ArticleMolecular medicine reports2018
Tenascin‑C promotes the migration of bone marrow stem cells via toll‑like receptor 4‑mediated signaling pathways: MAPK, AKT and Wnt.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Protective Effects and Mechanisms of Extracellular Vesicles in Remote Ischemic Preconditioning on Renal Injury Induced by Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- The Role of Tenascin-C in Neuroinflammation and Neuroplasticity.International journal of molecular sciences · 2025Review
- The role of autophagy in cardiovascular disease: Cross-interference of signaling pathways and underlying therapeutic targets.Frontiers in cardiovascular medicine · 2023Review
- MicroRNA‑218 inhibits the malignant phenotypes of glioma by modulating the TNC/AKT/AP‑1/TGFβ1 feedback signaling loop.International journal of molecular medicine · 2021Article
- Metformin regulates inflammation and fibrosis in diabetic kidney disease through TNC/TLR4/NF-κB/miR-155-5p inflammatory loop.World journal of diabetes · 2021Article
- The Extracellular Matrix Glycoprotein Tenascin C and Adult Neurogenesis.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There are currently limitations in stem cell therapy due to the low rate of homing and proliferation of cells following transplantation. The present study was designed to investigate the effects of Tenascin‑C (TN‑C) on bone marrow mesenchymal stem cells (BMSCs) and its underlying mechanisms. BMSCs were obtained from C57BL/6 mice. The survival and proliferation of BMSCs was analyzed by Cell Counting Kit‑8 assay, migration was evaluated using the Transwell method, and differentiation was assessed by immunocytochemistry and immunofluorescence. In addition, the levels of proteins were detected by western blotting. High concentrations of TN‑C promoted the migration of BMSCs. H2O2 at concentrations of 60‑90 µmol/ml induced cell death in BMSCs, and thus, it was used to simulate oxidative stress in the microenvironment of acute myocardial infarction (AMI). High concentrations of TN‑C were able to protect BMSCs from cell death, and promoted the migration of BMSCs (P<0.05). However, TAK‑242 [the inhibitor of Toll‑like receptor 4, (TLR4)] reduced the promoting effect of TN‑C (P<0.05). By contrast, TN‑C had no effect on the proliferation and differentiation of BMSCs. TN‑C reduced the phosphorylation levels of p38 mitogen‑activated protein kinase (MAPK), and increased the phosphorylation levels of Ser473 protein kinase B (AKT) and β‑catenin, all of which were inhibited by TAK‑242 (P<0.05). In the simulated AMI microenvironment, TN‑C promoted the migration of BMSCs via TLR4‑mediated signaling pathways, including MAPK, AKT and Wnt.
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Registered trials
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