scholarly journals Erratum to “Vitamin D Promotes MSC Osteogenic Differentiation Stimulating Cell Adhesion and αVβ3 Expression”

2018 ◽  
Vol 2018 ◽  
pp. 1-1
Author(s):  
Francesca Posa ◽  
Adriana Di Benedetto ◽  
Elisabetta A. Cavalcanti-Adam ◽  
Graziana Colaianni ◽  
Chiara Porro ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cell Adhesion ◽  
Osteogenic Differentiation

scholarly journals Vitamin D Promotes MSC Osteogenic Differentiation Stimulating Cell Adhesion and αVβ3 Expression

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Francesca Posa ◽  
Adriana Di Benedetto ◽  
Elisabetta A. Cavalcanti-Adam ◽  
Graziana Colaianni ◽  
Chiara Porro ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cell Adhesion ◽  
Osteogenic Differentiation ◽  
Matrix Protein ◽  
Active Form ◽  
Focal Adhesions ◽  
Supporting Cell ◽  
Integrin Expression ◽  
Dihydroxyvitamin D ◽  
Cell Commitment

Vitamin D (Vit D) by means of its biological active form, 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3), has a protective effect on the skeleton by acting on calcium homeostasis and bone formation. Furthermore, Vit D has a direct effect on mesenchymal stem cells (MSCs) in stimulating their osteogenic differentiation. In this work, we present for the first time the effect of 1,25(OH)2D3 on MSC adhesion. Considering that cell adhesion to the substrate is fundamental for cell commitment and differentiation, we focused on the expression of αVβ3 integrin, which has a key role in the commitment of MSCs to the osteoblastic lineage. Our data indicate that Vit D increases αVβ3 integrin expression inducing the formation of focal adhesions (FAs). Moreover, we assayed MSC commitment in the presence of the extracellular matrix (ECM) glycoprotein fibronectin (FN), which is able to favor cell adhesion on surfaces and also to induce osteopontin (OPN) expression: this suggests that Vit D and FN synergize in supporting cell adhesion. Taken together, our findings provide evidence that Vit D can promote osteogenic differentiation of MSCs through the modulation of αVβ3 integrin expression and its subcellular organization, thus favoring binding with the matrix protein (FN).

scholarly journals Testing the in vitro performance of hydroxyapatite coated magnesium (AZ91D) and titanium concerning cell adhesion and osteogenic differentiation

2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Claudia Kleinhans ◽  
Gabriele Vacun ◽  
Roman Surmenev ◽  
Maria Surmeneva ◽  
Petra Juliane Kluger
Keyword(s):  
Cell Adhesion ◽  
Osteogenic Differentiation ◽  
Cell Attachment ◽  
Human Mesenchymal Stem Cell ◽  
Adhesion Properties ◽  
Sputtering Deposition ◽  
Initial Cell ◽  
Tissue Culture Polystyrene ◽  
Diffraction Patterns

AbstractIn the current study the in vitro outcome of a degradable magnesium alloy (AZ91D) and standard titanium modified by nanostructured-hydroxyapatite (n-HA) coatings concerning cell adhesion and osteogenic differentiation was investigated by direct cell culture. The n-HA modification was prepared via radio-frequency magnetron sputtering deposition and proven by field emission scanning electron microscopy and X-ray powder diffraction patterns revealing a homogenous surface coating. Human mesenchymal stem cell (hMSCs) adhesion was examined after one and 14 days displaying an enhanced initial cell adhesion on the n-HA modified samples. The osteogenic lineage commitment of the cells was determined by alkaline phosphatase (ALP) quantification. On day one n-HA coated AZ91D exhibited a comparable ALP expression to standard tissue culture polystyrene samples. However, after 14 days solely little DNA and ALP amounts were measurable on n-HA coated AZ91D due to the lack of adherent cells. Titanium displayed excellent cell adhesion properties and ALP was detectable after 14 days. An increased pH of the culture was measured for AZ91D as well as for n-HA coated AZ91D. We conclude that n-HA modification improves initial cell attachment on AZ91D within the first 24 h. However, the effect does not persist for 14 days in in vitro conditions.

KR-12 coating of polyetheretherketone (PEEK) surface via polydopamine improves osteointegration and antibacterial activity in vivo

2020 ◽  
Vol 8 (44) ◽  
pp. 10190-10204
Author(s):  
Xiangchao Meng ◽  
Jue Zhang ◽  
Jun Chen ◽  
Binen Nie ◽  
Bing Yue ◽  
...  
Keyword(s):  
Antibacterial Activity ◽  
Cell Adhesion ◽  
Osteogenic Differentiation ◽  
Material Surface

KR-12 was grafted onto the surface of PEEK, which improved the hydrophilicity of the material surface, promoted cell adhesion, osteogenic differentiation and osseointegration, while also endowing the appreciable antibacterial activity on the material surface.

Zwitterionic PMCP‐Modified Polycaprolactone Surface for Tissue Engineering: Antifouling, Cell Adhesion Promotion, and Osteogenic Differentiation Properties

Small ◽  
2019 ◽  
Vol 15 (42) ◽  
pp. 1903784 ◽  
Author(s):  
Xingyu Chen ◽  
Zaifu Lin ◽  
Ying Feng ◽  
Hong Tan ◽  
Xinyuan Xu ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Cell Adhesion ◽  
Osteogenic Differentiation ◽  
Adhesion Promotion

Cell adhesion and osteogenic differentiation on three-dimensional pillar surfaces

2012 ◽  
Vol 101A (3) ◽  
pp. 842-852 ◽  
Author(s):  
Emilia Kaivosoja ◽  
Pia Suvanto ◽  
Gonçalo Barreto ◽  
Susanna Aura ◽  
Antti Soininen ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Osteogenic Differentiation ◽  
Three Dimensional

The Increased 1,25-(OH)2D3 Sensitivity of Myeloma Cells and Marrow Stromal Cells Enhances RANKL Production and Tumor Cell Growth

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3946-3946
Author(s):  
Jumpei Teramachi ◽  
Noriyoshi Kurihara ◽  
John M Chirgwin ◽  
G David Roodman
Keyword(s):  
Vitamin D ◽  
Cell Adhesion ◽  
Cell Growth ◽  
Stromal Cells ◽  
Marrow Stromal Cells ◽  
Integrin Expression ◽  
Myeloma Cells ◽  
Low Levels ◽  
Adhesive Interactions

Abstract Abstract 3946 Vitamin D plays multiple roles in normal and malignant cell function, regulating cell differentiation and proliferation as well as bone homeostasis. Epidemiologic studies suggest that low levels of vitamin D contribute to the progression of lung cancer, breast cancer, colorectal and prostate cancer as well as lymphoma and melanoma. However, the role of vitamin D in multiple myeloma (MM) is unclear. In contrast to its growth inhibition of solid tumors, vitamin D has little anti-proliferative effects on MM cells. The physiological responses of myeloma cells to vitamin D are unknown, as are its effects on the marrow microenvironment in myeloma bone disease. Vitamin D insufficiency or deficiency has been documented in the majority of myeloma patients. Vitamin D receptor (VDR) is expressed by RPMI8226 cells, but it is unknown if this is a common finding in MM. Further, the functional consequences of VDR expression in myeloma cells are not well characterized. We reported osteoclast (OCL) precursors from patients with Paget's disease (PD) of bone were hypersensitive to 1,25-(OH)2D3 (1,25-D3) and formed OCL at physiologic concentrations of 1,25-D3 rather than the pharmacologic concentrations of 1,25-D3 required for normal OCL formation in vitro. This enhanced sensitivity to 1,25-D3 was due to increased expression of a novel VDR co-activator, TAF12, a member of the TFIID transcription complex. We found TAF12 expression was increased in marrow stromal cells (BMSC) by increased NFκB signaling and enhanced the capacity of BMSC to produce RANKL in response to low levels of 1,25-D3. Because the marrow microenvironment in MM and PD has many similarities in terms of increased OCL activity and enhanced NFκB signaling, we determined if MM cells induced TAF12 expression in BMSC of MM patients and if 1,25-D3 could enhanced RANKL production in BMSC of MM patients, even in patients with low levels of 1,25-D3. We found that both BMSC and CD138+ primary myeloma cells from MM patients expressed increased TAF12 levels compared to normal BMSC and CD138+ bone marrow cells. Four of four human MM cell lines (MM1.S, ANBL6, JJN3 and RPMI8266) expressed VDR, TAF12 and ATF7, which potentiates TAF12-mediated gene transcription. MM1.S and JJN3 but not RPMI8266 produced increased amounts of RANKL in response to very low levels of 1,25-D3. Further, 1,25-D3 increased VEGF, DKK1 and α4β1 integrin expression by MM1.S, JJN3 and RPMI8266 cells and enhanced adhesive interactions between MM cells and BMSC that increase MM growth. To confirm the role of TAF12 in the increased RANKL expression by MM cells treated with 1,25-D3, we established a stable TAF12 anti-sense JJN3 cell line (AS-TAF12-JJN3). AS-TAF12-JJN3 cells had markedly decreased RANKL production, VDR content and CYP24A1 accumulation in response to 1,25-D3. MM1.S and JJN3 myeloma cells treated with a VDR antagonist (TEI-9647) decreased RANKL production and α4β1 integrin expression in response to low levels of 1,25-D3. Further, 1,25-D3 induced VCAM-1 expression on normal human BMSC. Co-culture of JJN3 cells with BMSC treated with 1,25-D3 induced both MM cell growth and cell adhesion. In contrast, co-culture with AS-TAF12-JJN3 cells resulted in decreased cell growth and cell adhesion. Further, 1,25-D3 treatment of mouse OCL precursors co-cultured with JJN3 cells, but not AS-TAF12-JJN3 cells, increased OCL formation. These results suggest that increased TAF12 levels in MM cells and BMSC allow low levels of 1,25-D3 significantly to increase RANKL production by both MM cells and BMSC, and enhance adhesive interactions between MM cells and BMSC, thus increasing MM cell growth and OCL formation. Disclosures: No relevant conflicts of interest to declare.

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