Bone marrow-derived mesenchymal stem cells mitigate caspase-3 and 8-hydroxy proline induced via β-adrenergic agonist in pulmonary injured rats

2017 ◽  
Vol 31 (8) ◽  
pp. e21913 ◽  
Author(s):  
Mai O Kadry ◽  
Rehab M Abdel-Megeed
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Caspase 3 ◽  
Adrenergic Agonist ◽  
Hydroxy Proline

Effect of αCGRP on Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells Through Smad/Runx2 Signaling Pathway

2020 ◽  
Vol 10 (6) ◽  
pp. 868-873
Author(s):  
Shengxiang Huang ◽  
Haibo Mei ◽  
Rongguo He ◽  
Kun Liu ◽  
Jin Tang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Real Time ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Alp Activity ◽  
Marrow Mesenchymal Stem Cells

The α-calcitonin gene-related peptide (α-CGRP) regulates bone metabolism and has potential applications in enhancing bone remodeling in vivo. However, α-CGRP's role in bone marrow mesenchymal stem cells (BMSCs) osteogenic differentiation remain unclear. Rat BMSCs were separated into control group, α-CGRP group and α-CGRP siRNA group, in which BMSCs were transfected with α-CGRP plasmid and α-CGRP siRNA respectively followed by analysis of α-CGRP level by real time PCR and ELISA, cell proliferation by MTT assay, Caspase 3 activity, ALP activity, formation of calcified nodules by alizarin red staining, Smad1 and Smad7 level by Western blot and Runx2 by real time PCR. αCGRP transfection into BMSCs significantly up-regulated CGRP, which could promote cell proliferation, inhibit Caspase 3 activity, promote ALP activity, increase calcified nodules formation and upregulate Smad1, Smad7 and Runx2 compared to control (P < 0.05); transfection of αCGRP siRNA significantly down-regulated CGRP in BMSCs, inhibited cell proliferation, promoted Caspase 3 activity, inhibited ALP activity, inhibited calcified nodules formation and downregulate Smad1, Smad7 and Runx2 (P < 0.05). αCGRP overexpression promotes the Smad/Runx2 signaling, which in turn promotes BMSCs proliferation and osteogenesis. Decreased αCGRP level inhibits Smad/Runx2 signaling, promotes BMSCs apoptosis, inhibits proliferation and osteogenic differentiation.

Effect of 25-Hydroxycholesterol on the Differentiation of Bone Marrow Mesenchymal Stem Cells Through Wnt5/TGF-β Signaling Pathway

2019 ◽  
Vol 9 (11) ◽  
pp. 1583-1588
Author(s):  
Shaoting Li ◽  
Jinhe Zhou ◽  
Zhiqing Ye ◽  
Shenglin Wu
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Control Group ◽  
Nodule Formation ◽  
Alp Activity ◽  
Marrow Mesenchymal Stem Cells

Bone marrow mesenchymal stem cells (BMSCs) can be multi-directionally differentiated and are widely used in tissue engineering. 25-hydroxycholesterol (25-HC) can induce osteogenesis and is involved in osteogenic formation. However, the role of 25-hydroxycholesterol in BMSCs is unclear. Rat BMSCs were isolated and divided into control group and 25-HC treatment (2 and 4 μM) group. Cell proliferation was detected by MTT assay. Caspase-3 and ALP activity was analyzed. Real time PCR was done to analyze Runx2, OPN, FABP4 and PPARγ2 expression. Red staining detects the calcified nodule formation. Wnt5 level was detected by western blot and TGF-β secretion was analyzed by ELISA. 25-HC treatment significantly inhibited cell proliferation, increased Caspase 3 activity, decreased ALP activity and the expression of Runx2 and OPN, increased expression of FABP4 and PPARγ2, decreased formation of calcified nodules, secretion of TGF-β and reduced expression of Wnt5 compared to control group (P < 0.05), and the above changes were significant with the increase of the concentration of 25-HC (P < 0.05). 25-hydroxycholesterol regulates the proliferation and apoptosis of BMSCs by regulating Wnt5/TGF-β signaling pathway, inhibiting the differentiation of BMSCs into osteogenic direction and promoting its adipogenic differentiation.

The Role of Integrin-Linked Kinase in Regulating Bone Differentiation of Metabolic Syndrome-Derived Bone Marrow Mesenchymal Stem Cells Through Autophagy

2019 ◽  
Vol 9 (9) ◽  
pp. 1266-1272
Author(s):  
Yonggang Zhang ◽  
Junqi Wang ◽  
Junqi Yang ◽  
Peng Liu ◽  
Kunzheng Wang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Caspase 3 ◽  
Diabetic Rat ◽  
Control Group ◽  
Marrow Mesenchymal Stem Cells ◽  
Integrin Linked Kinase ◽  
Apoptosis And Inflammation

Bone marrow mesenchymal stem cells (BMSCs) can differentiate into osteogenesis. Integrin-linked kinase (ILK) regulates several biological processes. However, whether ILK affects metabolic syndrome (MS)-derived BMSCs differentiation remains unclear. SD rats were divided into control group and MS group. Diabetic rat model was prepared. BMSCs were divided into control group, MS group and ILK group, in which ILK plasmid was transfected into BMSCs from MS group followed by analysis of ILK, Bcl-2, Bax, RUNX2 and OPN expression by real time PCR, BMSCs proliferation by MTT assay, BMSCs apoptosis, expression of Beclin-3 and LC-3 by Western blot as well as secretion of IL-1β and IL-6 by ELISA. MS group showed significantly reduced BMSCs proliferation, elevated Caspase 3 activity, downregulated Bcl-2, RUNX2 and OPN expression, upregulated Bax level and increased IL-1β and IL-6 secretion as well as decreased Beclin-3 and LC-3 expression compared to control group (P < 0.05). BMSCs with ILK overexpression in high glucose presented significantly promoted BMSCs proliferation, decreased Caspase 3 activity, increased Bcl-2, RUNX2 and OPN expression, decreased Bax expression and IL-1β and IL-6 secretion as well as reduced Beclin-3 and LC-3 expression compared to MS group (P < 0.05). ILK expression in MS-derived BMSCs is decreased. ILK overexpression in BMSCs can promote autophagy, inhibit apoptosis and inflammation, and promote their differentiation into osteoblasts.

scholarly journals Mesenchymal Stem Cells from Rat Bone Marrow Downregulate Caspase-3-mediated Apoptotic Pathway After Spinal Cord Injury in Rats

2007 ◽  
Vol 32 (12) ◽  
pp. 2080-2093 ◽  
Author(s):  
Venkata Ramesh Dasari ◽  
Daniel G. Spomar ◽  
Craig Cady ◽  
Meena Gujrati ◽  
Jasti S. Rao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Stem Cells ◽  
Bone Marrow ◽  
Spinal Cord Injury ◽  
Mesenchymal Stem Cells ◽  
Caspase 3 ◽  
Apoptotic Pathway ◽  
Cord Injury ◽  
Rat Bone

Effects of Melatonin on Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells in Inflammatory Environment by Regulating Mammalian Target of Rapamycin/Phosphatidylinositol 3-Kinase/Protein Kinase B Signaling

2021 ◽  
Vol 11 (4) ◽  
pp. 749-755
Author(s):  
Chi Zhang ◽  
Yuanhe Wang ◽  
Kang Sun ◽  
Dingzhu Yu ◽  
Shaoqi Tian
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Sod Activity ◽  
Alp Activity ◽  
Tnf Α ◽  
Marrow Mesenchymal Stem Cells

Human bone marrow mesenchymal stem cells (BMSCs) differentiation into special cell types is affected by inflammation. Melatonin has various effects such as anti-oxidation and immune regulation. However, melatonin’s effect on BMSCs osteogenic differentiation during inflammation has not been elucidated. Rat BMSCs were isolated and assigned into control group, inflammation group (1 μg/ml lipopolysaccharide, LPS) and melatonin group (100 μM melatonin was added to LPSstimulated BMSCs cells) followed by analysis of BMSCs proliferation by MTT assay, Caspase 3 and ALP activity, expression of Runx2 and OP by Real time PCR, ROS content and SOD activity, TNF-α and IL-1β secretion by ELISA and mTOR/PI3K/AKT signaling protein level by Western blot. LPS action on BMSCs significantly inhibits BMSCs proliferation, promotes Caspase 3 activity, inhibits ALP activity, decreases Runx2 and OP expression and SOD activity, increases ROS content and TNF-α and IL-1β secretion as well as reduced mTOR and p-PI3K level (P <0.05). Melatonin addition significantly reversed the above changes (P <0.05). Melatonin can regulate oxidative stress, inhibit inflammation, and promote BMSCs proliferation and osteogenic differentiation in inflammatory environment by activating mTOR/PI3K/AKT signaling pathway.

CXCR4-overexpressing bone marrow-derived mesenchymal stem cells improve repair of acute kidney injury

2013 ◽  
Vol 305 (7) ◽  
pp. F1064-F1073 ◽  
Author(s):  
Nanmei Liu ◽  
Andreas Patzak ◽  
Jinyuan Zhang
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Acute Kidney Injury ◽  
Cell Death ◽  
Mesenchymal Stem Cells ◽  
Renal Function ◽  
Caspase 3 ◽  
Kidney Injury ◽  
Nuclear Antigen ◽  
Tubular Cells

Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) can repair acute kidney injury (AKI), but with limited effect. We test the hypothesis that CXCR4 overexpression improves the repair ability of BMSCs and that this is related to increased homing of BMSCs and increased release of cytokines. Hypoxia/reoxygenation-pretreated renal tubular epithelial cells (HR-RTECs) were used. BMSCs, null-BMSCs, and CXCR4-BMSCs were cocultured with HR-RTECs. The number of migrating BMSCs was counted. Proliferating cell nuclear antigen (PCNA) expression, cell death, and expressions of cleaved caspase-3 and Bcl-2 in cocultured HR-RTECs were measured. Cytokeratin 18 (CK18) expression and cytokine secretions of the BMSCs cultured with HR-RTEC supernatant were detected. BMSC homing, renal function, proliferation, and cell death of tubular cells were assayed in the AKI mouse model. CXCR4-BMSCs showed a remarkable expression of CXCR4. Stromal cell-derived factor-1 in the HR-RTEC supernatant was increased. Migration of BMSCs was CXCR4-dependent. Proportions of CK18+ cells in BMSCs, null-BMSCs, and CXCR4-BMSCs showed no difference. However, CXCR4 overexpression in BMSCs stimulated secretion of bone morphogenetic protein-7, hepatocyte growth factor, and interleukin 10. The neutralizing anti-CXCR4 antibody AMD3100 abolished this. In cocultured HR-RTECs the proportions of PCNA+ cells and Bcl-2 expression were enhanced; however, the proportion of annexin V+ cells and expression of cleaved caspase-3 were reduced. The in vivo study showed increased homing of CXCR4-BMSCs in kidneys, which was associated with improved renal function, reduced acute tubular necrosis scoring, accelerated mitogenic response of tubular cells, and reduced tubular cell death. The enhanced homing and paracrine actions of BMSCs with CXCR4 overexpression suggest beneficial effects of such cells in BMSC-based therapy for AKI.

Effect of LncRNA DGCR5 on Bone Marrow Mesenchymal Stem Cells of Osteoporosis Rats Through Regulation of ERK/P38 Signaling Pathway

2019 ◽  
Vol 9 (11) ◽  
pp. 1589-1594
Author(s):  
Xu Tong ◽  
Renjian Zheng ◽  
Linjing Shu
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Control Group ◽  
Alp Activity ◽  
Marrow Mesenchymal Stem Cells

Bone marrow mesenchymal stem cells (BMSCs) osteogenic differentiation plays an important role in Osteoporosis (OP). LncRNA DGCR5 participates in OP development. However, LncRNA DGCR5's effect on BMSCs in osteoporosis rats and related mechanisms have not been elucidated. SD rats were divided into control group and OP group. Rat BMSCs were cultured and transfected with LncRNA DGCR5 siRNA followed by analysis of LncRNA DGCR5 expression by Real time PCR, cell proliferation by MTT assay, Caspase 3 activity, of ERK/P38 signaling pathway protein expression by Western blot, ALP activity, and the osteogenic genes Runx2 and OC expression by Real time PCR. LncRNA DGCR51 expression was increased in BMSCs of OP rats. Compared with control group, cell proliferation was significantly inhibited, Caspase 3 activity was increased, p-ERK1/2 and p-P38 were downregulated, ALP activity, Runx2 and OC expression was decreased (P < 0.05). DGCR51 siRNA transfection into OP rat BMSCs significantly reduced DGCR51 expression, promoted cell proliferation, decreased Caspase 3 activity, increased p-ERK1/2 and p-P38 expression, increased ALP activity, Runx2 and OC expression compared to OP group (P < 0.05). LncRNA DGCR51 expression is increased in OP rat BMSCs. Down-regulation of LncRNA DGCR51 promoted the activation of ERK/P38 signaling pathway, thereby inhibiting the apoptosis of BMSCs and promoting proliferation and osteogenic differentiation of BMSC in OP rats.

Protective mechanisms of melatonin against hydrogen-peroxide-induced toxicity in human bone-marrow-derived mesenchymal stem cells

2017 ◽  
Vol 95 (7) ◽  
pp. 773-786 ◽  
Author(s):  
Saeed Mehrzadi ◽  
Majid Safa ◽  
Seyed Kamran Kamrava ◽  
Radbod Darabi ◽  
Parisa Hayat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Inflammatory Cytokines ◽  
Caspase 3 ◽  
Ros Generation ◽  
Protective Agent ◽  
Antioxidant Power

Many obstacles compromise the efficacy of bone marrow mesenchymal stem cells (BM-MSCs) by inducing apoptosis in the grafted BM-MSCs. The current study investigates the effect of melatonin on important mediators involved in survival of BM-MSCs in hydrogen peroxide (H2O2) apoptosis model. In brief, BM-MSCs were isolated, treated with melatonin, and then exposed to H2O2. Their viability was assessed by MTT assay and apoptotic fractions were evaluated through Annexin V, Hoechst staining, and ADP/ATP ratio. Oxidative stress biomarkers including ROS, total antioxidant power (TAP), superoxide dismutase (SOD) and catalase (CAT) activity, glutathione (GSH), thiol molecules, and lipid peroxidation (LPO) levels were determined. Secretion of inflammatory cytokines (TNF-α and IL-6) were measured by ELISA assay. The protein expression of caspase-3, Bax, and Bcl-2, was also evaluated by Western blotting. Melatonin pretreatment significantly increased viability and decreased apoptotic fraction of H2O2-exposed BM-MSCs. Melatonin also decreased ROS generation, as well as increasing the activity of SOD and CAT enzymes and GSH content. Secretion of inflammatory cytokines in H2O2-exposed cells was also reduced by melatonin. Expression of caspase-3 and Bax proteins in H2O2-exposed cells was diminished by melatonin pretreatment. The findings suggest that melatonin may be an effective protective agent against H2O2-induced oxidative stress and apoptosis in MSC.

Effect of Chordin-Like 1 on Differentiation of Bone Marrow Mesenchymal Stem Cells Through Wnt5/TGF-β Signaling Pathway

2019 ◽  
Vol 9 (9) ◽  
pp. 1304-1310
Author(s):  
Qing Yang ◽  
Lei Wu ◽  
Yang Liu ◽  
Bing Yuan
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Control Group ◽  
Alp Activity ◽  
Marrow Mesenchymal Stem Cells

Chordin-like 1 (CHRDL1) functions in multiple tissues and organs. However, whether CHRDL1 affects bone marrow mesenchymal stem cells (BMSCs) differentiation remain unclear. Rat BMSCs were isolated and divided into control group, CHRDL1 group and CHRDL1 siRNA group followed by analysis of CHRDL1 level by real time PCR and ELISA, cell proliferation by MTT assay, Caspase 3 activity, ALP activity, expression of o Runx2, OC and PPARγ2 by Real time PCR, TGF-β secretion by ELIS, and Wnt5 protein expression by Western blot. CHRDL1 expression was significantly increased in CHRDL1 group, along with significantly promoted cell proliferation, decreased Caspase 3 activity, increased ALP activity and expression of Runx2 and OC, decreased PPARγ2 expression, increased TGF-β secretion and Wnt5 expression compared to control group (P < 0.05). However, CHRDL1 siRNA transfection significantly decreased CHRDL1 expression, inhibited cell proliferation, increased Caspase 3 activity, decreased ALP activity and Runx2 and OC expression, increased PPARγ2 expression, decreased TGF-β secretion and Wnt5 expression. (P < 0.05). Down-regulation of CHRDL1 expression in BMSCs promotes Wnt5/TGF-β signaling transduction, which in turn increases BMSCs proliferation and osteogenic differentiation. Up-regulation of CHRDL1 expression in BMSCs inhibited the activation of Wnt5/TGF-β signaling pathway, promoted BMSCs apoptosis, and inhibited BMSCs proliferation and osteogenic differentiation.

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