scholarly journals HIF-1α overexpression in adipose mesenchymal stem cell-derived exosomes ameliorate hypoxia-induced dysfunction and inflammation in HUVECs

2021 ◽  
Author(s):  
Xingxing Chen ◽  
Yonghong Sun ◽  
Xiaoyan Lei ◽  
Yunshan Cao ◽  
Mingdong Gao ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Growth ◽  
Mesenchymal Stem Cell ◽  
Tissue Repair ◽  
Tube Formation ◽  
Inflammatory Factors ◽  
Therapeutic Effects ◽  
Hypoxic Conditions ◽  
Angiogenic Effect ◽  
Culture Supernatants

Abstract Background Increasing evidence suggests that ADSCs execute their paracrine function via the secretion of exosomes, especially under hypoxic conditions. However, the mechanisms by which ADSCs-derived exosomes (ADSC-exos) enhance angiogenesis under hypoxia remain unclear. Methods Exosomes were isolated from HIF-1α-modified ADSCs culture supernatants. To investigate the effects HIF-1α-ADSC-exos on HUVECs, cell growth, apoptosis, and tube formation assay were performed with or without HIF-1α-ADSC-exos. Moreover, to determine the function of HIF-1α-ADSC-exos, the therapeutic effects of ADSC-exos and HIF-1α-ADSC-exos were examined in PAH rats. Results Exosomes released by HIF-1α-modified ADSCs rescued the impaired angiogenic ability, migratory function, and inflammatory factors of hypoxia-injured HUVECs, with increased SDF-1α, Rac1, Rac2, VEGF and IL-10 expression. Furthermore, exos-HIF-1α activated SIRT3 to enhance angiogenesis in HUVECs and induced IL-10 expression to inhibit inflammatory response. Block SIRT3 or SDF-1α abolished the angiogenic effect in HUVECs. Conclusion Our findings indicated that the SIRT3 contributed a crucial role in HIF-1α-ADSC-exos in tissue repair under hypoxia.

Enhancing therapeutic effects and in vivo tracking of adipose tissue derived mesenchymal stem cells for liver injury using bioorthogonal click chemistry

Nanoscale ◽  
2020 ◽  
Author(s):  
Naishun Liao ◽  
Da Zhang ◽  
Ming Wu ◽  
Huang-Hao Yang ◽  
Xiaolong Liu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Stem Cell ◽  
Liver Injury ◽  
Mesenchymal Stem Cell ◽  
Liver Diseases ◽  
Therapeutic Effects

Adipose tissue derived mesenchymal stem cell (ADSC)-based therapy is attractive for liver diseases, but the long-term therapeutic outcome is still far from satisfaction due to low hepatic engraftment efficiency of...

scholarly journals Positively Correlated CD47 Activation and Autophagy in Umbilical Cord Blood-Derived Mesenchymal Stem Cells during Senescence

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Gee-Hye Kim ◽  
Yun Kyung Bae ◽  
Ji Hye Kwon ◽  
Miyeon Kim ◽  
Soo Jin Choi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Cell Growth ◽  
Cell Therapy ◽  
Critical Role ◽  
Therapeutic Effects ◽  
Stem Cell Maintenance ◽  
Selection Of

Autophagy plays a critical role in stem cell maintenance and is related to cell growth and cellular senescence. It is important to find a quality-control marker for predicting senescent cells. This study verified that CD47 could be a candidate to select efficient mesenchymal stem cells (MSCs) to enhance the therapeutic effects of stem cell therapy by analyzing the antibody surface array. CD47 expression was significantly decreased during the expansion of MSCs in vitro ( p < 0.01 ), with decreased CD47 expression correlated with accelerated senescence phenotype, which affected cell growth. UCB-MSCs transfected with CD47 siRNA significantly triggered the downregulation of pRB and upregulation of pp38, which are senescence-related markers. Additionally, autophagy-related markers, ATG5, ATG12, Beclin1, and LC3B, revealed significant downregulation with CD47 siRNA transfection. Furthermore, autophagy flux following treatment with an autophagy inducer, rapamycin, has shown that CD47 is a key player in autophagy and senescence to maintain and regulate the growth of MSCs, suggesting that CD47 may be a critical key marker for the selection of effective stem cells in cell therapy.

Biocompatible succinic acid-based polyesters for potential biomedical applications: fungal biofilm inhibition and mesenchymal stem cell growth

RSC Advances ◽  
2015 ◽  
Vol 5 (104) ◽  
pp. 85756-85766 ◽  
Author(s):  
E. Jäger ◽  
R. K. Donato ◽  
M. Perchacz ◽  
A. Jäger ◽  
F. Surman ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Stem Cells ◽  
Stem Cell ◽  
Cell Growth ◽  
Mesenchymal Stem Cell ◽  
Medical Devices ◽  
Biomedical Applications ◽  
Growth Promotion ◽  
Intrinsic Properties ◽  
Biofilm Inhibition

Poly(alkene succinates) are promising materials for specialized medical devices and tissue engineering, presenting intrinsic properties, such as; fungal biofilm inhibition, biocompatibility and stem cells controlled growth promotion.

p21 is a critical suppressor of mesenchymal stem cell growth and differentiation after ionizing radiation

2008 ◽  
Vol 207 (3) ◽  
pp. S63
Author(s):  
Marc A. Soares ◽  
John G. Fernandez ◽  
Björn H. Schönmeyr ◽  
Nicholas W. Clavin ◽  
Babak J. Mehrara
Keyword(s):  
Stem Cell ◽  
Cell Growth ◽  
Mesenchymal Stem Cell ◽  
Ionizing Radiation ◽  
Cell Growth And Differentiation

Enhanced Therapeutic Effects of Mesenchymal Stem Cell-Derived Exosomes with an Injectable Hydrogel for Hindlimb Ischemia Treatment

2018 ◽  
Vol 10 (36) ◽  
pp. 30081-30091 ◽  
Author(s):  
Kaiyue Zhang ◽  
Xiangnan Zhao ◽  
Xiaoniao Chen ◽  
Yongzhen Wei ◽  
Wei Du ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Therapeutic Effects ◽  
Hindlimb Ischemia ◽  
Injectable Hydrogel

scholarly journals Poly(3-hydroxybutyrate) graft copolymer dense membranes for human mesenchymal stem cell growth

2018 ◽  
Vol 34 ◽  
pp. 59-66 ◽  
Author(s):  
Maykel González-Torres ◽  
Roberto Sánchez-Sánchez ◽  
Silvia G. Solís-Rosales ◽  
Witold Brostow ◽  
Eric Reyes-Cervantes ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Growth ◽  
Mesenchymal Stem Cell ◽  
Graft Copolymer ◽  
Human Mesenchymal Stem Cell

Adipose mesenchymal stem cell transplantation alleviates spinal cord injury-induced neuroinflammation partly by suppressing the Jagged1/Notch pathway

2019 ◽  
Author(s):  
Zhou Zhilai ◽  
Tian Xiaobo ◽  
Mo Biling ◽  
Xu Huali ◽  
Yao Shun ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Therapeutic Effects ◽  
Mesenchymal Stem Cell Transplantation ◽  
Cord Injury

Abstract Background The therapeutic effects of adipose-derived mesenchymal stem cell (ADSC) transplantation have been demonstrated in several models of central nervous system (CNS) injury and are thought to involve the modulation of the inflammatory response. However, the exact underlying molecular mechanism is poorly understood. Activation of the Jagged1/Notch signaling pathway is thought to involve inflammatory and gliotic events in the CNS. Here, we elucidated the effect of ADSC transplantation on the inflammatory reaction after spinal cord injury (SCI) and the potential mechanism mediated by Jagged1/Notch signaling pathway suppression.Methods Using a mouse model of compression SCI, ADSCs and Jagged1 small interfering RNA (siRNA) were injected into the spinal cord. Locomotor function, spinal cord tissue morphology and the levels of various proteins and transcripts were compared between groups.Results ADSC treatment resulted in significant downregulation of proinflammatory mediator expression and reduced ionized calcium binding adapter molecule 1 (Iba1) and ED1 staining in the injured spinal cord, promoting the survival of neurons. These changes were accompanied by improved functional recovery. The augmentation of the Jagged1/Notch signaling pathway after SCI was suppressed by ADSC transplantation. The inhibition of the Jagged1/Notch signaling pathway by Jagged1 siRNA resulted in a decrease in SCI-induced proinflammatory cytokines as well as the activation of microglia. Furthermore, Jagged1 knockdown suppressed the phosphorylation of JAK/STAT3 following SCI.Conclusion The results of this study demonstrated that the therapeutic effects of ADSCs in SCI mice were partly due to Jagged1/notch signaling pathway inhibition and a subsequent reduction in JAK/STAT3 phosphorylation.

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