scholarly journals LINC00473 regulated apoptosis, proliferation and migration but could not reverse cell cycle arrest of human bone marrow mesenchymal stem cells induced by a high-dosage of dexamethasone

2020 ◽  
Vol 48 ◽  
pp. 101954 ◽  
Author(s):  
Yingxing Xu ◽  
Yaping Jiang ◽  
Yingzhen Wang ◽  
Yuanzhong Ren ◽  
Zhiping Zhao ◽  
...  
2017 ◽  
Vol 95 (6) ◽  
pp. 628-633 ◽  
Author(s):  
Liang Wang ◽  
Guang Bai ◽  
Fei Chen

Bone marrow mesenchymal stem cells (BMSCs) have considerable therapeutic potential for the treatment of end-stage liver disease. Previous studies have demonstrated that BMSCs secrete growth factors and cytokines that inactivate hepatic stellate cells (HSCs), which inhibited the progression of hepatic fibrosis. The aim of this study was to determine the mechanism by which BMSCs suppress the function of HSCs in fibrosis. Our results showed that co-culture of BMSCs and HSCs induced cell cycle arrest at the G10/G1 phase and cell apoptosis of HSCs, which finally inhibited the cell proliferation of HSCs. Consistent with the cell cycle arrest, co-culture of BMSCs and HSCs increased the abundance of the cell cycle protein p27. Mechanistically, we further uncovered that following the co-culture with BMSCs, the expression level of the E3 ligase S-phase kinase-associated protein 2 (SKP2) that is responsible for the ubiquitination of p27 was decreased, which attenuated the ubiquitination of p27 and increased the stability of p27 in HSCs. Collectively, our results indicated the potential involvement of the SKP2–p27 axis for the inhibitory effect of BSMCs on the cell proliferation of HSCs.


2012 ◽  
Vol 36 (10) ◽  
pp. 917-922 ◽  
Author(s):  
Yan‑Hui Cen ◽  
Wen‑Wen Guo ◽  
Bin Luo ◽  
Yong‑Da Lin ◽  
Qing‑Mei Zhang ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Mingyu Zhang ◽  
Yue Du ◽  
Renzhong Lu ◽  
You Shu ◽  
Wei Zhao ◽  
...  

In the present study, we demonstrated that bone marrow mesenchymal stem cells (BMSCs) of the 3rd passage displayed the senescence-associated phenotypes characterized with increased activity of SA-β-gal, altered autophagy, and increased G1 cell cycle arrest, ROS production, and expression of p53 andp21Cip1/Waf1compared with BMSCs of the 1st passage. Cholesterol (CH) reduced the number of SA-β-gal positive cells in a dose-dependent manner in aging BMSCs induced by H2O2and the 3rd passage BMSCs. Moreover, CH inhibited the production of ROS and expression of p53 andp21Cip1/Waf1in both cellular senescence models and decreased the percentage of BMSCs in G1 cell cycle in the 3rd passage BMSCs. CH prevented the increase in SA-β-gal positive cells induced by RITA (reactivation of p53 and induction of tumor cell apoptosis, a p53 activator) or 3-MA (3-methyladenine, an autophagy inhibitor). Our results indicate that CH not only is a structural component of cell membrane but also functionally contributes to regulating cellular senescence by modulating cell cycle, autophagy, and the ROS/p53/p21Cip1/Waf1signaling pathway.


2021 ◽  
Vol 11 (12) ◽  
pp. 2357-2366
Author(s):  
Xiaopeng Guo ◽  
Yingsong Liu ◽  
Mingzhu Wei

We aimed to explore the mechanism by how LX4211 affects bone marrow mesenchymal stem cells (BMSCs) during ischemia-reperfusion (I/R). BMSCs were extracted and treated with LX4211 followed by analysis of cell proliferation and migration by CCK-8, Transwell assay and wound healing tests, cell apoptosis and cycle by flow cytometry, exosomes and VEGFA secretion by immunoenzyme-linked adsorption. BMSCs treated with LX4211 or DMSO were administrated into mice with blood perfusion and capillary or arteriolar density was detected. Treatment with LX4211 significantly inhibited BMSCs proliferation, increased apoptosis and activated AMPK/ACC signaling along with reduced the number of exosomes and VEGFA level and impaired physiological functions. In vivo experiments determined that LX4211 alleviated I/R of lower limbs by inhibiting the muscle retention of BMSCs and paracrine. In conclusion, LX4211 treatment can delay the blood recovery of ischemic non-diabetic mice by reducing the proliferation, migration and impairing paracrine of BMSCs.


Author(s):  
T. Zhao ◽  
G. Zadeh

Ionizing radiation (IR) is one of the conventional post-surgical treatments for Glioblastoma Multiforme (GBM). Mesenchymal stem cells (MSCs) constitute a subpopulation of bone marrow derived cells which are actively recruited to the site of radiation and/or tumour microenvironment (TME), both of which have important implications for neovascularization and tumor progression. The goal of this project is to investigate the functional contribution of MSCs in the TME. We postulate that Bone Marrow-MSCs promote radio-resistance in GBM via cell cycle arrest. We tested the effect of MSC on U87 glioblastoma cell line in response to IR. We found that MSC co-culture, MSC-conditioned media (MSCCM) and irradiated MSC-conditioned media (MSCIRCM) did not reduce IR-induced p53 (ser15) phosphorylation, signifying intact p53-dependent DNA damage pathway in all conditions. However, both MSCCM and MSCIRCM temporally increased phospho-Chk2, a kinase involved in ATM-dependent cascade and cell cycle arrest. This increase occurred at 24 hours and reverted to baseline levels by 48 hours. Interestingly, IR (15Gy) caused transiently heightened metabolic rate under MSC and MSC IRCM as opposed to IR-null treatment at 48 hours elevated cell proliferation. MSCCM, but not MSCIRCM, marginally reduced caspase 3/7-dependent apoptotic levels. The combination of IR and MSCCM as well as MSCIRCM first increased protein level of phospho-Chk2 at 24 hours; followed by increased metabolic rate at 48 hours; and lastly, boosted proliferation at 72 hours. This data combined proposes plausible machinery for BM-MSC mediated radio-resistance by initiating cell cycle arrest in tumour cells for DNA damage repair.


2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Anh Thi Mai Nguyen ◽  
Ha Le Bao Tran ◽  
Thuy Anh Vu Pham

Objective. To access the effects of platelet-rich plasma (PRP) on the behaviour of human bone marrow-derived mesenchymal stem cells (hBMSCs), including proliferation and migration. Methods. PRP was diluted with DMEM/F12, resulting in concentrations of 1%, 2%, and 5%. The proliferation of hBMSCs was examined by 2 methods: cell-number counting with the haemocytometer method and the colony-forming unit-fibroblast (CFU-F) assay. Cell migration was evaluated using the scratch wound healing (SWH) assay; after that, the recorded digital images were analysed by the Image-Analysis J 1.51j8 software to compare the cell-free areas between groups after 0, 24, and 48 hours. Results. hBMSCs cultured in DMEM/F12 at PRP concentrations of 1%, 2%, and 5% were all able to proliferate and migrate. In the 5% PRP group, hBMSCs proliferated greatly with a significantly higher cell number than reported for all other groups on days 5, 7, and 9. CFU-Fs were observed in all groups, except for the negative control group. The SWH assay demonstrated that hBMSCs cultured in 2% and 5% PRP almost filled the artificial wound scratch and significantly migrated more than those of all other groups at both 24 h and 48 h. Conclusion. This study indicated that, due to the significant enhancement of cell proliferation and migration, 5% PRP might be the optimal concentration that should be used to promote the potential of hBMSCs in wound healing.


2012 ◽  
Vol 46 (2) ◽  
pp. 81-88 ◽  
Author(s):  
Bok-Nam Park ◽  
Wooyoung Shim ◽  
Young Hwan Ahn ◽  
Jae-Ho Lee ◽  
Young-Sil An ◽  
...  

2021 ◽  
Author(s):  
Xia Yi ◽  
Ping Wu ◽  
Jianyun Liu ◽  
Shan He ◽  
Ying Gong ◽  
...  

Adipogenesis and osteoblastogenesis (adipo-osteoblastogenesis) are closely related processes involving with the phosphorylation of numerous cytoplasmic proteins and key transcription factors.


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