scholarly journals Adipose-derived Mesenchymal Stem Cells can Alleviate Hypertrophic Scars and Affect the Biological Activity and Oxidative Stress-related Factors of Hypertrophic Scar Fibroblasts

2021 ◽  
Author(s):  
Shiyi Li ◽  
Jinxiu Yang ◽  
Minliang Chen
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Biological Activity ◽  
Hypertrophic Scar ◽  
Hypertrophic Scars ◽  
Collagen Fibres ◽  
Related Factors ◽  
And Migration ◽  
And Oxidative Stress ◽  
Proliferation And Migration

Abstract Background As a fibrotic disease with a high incidence, the pathogenesis of hypertrophic scarring is still not fully understood, and its treatment is also very difficult. In recent years, human adipose-derived mesenchymal stem cells (ADSCs) have been considered an effective treatment for fibrotic diseases, such as keloids. This study mainly explores the therapeutic effect and possible mechanism of ADSCs on hypertrophic scars.Methods After coculture, western blotting and quantitative real-time polymerase chain reaction (qRT–PCR) were used to detect gene and protein expression in hypertrophic scar fibroblasts (HSFs). Flow cytometry was used to detect reactive oxygen species (ROS), and apoptosis, cell proliferation and migration were also detected. A nude mouse animal model was established, the effects of ADSCs on hypertrophic scars were observed, and H&E staining, Masson staining and nuclear factor erythroid 2-related factor 2 (Nrf2) protein content detection were performed.Results Our experimental results show that ADSCs can inhibit HSF proliferation and migration and promote apoptosis. Our experimental results show that ADSCs can inhibit the proliferation and migration of HSFs and promote apoptosis. ADSCs also increase the ROS of HSFs, reduce superoxide dismutase (SOD), NAD(P)H:quinone oxidoreductase 1 (NQO1), and heme oxygenase-1 (HO-1), and reduce the expression of Nrf2 and BCL2. In in vivo experiments, we found that ADSCs can reduce the weight of hypertrophic scars, rearrange collagen fibres, and significantly reduce the Nrf2 content in tissues.Conclusion ADSCs can alleviate hypertrophic scars, promote the rearrangement of collagen fibres, and affect the biological activity of hypertrophic scar fibroblasts and oxidative stress-related factors.

Cell proliferation and migration on collagen substrata in vitro

1980 ◽  
Vol 41 (1) ◽  
pp. 159-175
Author(s):  
S.L. Schor
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Collagen Gel ◽  
Collagen Fibres ◽  
3 Dimensional ◽  
Cell Proliferation And Migration ◽  
Native Collagen ◽  
And Migration ◽  
Collagen Gel Matrix ◽  
Proliferation And Migration

Quantitative data are presented regarding cell proliferation and migration on (a) collagen films (b) the surface of 3-dimensional gels of native collagen fibres and (c) within the 3-dimensional collagen gel matrix, as part of a study of the effects of the extracellular matrix on cell behaviour. The nature of the collagen environment was found to influence the proliferation of certain cell types, but not of others. For example, HeLa cells proliferate at approximately the same rate and reach the same saturation cell densities on all of the collagen substrata, while human skin fibroblasts grow more slowly within the 3-dimensional collagen gel matrix compared with cells either on the gel surface or on collagen films. The 3-dimensional gels of native collagen fibres may also be used to study cell migration on the gel surface, as well as cell migration (or ‘infiltration’) from the gel surface into the 3-dimensional collagen matrix. Two methods have been used to obtain quantitative information concerning cell infiltration into the collagen gel, one involving the selective removal of cells from the gel surface, while the other relies on direct microscopic examination. Of the cells examined to date, epithelial cells (both normal and tumour) do not show infiltrative behaviour, while both normal and virally transformed fibroblasts, as well as tumour cells of non-epithelial origin (e.g. melanoma), do infiltrate into the collagen gel matrix, at rates which vary considerably according to cell type.

Abstract 15984: Rpl13a Small Nucleolar RNAs Promote Oxidative Stress and Atherosclerosis

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Lisheng Zhang ◽  
Jiaohui Wu ◽  
Andrew J Vista ◽  
Leigh Brian ◽  
Yushi Bai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carotid Arteries ◽  
Neointimal Hyperplasia ◽  
Foam Cells ◽  
Slice Thickness ◽  
Small Nucleolar Rnas ◽  
And Migration ◽  
Nucleolar Rnas ◽  
Proliferation And Migration

Reactive oxygen species (ROS) contribute to atherogenesis. An unusual mechanism that increases cellular ROS levels and oxidative stress involves 4 ubiquitously expressed noncoding small nucleolar RNAs (snoRNAs) from introns of the ribosomal protein L13a ( Rpl13a ) locus: U32a , U33 , U34 , and U35a . We tested the hypothesis that these snoRNAs promote aortic smooth muscle cell (SMC) activation and vascular inflammation, by using “snoKO” mice with targeted deletion of the 4 snoRNAs (but not Rpl13a ). Compared with congenic WT SMCs, snoKO SMCs showed 40±20% lower ROS levels, assessed by DCF fluorescence ( p <0.02). Congruently, ROS levels were 35±5% lower in snoKO than WT aorta and carotid frozen sections ( p <0.01), assessed by CellROX Orange fluorescence. Proliferation and migration evoked by FBS and PDGF-BB, respectively, were each 30±10% less in snoKO than WT SMCs ( p <0.01 for each). To assess SMC migration and proliferation in vivo, we performed carotid artery endothelial denudation. Before injury, snoKO and WT carotid arteries were morphologically equivalent. Four wk after injury, carotid neointimal hyperplasia was 57±9% less and luminal area was 40±20 % more in snoKO than in WT mice ( p <0.01). WT and snoKO mice had equivalent heart rates and systolic blood pressures by tail-cuff plethysmography: 480±20 vs 420±80 beats/min; 133±5, 132±7 mm Hg, respectively (n=5/group). To test whether snoRNAs affect atherosclerosis, we orthotopically transplanted carotid arteries from WT and snoKO mice into congenic Apoe -/- mice. Six wk post-op, atherosclerotic neointima was 70±10% smaller in snoKO than in WT carotids ( p <0.01). To assess SMC-to-foam-cell transdifferentiation, which is ROS-dependent, carotid cross-sections were stained for apoE to identify graft-derived cells and for cholesteryl ester with BODIPY. BODIPY + foam cells comprised 21±3% and 11±7% of neointimal area in WT and snoKO carotids, respectively ( p <0.05). Confocal co-localization of apoE and BODIPY (optical slice thickness 1 μm) showed that graft-derived foam cells were 2.0±0.6-fold more prevalent in WT than in snoKO carotids ( p <0.01). We conclude that Rpl13a snoRNAs promote SMC ROS levels, proliferation and migration in vitro and in vivo, and that these snoRNAs augment atherosclerosis.

scholarly journals Long non-coding RNA FAM83H-AS1 induced by adipose-derived stem cells promotes breast and pancreatic cancer cell proliferation and migration

2020 ◽  
Author(s):  
Jianing Tang ◽  
Qiuxia Cui ◽  
Dan Zhang ◽  
Xing Liao ◽  
Yan Gong ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cell Proliferation ◽  
Adipose Derived Stem Cells ◽  
Unfolded Protein ◽  
Pancreatic Cancer Cells ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Protein Response ◽  
Proliferation And Migration

Abstract Background Stromal cells recruited to the tumor microenvironment and long non-coding RNAs (lncRNAs) in the tumor cells regulate cancer progression. However, their relationship is largely unknown. Methods In the current study, we identified the effects of lncRNA FAM83H-AS1, induced by adipose-derived stem cells (ADSCs) during tumor development, and explored the underlying mechanisms using a coculture cell model. Adipose tissues were obtained from healthy female donors, the expression of stromal markers on cell surface of expanded ADSCs were confirmed using immunofluorescence analysis. The breast and pancreatic cancer cells were cultured with or without ADSCs using 24-well transwell chamber systems with 8.0 µm pore size. Results Our results showed that FAM83H-AS1 was upregulated in breast and pancreatic cancers and associated with poor prognosis. ADSCs further induced FAM83H-AS1 and increased tumor cell proliferation via promoting G1/S transition through cyclin D1, CDK4 and CDK6. Wound healing, modified Boyden chamber and immunoblotting assays demonstrated that ADSCs induced epithelial-mesenchymal transition and migration of breast and pancreatic cancer cells in a FAM83H-AS1-dependent manner. And ADSC-induced FAM83H-AS1 increased unfolded protein response through AKT/XBP1 pathway. Conclusion In conclusion, our results indicated that ADSCs promoted breast and pancreatic cancer development via inducing cell proliferation and migration, as well as unfolded protein response through FAM83H-AS1.

scholarly journals Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Haijun Zhao ◽  
Yanhui He
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Inflammatory Response ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Marrow Mesenchymal Stem Cells ◽  
And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

Umbilical Cord Mesenchymal Stem Cell Exosomes Alleviate the Progression of Kidney Failure by Modulating Inflammatory Responses and Oxidative Stress in an Ischemia-Reperfusion Mice Model

2021 ◽  
Vol 17 (9) ◽  
pp. 1874-1881
Author(s):  
Yanqiang Zhang ◽  
Chongjuan Wang ◽  
Zhuxiao Bai ◽  
Peng Li
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Renal Failure ◽  
Stem Cell ◽  
Protein Expression ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Protein Expression Level ◽  
M1 Macrophages ◽  
And Oxidative Stress

The efficacy of stem cells for the treatment of renal failure is widely recognized; however, an excessive volume of stem cells can block the capillaries; thus, the potential risks should not be ignored. Stem cell exosomes are secretory extracellular vesicles with a size of 30–150 nm, which have similar functions to stem cells but are much smaller in size. This study aims to investigate the role of human umbilical cord mesenchymal stem cells (UCMSCs)-derived exosomes in the treatment of renal failure caused by ischemia-reperfusion. Fifty 8-week-old female C57 mice underwent bilateral renal ischemia-reperfusion surgery for 30 minutes. After 4 weeks, the treated group received UCMSCs-derived exosomes treatment, and the control group was solely injected with the same amount of PBS. At the age of 16 weeks, the kidney function, kidney damage, inflammatory responses and oxidative stress were measured. Moreover, the effect of UCMSCs-derived exosomes on the phenotype of M1 macrophages was also tested. The results showed that UCMSCsderived exosomes significantly reduced the levels of blood urea nitrogen (BUN), serum creatinine (SCR), and urinary albumin and creatinine (ACR) and 8-isoprostane. UCMSCs-derived exosomes also improved the atrophy of the kidney and glomerulus, decreased kidney pro-inflammatory factors expression (mRNA of II-1β, II-6, Tnf-α, and Mcp-1) and oxidative stress (malondialdehyde), and increased glutathione level. However, F4/80 immunohistochemistry did not show significant differences between the two groups. In systemic inflammation measurement, UCMSCs-derived exosomes decreased proinflammatory factors TNF-α, IL-6, and IL-1β levels, and increased anti-inflammatory factor IL-10 level. In vitro experiments showed that UCMSCs-derived exosomes decreased the protein expression level of TNF-α and increased the protein expression level of IL-10 in M1 macrophages. UCMSCs-derived exosomes reduce kidney inflammation and oxidative stress by improving systemic inflammation, and thus reduce kidney damage and improve kidney function. This study shows the potential application value of exosomes in the treatment of renal failure.

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