Mineral trioxide aggregate enhances the osteogenic capacity of periodontal ligament stem cells via NF-κB and MAPK signaling pathways

2017 ◽  
Vol 233 (3) ◽  
pp. 2386-2397 ◽  
Author(s):  
Yanqiu Wang ◽  
Yixiang Zhou ◽  
Lin Jin ◽  
Xiyao Pang ◽  
Yadie Lu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Signaling Pathways ◽  
Periodontal Ligament ◽  
Mineral Trioxide Aggregate ◽  
Mapk Signaling ◽  
Periodontal Ligament Stem Cells ◽  
Mapk Signaling Pathways

scholarly journals Adenosine Triphosphate Prevents Serum Deprivation-Induced Apoptosis in Human Mesenchymal Stem Cells via Activation of the MAPK Signaling Pathways

Stem Cells ◽  
2014 ◽  
Vol 33 (1) ◽  
pp. 211-218 ◽  
Author(s):  
Jessica L. Berlier ◽  
Sabrina Rigutto ◽  
Antoine Dalla Valle ◽  
Jessica Lechanteur ◽  
Muhammad S. Soyfoo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathways ◽  
Adenosine Triphosphate ◽  
Human Mesenchymal Stem Cells ◽  
Mapk Signaling ◽  
Serum Deprivation ◽  
Induced Apoptosis ◽  
Mapk Signaling Pathways

Abstract 3392: Regulation and maintenance of cancer stem cells of glioblastoma multiforme: The role of mTOR/MAPK signaling pathways

2011 ◽  
Author(s):  
Marissa D. Friedman ◽  
Craig M. Shannon ◽  
Michael Tobias ◽  
Alex Braun ◽  
Raj Murali ◽  
...  
Keyword(s):  
Stem Cells ◽  
Glioblastoma Multiforme ◽  
Cancer Stem Cells ◽  
Signaling Pathways ◽  
Mapk Signaling ◽  
Mapk Signaling Pathways

scholarly journals Transcriptome analysis reveals the mechanism of stromal cell-derived factor-1 and exendin-4 synergistically promoted periodontal ligament stem cells osteogenic differentiation

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e12091
Author(s):  
Wenyan Kang ◽  
Lingqian Du ◽  
Qianyu Liang ◽  
Rui Zhang ◽  
Chunxu Lv ◽  
...  
Keyword(s):  
Stem Cells ◽  
Osteogenic Differentiation ◽  
Signaling Pathways ◽  
Periodontal Ligament ◽  
Stromal Cell ◽  
Expression Patterns ◽  
Gene Clusters ◽  
Gene Set Enrichment Analysis ◽  
Periodontal Ligament Stem Cells ◽  
Stromal Cell Derived Factor

Stromal cell-derived factor-1 (SDF-1) and Exendin-4 (EX-4) play beneficial roles in promoting periodontal ligament stem cells (PDLSCs) osteogenic differentiation, while the detailed mechanism has not been clarified. In this study, we aimed to evaluate the biological mechanism of SDF-1 and EX-4 alone or synergistic application in regulating PDLSCs differentiation by RNA-sequencing (RNA-seq). A total of 110, 116 and 109 differentially expressed genes (DEGs) were generated in osteogenic medium induced PDLSCs treated by SDF-1, EX-4, and SDF-1+EX-4, respectively. The DEGs in SDF-1 group were enriched in signal transduction related signaling pathways; the DEGs in EX-4 group were enriched in metabolism and biosynthesis-related pathways; and the DEGs generated in SDF-1+EX-4 group were mainly enriched in RNA polymerase II transcription, cell differentiation, chromatin organization, protein phosphorylation pathways. Based on Venn analysis, a total of 37 specific DEGs were identified in SDF-1+EX-4 group, which were mainly enriched in negative regulation of autophagy and cellular component disassembly signaling pathways. Short time-series expression miner (STEM) analysis grouped all expressed genes of PDLSCs into 49 clusters according to the dynamic expression patterns and 25 genes, including NRSN2, CHD9, TUBA1A, distributed in 10 gene clusters in SDF-1+EX-4 treated PDLSCs were significantly up-regulated compared with the SDF-1 and EX-4 alone groups. The gene set enrichment analysis indicated that SDF-1 could amplify the role of EX-4 in regulating varied signaling pathways, such as type II diabetes mellitus and insulin signaling pathways; while EX-4 could aggravate the effect of SDF-1 on PDLSCs biological roles via regulating primary immunodeficiency, tight junction signaling pathways. In summary, our study confirmed that SDF-1 and EX-4 combined application could enhance PDLSCs biological activity and promote PDLSCs osteogenic differentiation by regulating the metabolism, biosynthesis and immune-related signaling pathways.

scholarly journals The Conditioned Medium of Calcined Tooth Powder Promotes the Osteogenic and Odontogenic Differentiation of Human Dental Pulp Stem Cells via MAPK Signaling Pathways

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Jintao Wu ◽  
Na Li ◽  
Yuan Fan ◽  
Yanqiu Wang ◽  
Yongchun Gu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Signaling Pathways ◽  
Conditioned Medium ◽  
Dental Pulp ◽  
Mapk Signaling ◽  
Dental Pulp Stem Cells ◽  
Control Group ◽  
Odontogenic Differentiation ◽  
Human Dental Pulp ◽  
Mapk Signaling Pathways

The calcined tooth powder (CTP), a type of allogeneic biomimetic mineralized material, has been confirmed that can promote new bone formation when obtained at high temperature. The aim of this study was to investigate effects of the conditioned medium of calcined tooth powder (CTP-CM) on the osteogenic and odontogenic differentiation of human dental pulp stem cells (hDPSCs) and the underlying mechanisms involved. First, ALP activity assay determined that 200 μg/mL was the optimal concentration of CTP-CM for the following experiments. CTP-CM had no significant effect on the proliferation of hDPSCs as indicated by CCK-8 and FCM analysis. Both the gene and protein (DSPP/DSPP, RUNX2/RUNX2, OCN/OCN, OSX/OSX, OPN/OPN, ALP/ALP, and COL-1/COL-1) expression levels increased in the CTP-CM-induced hDPSC group as compared with those in the control group at day 3 or 7, showing the positive regulation of CTP-CM on the osteo/odontogenic differentiation of hDPSCs. Mechanistically, MAPK signaling pathways were activated after the CTP-CM treatment, and the inhibitors targeting MAPK were identified which weakened the effects of CTM-CM on the committed differentiation of hDPSCs. These findings could lead to the creation of stem cell therapies for dental regeneration.

scholarly journals SPARC promotes self-renewal of limbal epithelial stem cells and ocular surface restoration through JNK and p38-MAPK signaling pathways

Stem Cells ◽  
2019 ◽  
Vol 38 (1) ◽  
pp. 134-145 ◽  
Author(s):  
Jing Zhu ◽  
Le-yi Wang ◽  
Chong-yun Li ◽  
Jia-yin Wu ◽  
Yu-ting Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Ocular Surface ◽  
Mapk Signaling ◽  
Epithelial Stem Cells ◽  
Self Renewal ◽  
Limbal Epithelial Stem Cells ◽  
Mapk Signaling Pathways

scholarly journals Melatonin induces the rejuvenation of long-term ex vivo expanded periodontal ligament stem cells by modulating the autophagic process

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yi-Zhou Tan ◽  
Xin-Yue Xu ◽  
Ji-Min Dai ◽  
Yuan Yin ◽  
Xiao-Tao He ◽  
...  
Keyword(s):  
Stem Cells ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Cellular Senescence ◽  
Periodontal Ligament ◽  
Ex Vivo ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Periodontal Ligament Stem Cells

Abstract Background Stem cells that have undergone long-term ex vivo expansion are most likely functionally compromised (namely cellular senescence) in terms of their stem cell properties and therapeutic potential. Due to its ability to attenuate cellular senescence, melatonin (MLT) has been proposed as an adjuvant in long-term cell expansion protocols, but the mechanism underlying MLT-induced cell rejuvenation remains largely unknown. Methods Human periodontal ligament stem cells (PDLSCs) were isolated and cultured ex vivo for up to 15 passages, and cells from passages 2, 7, and 15 (P2, P7, and P15) were used to investigate cellular senescence and autophagy change in response to long-term expansion and indeed the following MLT treatment. Next, we examined whether MLT could induce cell rejuvenation by restoring the autophagic processes of damaged cells and explored the underlying signaling pathways. In this context, cellular senescence was indicated by senescence-associated β-galactosidase (SA-β-gal) activity and by the expression of senescence-related proteins, including p53, p21, p16, and γ-H2AX. In parallel, cell autophagic processes were evaluated by examining autophagic vesicles (by transmission electronic microscopy), autophagic flux (by assessing mRFP-GFP-LC3-transfected cells), and autophagy-associated proteins (by Western blot assay of Atg7, Beclin-1, LC3-II, and p62). Results We found that long-term in vitro passaging led to cell senescence along with impaired autophagy. As expected, MLT supplementation not only restored cells to a younger state but also restored autophagy in senescent cells. Additionally, we demonstrated that autophagy inhibitors could block MLT-induced cell rejuvenation. When the underlying signaling pathways involved were investigated, we found that the MLT receptor (MT) mediated MLT-related autophagy restoration by regulating the PI3K/AKT/mTOR signaling pathway. Conclusions The present study suggests that MLT may attenuate long-term expansion-caused cellular senescence by restoring autophagy, most likely via the PI3K/AKT/mTOR signaling pathway in an MT-dependent manner. This is the first report identifying the involvement of MT-dependent PI3K/AKT/mTOR signaling in MLT-induced autophagy alteration, indicating a potential of autophagy-restoring agents such as MLT to be used in the development of optimized clinical-scale cell production protocols.

scholarly journals Wharton Jelly Stem Cells inhibits AGS Gastric Cancer Cells through Induction of Apoptosis and Modification of MAPK and NF‑κB Signaling Pathways

2021 ◽  
Author(s):  
Samaneh Abbasi ◽  
Reza Bazyar ◽  
Mohammad Ali Saremi ◽  
Gholamhoseen Alishiri ◽  
Nasrin Seyyedsani ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cell Line ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Induction Of Apoptosis ◽  
Mapk Signaling Pathways

Abstract Background and aim: Gastric cancer) GC) is one of the most common cancer with high mortality worldwide. The human Wharton's jelly stem cells (hWJSCs) can inhibit several cancer cells through several molecular pathways. Therefore, the present study aimed to investigate anticancer effects of hWJSCs conditioned medium (hWJSC-CM) and cell-free lysate (hWJSC-CL) against of GC cell line AGS and underlying signaling pathways. Methods: In this study, we evaluated the effects of hWJSC-CM and hWJSC-CL on viability, proliferation, migration, invasion, apoptosis, and MAPK and NF‑κB signaling pathways in AGS cells. Moreover, mRNA expression of genes involved in apoptosis (BAX, BCL2, SMAC, and SURVIVIN), as well as expression of proteins involved in NF-κB and MAPK signaling pathways were evaluated. Results: The obtained results showed that the hWJSC-CM and hWJSC-CL decreased viability, migration, and invasion of GC cell line AGS in a concentration and time dependent manner. We observed that the hWJSC-CM and hWJSC-CL induced apoptosis pathway through regulation of apoptosis involved genes mRNA expression. In addition, the hWJSC-CM and hWJSC-CL suppressed NF-κB signaling pathways as well as promoted MAPK signaling pathways. Conclusions: In general, our study suggested that the hWJSC-CM and hWJSC-CL inhibits proliferation and viability of GC cell line AGS through induction of apoptosis, as well as modification of NF-κB and MAPK signaling pathways.

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