrogen biosynthesis. In normal adipose tissue, transcription of the aromatase gene is initiated from a relatively weak adipose-specific promoter (I.4). However, in breast cancer, a switch of promoter utilization from I.4 to a strong ovary-specific promoter, PII, leads to increased aromatase expression and, hence, elevated estrogen production. Here, we report an intriguing relationship between the breast cancer susceptibility gene BRCA1 and aromatase expression in human adipose stromal cells (ASCs). Upon stimulation by phorbol ester or dexamethasone, increased aromatase expression in ASCs was accompanied by significant reduction of the BRCA1 level. In addition, adipogenesis-induced aromatase expression was also inversely correlated with BRCA1 abundance. Downregulation of BRCA1 expression in response to various stimuli was through distinct transcription or posttranscription mechanisms. Importantly, siRNA-mediated knockdown of BRCA1 led to specific activation of the breast cancer-associated PII promoter. Therefore, in addition to its well-characterized activities in breast epithelial cells, a role of BRCA1 in modulation of estrogen biosynthesis in ASCs may also contribute to its tissue-specific tumor suppressor function.


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