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2022 ◽  
Vol 12 (5) ◽  
pp. 978-983
Author(s):  
Shengdi Ding ◽  
Shitong Xing ◽  
Zhanfeng Zhang ◽  
Zhenguo Sun ◽  
Xiaojie Dou ◽  
...  

The menopausal hormone abnormal changes such as estrogen deficiency and increased FSH secretion in female patients in old age may cause osteoporosis which is plagued by patients. The pathogenesis of osteoporosis is not yet fully understood. BMP in the transforming growth factor-β superfamily is a key member in the process of bone growth and development, among which BMP-2 exerts critical roles. Impaired osteogenic differentiation of bone marrow mesenchymal stem cells (BMSC) contributes to the progress of osteoporosis. BMSC plays an indispensable role in treating osteoporosis and can develop into different directions through induction. As the regenerative medicine nanotechnology has become a new medical method, it is believed that BMSC can be used to treat osteoporosis and other related diseases. Our study analyzed the effects of BMP-2/estrogen composite nanoparticles on the proliferation and differentiation of osteoporotic BMSC cells to provide a reliable reference for the future treatment. Our results showed that BMP-2/estrogen composite nanoparticles promoted BMSC cell proliferation, increased ALP activity, decreased apoptosis rate, increased the expression of Col-1, Runx2 and Osterix, upregulated the osteogenic marker BMP-2. As confirmed by Alizarin Red staining, it could differentiate into osteoblasts and the content of Trap was decreased. In conclusion, our study confirms that BMP-2/estrogen composite nanoparticles can promote BMSC cell proliferation, osteogenic differentiation, and inhibit osteoclast differentiation, thereby providing new treatments and theoretical reference basis for treating osteoporosis.


2022 ◽  
Vol 12 (4) ◽  
pp. 854-861
Author(s):  
Jing Li ◽  
Bo Xie ◽  
Hu Wang ◽  
Chengsong Chen ◽  
Chengwu Pan ◽  
...  

Certain progress has been made in the therapeutic method against gastric cancer such as surgical operation combined with chemotherapy and radiation therapy in recent years. But the therapeutic efficacy and prognosis on gastric cancer was still not satisfactory. The function of exosome of miR-328–3p secreted by bone marrow stromal cells (BMSCs) on restraining the gastric cancer was studied in the present study. The BMSCs with highly-expressed miR-328-3p was established. The exosome in cell supernatant was collected. The exosome of BMSCs and MSCs with highlyexpressed miR-328-3p was added into SGC-7901 cells followed by analysis of miR-328-3p level by Real-time PCR and TFF3 (Trefoil Factor 3) level in exosome by Western blot, cell proliferation, expression of E-cadherin, Vimentin and Caspase-3. miR-328-39 expression was reduced and TFF3 was elevated in gastric cancer tissue (P < 0.05). miR-328-3p was upregulated and TFF3 was downregulated after addition of BMSCs exosomes along with increased cell proliferation and reduced E-cadherin and Caspase3 expression (P < 0.05). In conclusion, exosome of BMSCs could be regulated by miR-328-3p and TFF3 expression is restrained so as to regulate the biological behaviors of gastric cancer cell.


2022 ◽  
Vol 12 (4) ◽  
pp. 862-866
Author(s):  
Qiuxiang Ning ◽  
Fa Guo ◽  
Pengfei Xiao ◽  
Xiulan Liu ◽  
Ya Ding

The tumorigenesis mechanism of cervical cancer (CC) is complicated as several pathways deserve exploration. LncRNAs are recently highlighted to be involved in various biological processes. The role of bone marrow mesenchymal stem cells (BMSCs) in tumor regulation is recently investigated. Herein, we aimed to explore the interaction between lncRNA Neu and microRNA (miR)-625 and BMSCs in CC. Expression levels of lncRNA Neu and miR-625 in CC cells and BMSCs were determined by RT-qPCR. The relationship between lncRNA Neu and miR-625 was analyzed by Pearson correlation analysis. After cancer cells were transfected with siRNA-Neu, CCK-8 assay and clone formation assay were conducted to determine cell proliferation and viability. LncRNA Neu was highly expressed in CC cells and poorly expressed in BMSCs. Knockdown of lncRNA Neu attenuated cell viability and proliferation while increased miR-625 expression. MiR-625 expression was negatively correlated with expression of lncRNA Neu in CC cells. Overexpression of miR-625 resulted in weakened CC cell viability. Collectively, lncRNA Neu was highly expressed in CC and promoted the development of CC through stimulating the growth of BMSCs and suppressing miR-625 expression. These findings provide a novel insight into targeted therapy for CC.


2022 ◽  
Vol 12 (4) ◽  
pp. 695-700
Author(s):  
Xiumei He ◽  
Xiong Zhou ◽  
Yueyue Feng

This study intends to identify the expression profiles of micoRNAs during the recovery of damaged corneal epithelium induced by BMSCs. Differential expressions of miRNA after damage of corneal epithelium stimulated by BMSCs were analyzed based on micro-array and validated by qRT-PCR. The miRNA’s effect on cell proliferative and apoptotic activity was evaluated through transfection of plasmid with over presentation of miRNA and inhibitor of miRNA. miR-339 was significantly down-regulated in the process of recovery of the damaged corneal epithelium induced by BMSCs. Importin 13 and EGF expression was reduced after transfection of plasmid with over presentation of miR-339, which were reversed by transfection of the inhibitor of miR-339. Importin 13 was a target of miR-339. The cell proliferation and apoptosis could be restrained by miR-339 through regulation of the expression of Importin 13. In conclusion, the damaged corneal epithelium induced by BMSCs could be recovered by miR-339 through restraining Importin 13 expression, indicating that it might be a novel target for amelioration of corneal epithelium damage.


2022 ◽  
Vol 12 (4) ◽  
pp. 770-777
Author(s):  
Siyuan Chen ◽  
Weixiong Guo ◽  
Jinsong Wei ◽  
Han Lin ◽  
Fengyan Guo

Objective: The aim of this study was to explore the role of has_circ_0010452 in the progression of osteoporosis (OP) targeting miR-543, as well as their functions in regulating proliferation and osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs). Methods: The expression levels of circ_0010452 and miR-543 in hBMSCs at different time points of osteogenic differentiation were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). After transfection of circ_0010452 siRNA or miR-543 inhibitor in hBMSCs, the relative expression levels of osteogenic marker proteins, including oat spelt xylan (OSX), osteocalcin (OCN) and collagen I (Col-1), were determined by western blot. Cell proliferation of hBMSCs was valued by Cell Counting Kit 8 (CCK-8) assay. Dual-Luciferase reporter gene assay was performed to verify the relationship between circ_0010452 and miR-543. Subsequently, the regulatory effects of circ_0010452 and miR-543 on osteogenic differentiation and the capability of mineralization were evaluated by alkaline phosphatase (ALP) determination and alizarin red staining, respectively. Results: The expression of circ_0010452 decreased gradually and miR-543 increased in hBMSCs with the prolongation of osteogenic differentiation. circ_0010452 could bind to miR-543, which was negatively regulated by miR-543 in hBMSCs. Moreover, knockdown of circ_0010452 inhibited proliferation and osteogenic differentiation by upregulating miR-543, as well as upregulating expressions of OSX, OCN and Col-1. Furthermore, knockdown of circ_0010452 markedly promoted the capability of mineralization of hBMSCs, which was further reversed by transfection of miR-543 inhibitor. The knockdown of miR-543 partially reversed the inhibitory effect of circ_0010452 on the osteogenesis of hBMSCs. Conclusions: Silence of circ_0010452 promotes the development of OP via binding to miR-543 regulating proliferation and osteogenic differentiation of hBMSCs, thus promoting the progression of osteoporosis.


2022 ◽  
Vol 12 (3) ◽  
pp. 581-587
Author(s):  
Wenxu Rao ◽  
Kang Yin

This study aims at investigating the mechanism underlying bone marrow mesenchymal stem cells (BMSC) function in glioma. Glioma cells were administered with plasmids loading NF-κB siRNA, microRNA (miRNA)-189 inhibitor, or miR-189 mimics for transfection followed by analysis of miR-189 expression by RT-qPCR, cell apoptosis by flow cytometry, cell proliferation by MTT assay,invasion and migration by Transwell assay, inflammatory factors secretion by ELISA as well as proteins expression by western blot. A mouse model of glioma was established to detect the in vivo effect of BMSCs. miR-189 was lowly expressed in glioma cell lines but enriched in BMSCs. When miR-189 was silenced, cell proliferation, invasion and migration were potentiated and apoptosis was decreased, along with enhancement of N-cadherin, Vimentin, MMP-2 and and MMP-9, and decline in Bax, cleaved casepase-3 and cleaved PARP. Silencing of NF-κB reversed the effect of miR-189 inhibitor on cell progression, accompanied with reduction of inflammatory factors. BMSCs treatment effectively promoted miR-189 expression in glioma and inactivated TNF-α/NF-κB signaling, thereby suppressing tumor growth. In conclusion, miR-189 derived from BMSC inhibits glioma progression through regulation of TNF-α/NF-κB signaling pathway.


2022 ◽  
Vol 12 (3) ◽  
pp. 514-522
Author(s):  
Xiongsheng Xiao ◽  
Zhi Zhang ◽  
Hongpo Xie ◽  
Siyi Li ◽  
Jianwen Li

Our current study plans to dissect the impacts and its underlying mechanisms of bone marrow mesenchymal stem cells (BMSCs) on the invasive and metastatic features of PTC. Clinical specimens from distantly metastatic PTC were collected to measure DRR2 level. After being identified via tri-lineage differentiation and flow cytometry, BMSCs were co-cultured with PTC cells followed by analysis of cell proliferation and migration by CCK-8 and Transwell assays, expression of DDR2 and EMT-associated proteins by Western blot. Eventually, shDDR2-transfected BMSCs were infused with PTC cells into the abdominal cavity of mice to establish a mouse model assess their effect on tumor growth and distant metastasis. DDR2 was upregulated in BMSCs and malignant cells located in the metastatic sites. Co-culture with BMSCs enhanced DRR2 expression in PTC cells, which was simultaneously accompanied by the escalated mesenchymalization process. In vivo experiments exhibited that co-injection with BMSCs facilitated disease progression and distant metastasis of malignancies. Instead, DDR2 knockdown significantly impeded BMSCs-triggered migrative and proliferative behaviors of malignant cells. In conclusion, DDR2 derived from BMSCs can function as a communication mediator to strengthen the invasiveness and metastasis of PTC.


2022 ◽  
Vol 42 (3) ◽  
pp. 299-305
Author(s):  
Akriti G. Jain ◽  
Ling Zhang ◽  
John M. Bennett ◽  
Rami Komrokji

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