Orbital fluid shear stress promotes osteoblast metabolism, proliferation and alkaline phosphates activity in vitro

Aisha, M.D.; Нор-Ашикин, М. Н. К.; Sharaniza, A.B.R.; Nawawi, H.; Froemming, Gabriele Ruth Anisah

doi:10.1016/j.yexcr.2015.07.002

Cited by 29 publications

(29 citation statements)

References 41 publications

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“…Osteoblast responses to low FSS below 0.5 Pa have also been shown in vitro (Liegibel et al, 2004; Yu et al, 2014; Aisha et al, 2015). Responses of osteoblasts, which were cultured on planar surfaces as monolayer, to low FSS were comparable to high FSS responses (Table 2).…”

Section: Bone Mechanotransductionmentioning

confidence: 86%

“…Low FSS resulted in an increased production of PGE 2 (Liegibel et al, 2004), ALP (Xing et al, 2014; Aisha et al, 2015), and collagen (Xing et al, 2014). Furthermore, osteoblasts tended to proliferate more under low flow (Liegibel et al, 2004; Xing et al, 2014; Aisha et al, 2015). mRNA expression of osteogenic genes Runx2, ALP, Col I, and osteocalcin was also increased under low FSS (Yu et al, 2014).…”

Section: Bone Mechanotransductionmentioning

confidence: 99%

“…Similar to high FSS experiments, PPFC were often used to provide the required stimuli in low FSS applications (Kou et al, 2011; Xing et al, 2014). In addition, rockers and orbital shakers were also used to generate FSS in this range (Liegibel et al, 2004; Aisha et al, 2015). …”

Section: Bone Mechanotransductionmentioning

confidence: 99%

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In Vitro Bone Cell Models: Impact of Fluid Shear Stress on Bone Formation

Wittkowske

Reilly

Lacroix

et al. 2016

Front. Bioeng. Biotechnol.

236

225

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This review describes the role of bone cells and their surrounding matrix in maintaining bone strength through the process of bone remodeling. Subsequently, this work focusses on how bone formation is guided by mechanical forces and fluid shear stress in particular. It has been demonstrated that mechanical stimulation is an important regulator of bone metabolism. Shear stress generated by interstitial fluid flow in the lacunar-canalicular network influences maintenance and healing of bone tissue. Fluid flow is primarily caused by compressive loading of bone as a result of physical activity. Changes in loading, e.g., due to extended periods of bed rest or microgravity in space are associated with altered bone remodeling and formation in vivo. In vitro, it has been reported that bone cells respond to fluid shear stress by releasing osteogenic signaling factors, such as nitric oxide, and prostaglandins. This work focusses on the application of in vitro models to study the effects of fluid flow on bone cell signaling, collagen deposition, and matrix mineralization. Particular attention is given to in vitro set-ups, which allow long-term cell culture and the application of low fluid shear stress. In addition, this review explores what mechanisms influence the orientation of collagen fibers, which determine the anisotropic properties of bone. A better understanding of these mechanisms could facilitate the design of improved tissue-engineered bone implants or more effective bone disease models.

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Section: Bone Mechanotransductionmentioning

confidence: 86%

Section: Bone Mechanotransductionmentioning

confidence: 99%

See 1 more Smart Citation

In Vitro Bone Cell Models: Impact of Fluid Shear Stress on Bone Formation

Wittkowske

Reilly

Lacroix

et al. 2016

Front. Bioeng. Biotechnol.

236

225

View full text Add to dashboard Cite

show abstract

“…It is also firmly established that mechanical loading of bone results in increased bone formation and remodeling[1, 2]. However, when physiological mechanical stimulation is absent, for example, during exposure to an environment of microgravity, after prolonged bed rest or following joint immobilization after surgery, bone resorption increases and bone mass is lost[3, 4].…”

Section: Introductionmentioning

confidence: 99%

“…However, the response of monolayer osteoblasts to mechanical stress generated by liquid drops has never been reported. It is widely accepted that physiological mechanical loading leads to an anti-apoptotic effect and increased proliferation and differentiation of osteoblasts which results in extracellular matrix formation[2, 6, 11–13]. At present, some studies have suggested that mechanical overloading acts as a negative regulator of bone formation and induces cell apoptosis, but the precise cellular mechanism is poorly understood[7, 14–16].…”

Section: Introductionmentioning

confidence: 99%

Cyclic Compressive Stress Regulates Apoptosis in Rat Osteoblasts: Involvement of PI3K/Akt and JNK MAPK Signaling Pathways

et al. 2016

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It is widely accepted that physiological mechanical stimulation suppresses apoptosis and induces synthesis of extracellular matrix by osteoblasts; however, the effect of stress overloading on osteoblasts has not been fully illustrated. In the present study, we investigated the effect of cyclic compressive stress on rat osteoblasts apoptosis, using a novel liquid drop method to generate mechanical stress on osteoblast monolayers. After treatment with different levels of mechanical stress, apoptosis of osteoblasts and activations of mitogen-activated protein kinases (MAPKs) and PI3-kinase (PI3K)/Akt signaling pathways were investigated. Osteoblasts apoptosis was observed after treated with specific inhibitors prior to mechanical stimulation. Protein levels of Bax/Bcl-2/caspase-3 signaling were determined using western blot with or without inhibitors of PI3K/Akt and phosphorylation of c-jun N-terminal kinase (JNK) MAPK. Results showed that mechanical stimulation led to osteoblasts apoptosis in a dose-dependent manner and a remarkable activation of MAPKs and PI3K/Akt signaling pathways. Activation of PI3K/Akt protected against apoptosis, whereas JNK MAPK increased apoptosis via regulation of Bax/Bcl-2/caspase-3 activation. In summary, the PI3K/Akt and JNK MAPK signaling pathways played opposing roles in osteoblasts apoptosis, resulting in inhibition of apoptosis upon small-magnitude stress and increased apoptosis upon large-magnitude stress.

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Bioprinting Organotypic Hydrogels with Improved Mesenchymal Stem Cell Remodeling and Mineralization Properties for Bone Tissue Engineering

Campos

Blaeser

Buellesbach

et al. 2016

Adv Healthcare Materials

154

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3D-manufactured hydrogels with precise contours and biological adhesion motifs are interesting candidates in the regenerative medicine field for the culture and differentiation of human bone-marrow-derived mesenchymal stem cells (MSCs). 3D-bioprinting is a powerful technique to approach one step closer the native organization of cells. This study investigates the effect of the incorporation of collagen type I in 3D-bioprinted polysaccharide-based hydrogels to the modulation of cell morphology, osteogenic remodeling potential, and mineralization. By combining thermo-responsive agarose hydrogels with collagen type I, the mechanical stiffness and printing contours of printed constructs can be improved compared to pure collagen hydrogels which are typically used as standard materials for MSC osteogenic differentiation. The results presented here show that MSC not only survive the 3D-bioprinting process but also maintain the mesenchymal phenotype, as proved by live/dead staining and immunocytochemistry (vimentin positive, CD34 negative). Increased solids concentrations of collagen in the hydrogel blend induce changes in cell morphology, namely, by enhancing cell spreading, that ultimately contribute to enhanced and directed MSC osteogenic differentiation. 3D-bioprinted agarose-collagen hydrogels with high-collagen ratio are therefore feasible for MSC osteogenic differentiation, contrarily to low-collagen blends, as proved by two-photon microscopy, Alizarin Red staining, and real-time polymerase chain reaction.

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Orbital fluid shear stress promotes osteoblast metabolism, proliferation and alkaline phosphates activity in vitro

Cited by 29 publications

References 41 publications

In Vitro Bone Cell Models: Impact of Fluid Shear Stress on Bone Formation

In Vitro Bone Cell Models: Impact of Fluid Shear Stress on Bone Formation

Cyclic Compressive Stress Regulates Apoptosis in Rat Osteoblasts: Involvement of PI3K/Akt and JNK MAPK Signaling Pathways

Bioprinting Organotypic Hydrogels with Improved Mesenchymal Stem Cell Remodeling and Mineralization Properties for Bone Tissue Engineering

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