Benchtop Isolation and Characterisation of Small Extracellular Vesicles from Human Mesenchymal Stem Cells

Tan, Kian L.; Chia, Wui Chuen; How, Chee Wun; Tor, Yin Sim; Show, Pau Loke; Looi, Qi Hao; Foo, Jhi Biau

doi:10.1007/s12033-021-00339-2

Cited by 35 publications

(20 citation statements)

References 30 publications

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“…Mesenchymal stem cells (MSCs; also referred to as mesenchymal stromal cells) [ 15 ] are adherent fibroblast-like cells, capable of self-renewal and differentiation into chondrocytes, osteocytes, and adipocytes [ 16 ]. In terms of their phenotype, they are typically identified by their co-expression of CD29, CD44 [ 17 , 18 ], CD73, CD90, CD105, and Sca-1 [ 19 ], and their non-expression of hematopoietic markers CD34, CD45, and CD11b [ 20 ]. Sufficiently high levels of proinflammatory cytokines can induce MSCs to exert immunosuppressive effects, making them suitable for controlling aberrant inflammatory responses [ 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Current status of clinical trials assessing mesenchymal stem cell therapy for graft versus host disease: a systematic review

Liu

Hao

et al. 2022

Stem Cell Res Ther

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Background Graft-versus-host disease (GVHD) is a common fatal complication of hematopoietic stem cell transplantation (HSCT), where steroids are used as a treatment option. However, there are currently no second-line treatments for patients that develop steroid-resistance (SR). Mesenchymal stem cells (MSCs) have immunomodulatory functions and can exert immunosuppressive effects on the inflammatory microenvironment. A large number of in vitro experiments have confirmed that MSCs can significantly inhibit the proliferation or activation of innate and adaptive immune cells. In a mouse model of GVHD, MSCs improved weight loss and increased survival rate. Therefore, there is great promise for the clinical translation of MSCs for the prevention or treatment of GVHD, and several clinical trials have already been conducted to date. Main body In this study, we searched multiple databases and found 79 clinical trials involving the use of MSCs to prevent or treat GVHD and summarized the characteristics of these clinical trials, including study design, phase, status, and locations. We analyzed the results of these clinical trials, including the response and survival rates, to enable researchers to obtain a comprehensive understanding of the field’s progress, challenges, limitations, and future development trends. Additionally, factors that might result in inconsistencies in clinical trial results were discussed. Conclusion In this study, we attempted to analyze the clinical trials for MSCs in GVHD, identify the most suitable group of patients for MSC therapy, and provide a new perspective for the design of such trials in the future.

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Section: Introductionmentioning

confidence: 99%

Current status of clinical trials assessing mesenchymal stem cell therapy for graft versus host disease: a systematic review

Liu

Hao

et al. 2022

Stem Cell Res Ther

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“…Preclinical studies supported that neuroinflammation is a potential pathogenic mechanism of POCD. In some cases, mesenchymal stem cell-derived extracellular vesicles attenuate elevated neuroinflammation [ 6 ]. Sevoflurane is an inhalational anesthetic with common application in surgery.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane induces inflammation in primary hippocampal neurons by regulating Hoxa5/Gm5106/miR-27b-3p positive feedback loop

Zhu

2021

Bioengineered

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Postoperative cognitive dysfunction (POCD) is a normal condition that develops after surgery with anesthesia, leading to deterioration of cognitive functions. However, the mechanism of POCD still remains unknown. To elucidate the POCD molecular mechanism, sevoflurane was employed in the present study to generate neuroinflammation mice model. Sevoflurane treatment caused inflammatory markers IL6, IL-10 and TNF-α high expression in primary hippocampal neurons and blood samples. Long non-coding RNA Gm5106 was found to be increased after being stimulated with sevoflurane. Silencing Gm5106 inhibited neuron inflammation. In the meanwhile, Gm5106 was identified as a direct target of miR-27b-3p that was inhibited by sevoflurane and related to inflammation suppression. In addition, transcription factor (TF) Hoxa5 was validated to activate Gm5106 through two binding motifs in the promoter region after sevoflurane exposure. Furthermore, miR-27b-3p also directly targeted Hoxa5 3ʹUTR, which affected nuclear Hoxa5 protein served as TF. Hoxa5 protein instead of 3ʹUTR reduced miR-27b-3p, in which Gm5106 knocking down abrogated this effect. In conclusion, sevoflurane induces neuroinflammation through increasing long non-coding RNA Gm5106, which is transcriptionally activated by Hoxa5 and directly targeted by miR-27-3p. Apart from that, Hoxa5, Gm5106, and miR-27b-3p form a positive feedback loop in sevoflurane stimulation.

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“…Chemotherapy resistance is a critical obstacle for the human cancer therapy [ 23 ]. For BC, adriamycin (ADR) acts as a pivotal first-line drug; however, a remarkable ADR-resistance has been formed in the chemotherapy using ADR [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

N⁶-methyladenosine (m⁶A)-mediated lncRNA DLGAP1-AS1enhances breast canceradriamycin resistance through miR-299-3p/WTAP feedback loop

et al. 2021

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Chemotherapy resistance is identified as an obstacle for breast cancer (BC) therapy, and, besides, increasing evidence indicates that long-noncoding RNAs (lncRNAs) participate in the regulation of BC adriamycin (ADR) resistance. Here, our work shows that lncRNA DLGAP1 antisense RNA 1 (DLGAP1-AS1) is up-regulated in ADR-resistant BC cells (MCF-7/ADR). Clinically, higher DLGAP1-AS1 expression was closely correlated to poorer clinical prognosis. Results showed that DLGAP1-AS1 promoted the ADR IC 50 and proliferation of ADR-resistant cells. Moreover, N 6 -methyladenosine (m 6 A) methyltransferase WT1 associated protein (WTAP) binds to the m 6 A modified site of DLGAP1-AS1 and motivates its stability. Mechanistically, DLGAP1-AS1 sponged miR-299-3p through 3ʹ-untranslated region (3ʹ-UTR) binding, which in turn relieved the repression of WTAP and thus upregulated WTAP expression. In conclusion, above findings conclude that lncRNA DLGAP1-AS1 promotes BC ADR-resistance through WTAP/DLGAP1-AS1/miR-299-3p feedback loop.

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Benchtop Isolation and Characterisation of Small Extracellular Vesicles from Human Mesenchymal Stem Cells

Cited by 35 publications

References 30 publications

Current status of clinical trials assessing mesenchymal stem cell therapy for graft versus host disease: a systematic review

Current status of clinical trials assessing mesenchymal stem cell therapy for graft versus host disease: a systematic review

Sevoflurane induces inflammation in primary hippocampal neurons by regulating Hoxa5/Gm5106/miR-27b-3p positive feedback loop

N⁶-methyladenosine (m⁶A)-mediated lncRNA DLGAP1-AS1enhances breast canceradriamycin resistance through miR-299-3p/WTAP feedback loop

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Benchtop Isolation and Characterisation of Small Extracellular Vesicles from Human Mesenchymal Stem Cells

Cited by 35 publications

References 30 publications

Current status of clinical trials assessing mesenchymal stem cell therapy for graft versus host disease: a systematic review

Current status of clinical trials assessing mesenchymal stem cell therapy for graft versus host disease: a systematic review

Sevoflurane induces inflammation in primary hippocampal neurons by regulating Hoxa5/Gm5106/miR-27b-3p positive feedback loop

N6-methyladenosine (m6A)-mediated lncRNA DLGAP1-AS1enhances breast canceradriamycin resistance through miR-299-3p/WTAP feedback loop

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N⁶-methyladenosine (m⁶A)-mediated lncRNA DLGAP1-AS1enhances breast canceradriamycin resistance through miR-299-3p/WTAP feedback loop