2020
DOI: 10.1016/j.diff.2020.05.002
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Laminins in osteogenic differentiation and pluripotency maintenance

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Cited by 17 publications
(10 citation statements)
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“…N-cadherin is a key factor in directing cell–cell interaction during the mesenchymal condensation and it is also considered as a mimetic peptide that enhanced the osteogenic differentiation of the MSCs, leading to bone matrix deposition on the titanium implants [ 51 ]. Laminins are glycoproteins and major structural components in the basal lamina and showed a critical role to cell adhesion, differentiation and migration [ 52 ].…”
Section: Discussionmentioning
confidence: 99%
“…N-cadherin is a key factor in directing cell–cell interaction during the mesenchymal condensation and it is also considered as a mimetic peptide that enhanced the osteogenic differentiation of the MSCs, leading to bone matrix deposition on the titanium implants [ 51 ]. Laminins are glycoproteins and major structural components in the basal lamina and showed a critical role to cell adhesion, differentiation and migration [ 52 ].…”
Section: Discussionmentioning
confidence: 99%
“…The FAK/PI3K/AKT signaling pathways could play a crucial role in promoting osteogenic differentiation. [34][35][36] For example, Liu et al reported that platelet-rich plasma (PRP) could improve the healing effect of mandibular alveolar bone defects by activating the FAK/PI3K/ AKT signaling pathways. 37 Schreiber et al reported that disorders of FAK/PI3K/AKT signaling would inhibit the differentiation of MSCs to osteoblasts.…”
Section: Discussionmentioning
confidence: 99%
“…In addition, integrin-ECM interaction was identified to be capable of triggering the signaling mechanism of osteoblast specific gene expression. For instance, integrin α5 in the ECM bound to intracellular protein kinases and phosphatases such as focal adhesion kinase (FAK) and PI3K, and participated in signal transduction through PI3K-Akt pathway, which could activate the phosphorylation levels of Runx2 and promoted osteogenic gene levels. , Moreover, the ECM can also activate the FAK-ERK signaling pathway through integrin α2, upregulate the expression of Runx2 and ALP, and induce osteoblastic differentiation. ,, By comparing the osteogenic differentiation ability of MSCs on ECM with different stiffness, the important regulation of the classical Wnt/β-catenin pathway in ECM-induced osteogenic differentiation is noted …”
Section: Discussionmentioning
confidence: 99%
“…41,42 Moreover, the ECM can also activate the FAK-ERK signaling pathway through integrin α2, upregulate the expression of Runx2 and ALP, and induce osteoblastic differentiation. 41,43,44 By comparing the osteogenic differentiation ability of MSCs on ECM with different stiffness, the important regulation of the classical Wnt/β-catenin pathway in ECM-induced osteogenic differentiation is noted. 41 Overall, it would be confidently stated that ECM/PLGA scaffolds contained a variety of active ECM components and could upregulate the expressions of Runx2, BSP, OPN, OCN, and endogenous growth factors by activating one or more signal pathways such as the MAPK pathway, integrin-dependent pathway, Wnt/catenin pathway, and BMP/Smad pathway, thereby enhancing the osteogenic differentiation of MSCs (the possible regulatory mechanism of ECM on osteoblastogenesis is shown in Figure 11).…”
Section: ■ Materials and Methodsmentioning
confidence: 99%