scholarly journals Glioblastoma-mesenchymal stem cell communication modulates expression patterns of kinin receptors: Possible involvement of bradykinin in information flow

2015 ◽  
Vol 89 (4) ◽  
pp. 365-375 ◽  
Author(s):  
Micheli M. Pillat ◽  
Mona N. Oliveira ◽  
Helena Motaln ◽  
Barbara Breznik ◽  
Talita Glaser ◽  
...  
Author(s):  
G. Dostert ◽  
V. Jouan-Hureaux ◽  
H. Louis ◽  
É. Velot

Background: In peripheral blood, human natural killer (NK) cells are immunological cells that nearly don’t express the ectonucleotidase CD73 on their plasma membrane. When exposed to mesenchymal stem cells (MSCs), NK cells are able to acquire CD73. MSCs are known to be CD73-positive (CD73+) and also to modulate the immune system, e.g. through adenosynergic pathway by ectonucleosidases, such as CD73. Extracellular vesicles (EVs) are involved in cell-to-cell communication. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have emerged as paracrine mediators that are part of MSC immunomodulatory effects including immunosuppressive properties and immune privilege. Objective: The aim of our work was to study if CD73 could be acquired by NK cells through cell-to-cell communication with MSC-EVs as cell culture additives. We also hypothesised that MSC-EVs would act as tolerance inducers to attenuate NK cell cytotoxicity. Methods: Cell isolation was made from human umbilical cords for MSCs and from human peripheral blood for NK cells. MSC-EVs were isolated by ultracentrifugation and filtration, then characterized by nanoparticle tracking assay and flow cytometry (CD9, 63, 81 and 73). MSC-EV interaction with NK cells was monitored by PKH67 staining. NK cell activation was followed by measuring the expression of CD73 and NK-activating receptor natural-killer group 2, member D (NKG2D) by flow cytometry. The cytotoxicity of NK cells or EV-conditioned NK cells was evaluated after co-culture with K562 cells. Results: We showed that MSC-EVs are nanoparticles able to express CD73 and interact with NK cells. MSC-EV conditioned NK cells seem to increase CD73 and decrease NKG2D through an EV-mediated mechanism. MSC-EVs have an immunosuppressive effect on NK cells by preventing NK cell activation and NK cell cytotoxicity towards K562 cells. Conclusions: Our results demonstrate that MSC-EVs could influence NK cell behaviour and act as immunosuppressant cell-based products.


2011 ◽  
Vol 286 (48) ◽  
pp. 41489-41498 ◽  
Author(s):  
Noboru Taniguchi ◽  
Beatriz Caramés ◽  
Emily Hsu ◽  
Stephanie Cherqui ◽  
Yasuhiko Kawakami ◽  
...  

2013 ◽  
Vol 48 (2) ◽  
pp. 107 ◽  
Author(s):  
Myoung Woo Lee ◽  
Dae Seong Kim ◽  
Keon Hee Yoo ◽  
Hye Ryung Kim ◽  
In Keun Jang ◽  
...  

2021 ◽  
Vol 99 (2) ◽  
pp. 152-163
Author(s):  
Micheli Mainardi Pillat ◽  
Ágatha Oliveira‐Giacomelli ◽  
Mona Neves Oliveira ◽  
Roberta Andrejew ◽  
Natalia Turrini ◽  
...  

2018 ◽  
Vol 178 (4) ◽  
pp. 353-364 ◽  
Author(s):  
Zhanna Belaya ◽  
Tatiana Grebennikova ◽  
Galina Melnichenko ◽  
Alexey Nikitin ◽  
Alexander Solodovnikov ◽  
...  

Objective To evaluate the response of bone to chronic long-term growth hormone (GH) and insulin-like growth factor-1 (IGF1) excess by measuring the expression of selected mRNA and microRNA (miR) in bone tissue samples of patients with active acromegaly. Design Case–control study. Methods Bone tissue samples were obtained during transsphenoidal adenomectomy from the sphenoid bone (sella turcica) from 14 patients with clinically and biochemically confirmed acromegaly and 10 patients with clinically non-functioning pituitary adenoma (NFPA) matched by sex and age. Expression of genes involved in the regulation of bone remodeling was studied using quantitative polymerase chain reaction (qPCR). Results Of the genes involved in osteoblast and osteoclast activity, only alkaline phosphatase (ALP) mRNA was 50% downregulated in patients with acromegaly. GH excess caused increased expression of the Wnt signaling antagonists (DKK1) and agonists (WNT10B) and changes in the levels of miR involved in mesenchymal stem cell commitment to chondrocytes (miR-199a-5p) or adipocytes (miR-27-5p, miR-125b-5p, miR-34a-5p, miR-188-3p) P < 0.05; q < 0.1. Relevant compensatory mechanisms were found through the changes in miR involved in osteoblastogenesis (miR-210-5p, miR-135a-5p, miR-211, miR-23a-3p, miR-204-5p), but the expression of TWIST1 was 50% downregulated and RUNX2 was unchanged. Conclusions Acromegaly had minimal effects on tested mRNAs specific to osteoblast or osteoclast function except for downregulated ALP expression. The expressions of miR known to be involved in mesenchymal stem cell commitment and downregulated TWIST1 expression suggest acromegaly has a negative effect on osteoblastogenesis.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wenyi Chen ◽  
Jiaqi Zhu ◽  
Feiyan Lin ◽  
Yanping Xu ◽  
Bing Feng ◽  
...  

Abstract Background Cholangiocyte senescence is an important pathological process in diseases such as primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC). Stem cell/induced pluripotent stem cell-derived exosomes have shown anti-senescence effects in various diseases. We applied novel organoid culture technology to establish and characterize cholangiocyte organoids (cholangioids) with oxidative stress-induced senescence and then investigated whether human placenta mesenchymal stem cell (hPMSC)-derived exosomes exerted a protective effect in senescent cholangioids. Methods We identified the growth characteristics of cholangioids by light microscopy and confocal microscopy. Exosomes were introduced concurrently with H2O2 into the cholangioids. Using immunohistochemistry and immunofluorescence staining analyses, we assessed the expression patterns of the senescence markers p16INK4a, p21WAF1/Cip1, and senescence-associated β-galactosidase (SA-β-gal) and then characterized the mRNA and protein expression levels of chemokines and senescence-associated secretory phenotype (SASP) components. Results Well-established cholangioids expressed cholangiocyte-specific markers. Oxidative stress-induced senescence enhanced the expression of the senescence-associated proteins p16INK4a, p21WAF1/Cip1, and SA-β-gal in senescent cholangioids compared with the control group. Treatment with hPMSC-derived exosomes delayed the cholangioid aging progress and reduced the levels of SASP components (i.e., interleukin-6 and chemokine CC ligand 2). Conclusions Senescent organoids are a potential novel model for better understanding senescence progression in cholangiocytes. hPMSC-derived exosomes exert protective effects against senescent cholangioids under oxidative stress-induced injury by delaying aging and reducing SASP components, which might have therapeutic potential for PSC or PBC.


Stem Cells ◽  
2017 ◽  
Vol 35 (4) ◽  
pp. 1093-1105 ◽  
Author(s):  
Enrico Ragni ◽  
Federica Banfi ◽  
Mario Barilani ◽  
Alessandro Cherubini ◽  
Valentina Parazzi ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document