Periostin improves cell adhesion to implantable biomaterials and osteoblastic differentiation on implant titanium surfaces in a topography-dependent fashion
Abstract:Periostin is a matricellular protein highly expressed in periodontal ligament and periostium and has been shown to be required for tissue development and maintenance. We showed that the adhesion of murine osteoblastic MC3T3 cells to thiolated hyaluronic acid/polyethyleneglycol hydrogels was greatly improved by enrichment with periostin. Polished or sand-blasted/acid-etched (SLA) commercially pure titanium surfaces were also coated with this protein and periostin ameliorated cell adhesion and dramatically affec… Show more
“…The function of POSTN as an ECM protein in bone formation has been determined recently. POSTN is a secreted protein that is highly expressed in MSCs/preosteoblasts and supports cell adhesion, spreading, and differentiation [ 18 ]. In addition, expression of integrin α v β 3, the receptor of POSTN, has been observed in MSCs/preosteoblasts [ 19 , 20 ].…”
Erythropoietin-producing hepatocyte B4 (EphB4) has been reported to be a key molecular switch in the regulation of bone homeostasis, but the underlying mechanism remains poorly understood. In this study, we investigated the role of EphB4 in regulating the expression of periostin (POSTN) within bone marrow-derived mesenchymal stem cells (MSCs) and assessed its effect and molecular mechanism of osteogenic induction in vitro. Treatment with ephrinB2-FC significantly increased the expression of POSTN in MSCs, and the inhibition of EphB4 could abrogate this effect. In addition, osteogenic markers were upregulated especially in MSCs overexpressing EphB4. To elucidate the underlying mechanism of cross talk between EphB4 and the Wnt pathway, we detected the change in protein expression of phosphorylated-glycogen synthase kinase 3β-serine 9 (p-GSK-3β-Ser9) and β-catenin, as well as the osteogenic markers Runx2 and COL1. The results showed that GSK-3β activation and osteogenic marker expression levels were downregulated by ephrinB2-FC treatment, but these effects were inhibited by blocking integrin αvβ3 in MSCs. Our findings demonstrate that EphB4 can promote osteogenic differentiation of MSCs via upregulation of POSTN expression. It not only helps to reveal the interaction mechanism between EphB4 and Wnt pathway but also brings a better understanding of EphB4/ephrinB2 signaling in bone homeostasis.
“…The function of POSTN as an ECM protein in bone formation has been determined recently. POSTN is a secreted protein that is highly expressed in MSCs/preosteoblasts and supports cell adhesion, spreading, and differentiation [ 18 ]. In addition, expression of integrin α v β 3, the receptor of POSTN, has been observed in MSCs/preosteoblasts [ 19 , 20 ].…”
Erythropoietin-producing hepatocyte B4 (EphB4) has been reported to be a key molecular switch in the regulation of bone homeostasis, but the underlying mechanism remains poorly understood. In this study, we investigated the role of EphB4 in regulating the expression of periostin (POSTN) within bone marrow-derived mesenchymal stem cells (MSCs) and assessed its effect and molecular mechanism of osteogenic induction in vitro. Treatment with ephrinB2-FC significantly increased the expression of POSTN in MSCs, and the inhibition of EphB4 could abrogate this effect. In addition, osteogenic markers were upregulated especially in MSCs overexpressing EphB4. To elucidate the underlying mechanism of cross talk between EphB4 and the Wnt pathway, we detected the change in protein expression of phosphorylated-glycogen synthase kinase 3β-serine 9 (p-GSK-3β-Ser9) and β-catenin, as well as the osteogenic markers Runx2 and COL1. The results showed that GSK-3β activation and osteogenic marker expression levels were downregulated by ephrinB2-FC treatment, but these effects were inhibited by blocking integrin αvβ3 in MSCs. Our findings demonstrate that EphB4 can promote osteogenic differentiation of MSCs via upregulation of POSTN expression. It not only helps to reveal the interaction mechanism between EphB4 and Wnt pathway but also brings a better understanding of EphB4/ephrinB2 signaling in bone homeostasis.
“…Artificial matrices derived from tissues with cells either lacking or overexpressing a particular matricellular molecule could direct host cellular responses via alteration of tissue repair processes such as angiogenesis, matrix assembly, and myofibroblast induction ( Barker et al, 2005b ; Elliott et al, 2012 ; Calabro et al, 2014 ; Morris and Kyriakides, 2014 -in this issue). For example, coating either smooth or etched titanium implants with periostin increased cell adhesion as compared to metal surfaces without periostin, although periostin only improved osteoblastic differentiation of cells adherent to smooth titanium surface, suggesting that perhaps the surface bound conformation of periostin can differentially regulate cell behavior ( Galli et al, 2013 ). One can also take advantage of sequence-specific matricellular interactions with growth factors or receptors to target molecules to biologic scaffolds: one of the TGF-β binding motifs of TSP-1 (GGWSHW) was coupled to a scaffold to localize TGF-β to hydrogels for local growth factor delivery ( McCall et al, 2011 ).…”
Section: Matricellular Proteins In Tissue Engineering and Responsementioning
The concept of a matricellular protein was first proposed by Paul Bornstein in the mid-1990s to account for the non-lethal phenotypes of mice with inactivated genes encoding thrombospondin-1, tenascin-C, or SPARC. It was also recognized that these extracellular matrix proteins were primarily counter or de-adhesive. This review reappraises the matricellular concept after nearly two decades of continuous investigation. The expanded matricellular family as well as the diverse and often unexpected functions, cellular location, and interacting partners/receptors of matricellular proteins are considered. Development of therapeutic strategies that target matricellular proteins are discussed in the context of pathology and regenerative medicine.
“…Interestingly, Postn is highly expressed in human BMSCs and their derived adipocytes, chondrocytes, and osteoblasts [26,27]. Postn is a secreted protein that is highly expressed in MSCs/preosteoblasts and supports cell adhesion, spreading, and differentiation [28]. Heo et al [29] found that delivery of recombinant Postn to human adipose tissue-derived MSCs embedded within a hydroxyapatite/tricalcium phosphate scaffold can accelerate healing of calvarial defects.…”
Perimenopausal period causes a significant amount of bone loss, which results in
primary osteoporosis (OP). The Periostin (Postn) may play important roles in the
pathogenesis of OP after ovariectomized (OVX) rats. To identify the roles of
Postn in the bone marrow mesenchymal stem cell derived osteoblasts (BMSC-OB) in
OVX rats, we investigated the expression of Wnt/β-catenin
signaling pathways in BMSC-OB and the effects of Postn on bone formation by
development of BMSC-OB cultures. Twenty-four female Sprague–Dawley rats
at 6 months were randomized into 3 groups: sham-operated (SHAM) group, OVX group
and OVX+Postn group. The rats were killed after 3 months, and their
bilateral femora and tibiae were collected for BMSC-OB culture, Micro-CT
Analysis, Bone Histomorphometric Measurement, Transmission Electron Microscopy
and Immunohistochemistry Staining. The dose/time-dependent effects of
Postn on the proliferation, differentiation and mineralization of BMSC-OB and
the expression of osteoblastic markers were measured in in vitro experiments. We
found increased Postn increased bone mass, promoted bone formation of
trabeculae, Wnt signaling and the osteogenic activity in osteoblasts in
sublesional femur. Postn have the function to enhance cell proliferation,
differentiation and mineralization at a proper concentration and incubation
time. Interestingly, in BMSC-OB from OVX rats treated with the different dose of
Postn, the osteoblastic markers expression and Wnt/β-catenin
signaling pathways were significantly promoted. The direct effect of Postn may
lead to inhibit excessive bone resorption and increase bone formation through
the Wnt/β-catenin signaling pathways after OVX. Postn may play a
very important role in the pathogenesis of OP after OVX.
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