Periostin promotes migration and osteogenic differentiation of human periodontal ligament mesenchymal stem cells via the Jun amino-terminal kinases (JNK) pathway under inflammatory conditions

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Abstract

Mesenchymal stem cell ( MSC )‐mediated periodontal tissue regeneration is considered to be a promising method for periodontitis treatment. The molecular mechanism of functional regulation by MSC s remains unclear, thus limiting their application. Our previous study discovered that Periostin ( POSTN ) promoted the migration and osteogenic differentiation of periodontal ligament mesenchymal stem cells ( PDLSC s), but it is still unclear whether POSTN is able to restore the regenerative potential of PDLSC s under inflammatory conditions. In this study, we investigated the effect of POSTN on PDLSC s under inflammatory conditions and its mechanism. PDLSC s were isolated from periodontal ligament tissue. TNF ‐α was used at 10 ng/ mL to mimic inflammatory conditions. Lentivirus POSTN sh RNA was used to knock down POSTN . Recombinant human POSTN (rh POSTN ) was used to stimulate PDLSC s. A scratch assay was used to analyse cell migration. Alkaline phosphatase ( ALP ) activity, Alizarin Red staining and expression of osteogenesis‐related genes were used to investigate the osteogenic differentiation potential. Western blot analysis was used to detect the mitogen‐activated protein kinases ( MAPK ) and AKT signalling pathways. After a 10 ng/mL TNF ‐α treatment, knockdown of POSTN impeded scratch closure, inhibited ALP activity and mineralization in vitro, and decreased expression of RUNX 2, OSX , OPN and OCN in PDLSC s, while 75 ng/mL rh POSTN significantly accelerated scratch closure, enhanced ALP activity and mineralization in vitro, and increased expression of RUNX 2, OSX , OPN and OCN . In addition, knockdown of POSTN inhibited expression of phosphorylated c‐Jun N‐terminal kinase (p‐ JNK ), while 75 ng/mL rh POSTN increased expression of p‐ JNK in PDLSC s with TNF ‐α treatment. Furthermore, inhibition of JNK by its inhibitor SP 600125 dramatically blocked POSTN ‐enhanced scratch closure, ALP activity and mineralization in PDLSCs. Our results revealed that POSTN might promote the migration and osteogenic differentiation potential of PDLSC s via the JNK pathway, providing insight into the mechanism underlying MSC biology under inflammatory conditions and identifying a potential target for improving periodontal tissue regeneration.

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Yu-Chen Sun, Wen-Zhou Liu, Tao Liu … (2015)

The generic mitogen-activated protein kinases (MAPK) signaling pathway is shared by four distinct cascades, including the extracellular signal-related kinases (ERK1/2), Jun amino-terminal kinases (JNK1/2/3), p38-MAPK and ERK5. Mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) pathway is reported to be associated with the cell proliferation, differentiation, migration, senescence and apoptosis. The literatures were searched extensively and this review was performed to review the role of MAPK/ERK signaling pathway in cell proliferation, differentiation, migration, senescence and apoptosis.

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Periostin is required for maturation and extracellular matrix stabilization of noncardiomyocyte lineages of the heart.

Suzanne Field, Donald Menick, Tara Lindsley … (2008)

The secreted periostin protein, which marks mesenchymal cells in endocardial cushions following epithelial-mesenchymal transformation and in mature valves following remodeling, is a putative valvulogenesis target molecule. Indeed, periostin is expressed throughout cardiovascular morphogenesis and in all 4 adult mice valves (annulus and leaflets). Additionally, periostin is expressed throughout the fibrous cardiac skeleton and endocardial cushions in the developing heart but is absent from both normal and/or pathological mouse cardiomyocytes. Periostin (peri(lacZ)) knockout mice exhibit viable valve disease, with neonatal lethality in a minority and latent disease with leaflet abnormalities in the viable majority. Surviving peri(lacZ)-null leaflets are truncated, contain ectopic cardiomyocytes and smooth muscle, misexpress the cartilage proteoglycan aggrecan, demonstrate disorganized matrix stratification, and exhibit reduced transforming growth factor-beta signaling. Neonatal peri(lacZ) nulls that die (14%) display additional defects, including leaflet discontinuities, delamination defects, and deposition of acellular extracellular matrix. Assessment of collagen production, 3D lattice formation ability, and transforming growth factor-beta responsiveness indicate periostin-deficient fibroblasts are unable to support normal valvular remodeling and establishment of a mature cardiac skeleton. Furthermore, pediatric stenotic bicuspid aortic valves that have lost normal extracellular matrix trilaminar stratification have greatly reduced periostin. This suggests that loss of periostin results in inappropriate differentiation of mesenchymal cushion cells and valvular abnormalities via a transforming growth factor-beta-dependent pathway during establishment of the mature heart. Thus, peri(lacZ) knockouts provide a new model of viable latent valve disease.