Mild Heat Shock Induces Proliferation, Alkaline Phosphatase Activity, and Mineralization in Human Bone Marrow Stromal Cells and Mg-63 Cells In Vitro

Shui, Chaoxiang; Scutt, Andrew

doi:10.1359/jbmr.2001.16.4.731

Cited by 134 publications

(132 citation statements)

References 42 publications

(62 reference statements)

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“…This observed regenerative response is in agreement with previous studies that showed that exposure of osteoprogenitor cells to mild heat-shock (39-42.58C)-induced differentiation along the osteoblastic line and enhanced mineralized nodule formation [15,24]. In these studies, however, the duration of exposure to elevated temperatures is much longer than what is likely to occur during surgical cutting procedures.…”

Section: Discussionsupporting

confidence: 92%

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Heat-shock-induced cellular responses to temperature elevations occurring during orthopaedic cutting

Duffy

Haugh

Tallon

et al. 2012

J. R. Soc. Interface.

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Severe heat-shock to bone cells caused during orthopaedic procedures can result in thermal damage, leading to cell death and initiating bone resorption. By contrast, mild heat-shock has been proposed to induce bone regeneration. In this study, bone cells are exposed to heat-shock for short durations occurring during surgical cutting. Cellular viability, necrosis and apoptosis are investigated immediately after heat-shock and following recovery of 12, 24 h and 4 days, in osteocyte-like MLO-Y4 and osteoblast-like MC3T3-E1 cells, using flow cytometry. The regeneration capacity of heat-shocked Balb/c mesenchymal stem cells (MSCs) and MC3T3-E1s has been investigated following 7 and 14 day's recovery, by quantifying proliferation, differentiation and mineralization. An immediate necrotic response to heat-shock was shown in cells exposed to elevated temperatures (458C, 478C and most severe at 608C). A longer-term apoptotic response is induced in MLO-Y4s and, to a lesser extent, in MC3T3-E1s. Heat-shock-induced differentiation and mineralization by MSCs. These findings indicate that heat-shock is more likely to induce apoptosis in osteocytes than osteoblasts, which might reflect their role as sensors detecting and communicating damage within bone. Furthermore, it is shown for the first time that mild heat-shock (less than equal to 478C) for durations occurring during surgical cutting can positively enhance osseointegration by osteoprogenitors.

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Section: Discussionsupporting

confidence: 92%

“…The mineralized matrix was quantified by alizarin red S staining methods [15,24]. Alizarin red S (1 mole) binds to two moles of calcium, forming an alizarin red S-calcium complex.…”

Section: Quantification Of Mineralizationmentioning

confidence: 99%

Heat-shock-induced cellular responses to temperature elevations occurring during orthopaedic cutting

Duffy

Haugh

Tallon

et al. 2012

J. R. Soc. Interface.

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“…Nevertheless, some previous studies showed that HS induces a positive effect on bone growth and remodeling in vitro and in vivo. 13,33 Recently, conditions involving heating and growth factors in combination resulted in the inhibition of osteoclast differentiation and bone-resorptive processes in the bone microenvironment. 32 The close relationship between HSP synthesis and tissue regeneration under HS conditions has also been reported.…”

Section: Et Almentioning

confidence: 99%

“…12 Furthermore, MHS induces the proliferation and differentiation of human bone marrow stromal cells and MG-63 cells in vitro. 13 The conditioned culture media acquired from heat-treated osteoblasts enhances osteocalcin secretion and mineralization in bone marrow mesenchymal cells.…”

Section: Introductionmentioning

confidence: 99%

Mild Heat Stress Enhances Angiogenesis in a Co-culture System Consisting of Primary Human Osteoblasts and Outgrowth Endothelial Cells

Fuchs²,

Böse³

et al. 2014

Tissue Engineering Part C: Methods

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The repair and regeneration of large bone defects, including the formation of functional vasculature, represents a highly challenging task for tissue engineering and regenerative medicine. Recent studies have shown that vascularization and ossification can be stimulated by mild heat stress (MHS), which would offer the option to enhance the bone regeneration process by relatively simple means. However, the mechanisms of MHS-enhanced angiogenesis and osteogenesis, as well as potential risks for the treated cells are unclear. We have investigated the direct effect of MHS on angiogenesis and osteogenesis in a co-culture system of human outgrowth endothelial cells (OECs) and primary osteoblasts (pOBs), and assessed cytotoxic effects, as well as the levels of various heat shock proteins (HSPs) synthesized under these conditions. Enhanced formation of microvessel-like structures was observed in co-cultures exposed to MHS (41°C, 1 h), twice per week, over a time period of 7-14 days. As shown by real-time polymerase chain reaction (PCR), the expression of vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), and tumor necrosis factor-alpha was up-regulated in MHS-treated co-cultures 24 h post-treatment. At the protein level, significantly elevated VEGF and Ang-1 concentrations were observed in MHS-treated co-cultures and pOB mono-cultures compared with controls, indicating paracrine effects associated with MHS-induced angiogenesis. MHS-stimulated co-cultures and OEC mono-cultures released higher levels of Ang-2 than untreated cultures. On the other hand MHS treatment of cocultures did not result in a clear effect regarding osteogenesis. Nevertheless, real-time PCR demonstrated that MHS increased the expression of mitogen-activated protein kinase, interleukin-6, and bone morphogenetic protein 2, known as HSP-related molecules in angiogenic and osteogenic regulation pathways. In agreement with these observations, the expression of some selected HSPs also increased at both the mRNA and protein levels in MHS-treated co-cultures.

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“…However, mild heat shock has been shown to positively regulate cell survival and proliferation. For example, mild heat shock facilitates activation of resting lymphocytes for proliferation and effecter formation (17), stimulates bone marrow stromal cell proliferation (18), and induces the synthesis of cyclin D1, which plays a critical role(s) in the G1 progression of the cell cycle through multiple Ras signal pathways involving Rac1/NADPH oxidase, ERK, and PI3K (19). Furthermore, mild heat shock-induced heat shock protein (HSP) expression is regulated by a small GTPase Rac1, while harsh heat shock-induced HSP expression is not (20).…”

Section: Introductionmentioning

confidence: 99%

Implication of PI3K-dependent HSP27 and p53 expression in mild heat shock-triggered switch of metabolic stress-induced necrosis to apoptosis in A549 cells

Lim

Duong²,

Choi³

et al. 2009

Int J Oncol

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Abstract. Previously, we showed that mild heat shock modulates patterns of cell death in response to glucose deprivation (GD), a common characteristic of the tumor microenvironment, by switching necrosis to apoptosis through ERK-dependent suppression of reactive oxygen species production in A549 cells. In the present study, we further examined the molecular mechanism underlying mild heat shock-induced necrosisto-apoptosis switch. We examined the possible implication of p53 and heat shock proteins (HSPs) in the mechanism. Inhibition of p53 by pifithrin-· or p53 siRNA markedly suppressed apoptosis induced by heat shock/GD. On the other hand, silencing of HSP27, but not of HSP70, reversed heat shock/GD-induced apoptosis to necrosis, and HSP27 overexpression suppressed GD-induced necrosis. We further demonstrate that mild heat shock activated AKT and ERK1/2 through phosphorylation. Prevention of PI3K by LY294002 blocked heat shock/GD-induced apoptosis without reversing the cell death mode to necrosis, while inhibition of MEK1/2 by U0126 reversed heat shock/GD-induced apoptosis to necrosis, indicating a different role(s) of PI3K and ERK1/2 in heat shock/GD-induced cell death mode determination. We also found that mild heat shock increased HSP27 and p53 protein levels dependent on PI3K and suppressed the GD-induced increase in RIPA-insoluble HSP27 and p53 protein levels dependent on PI3K and ERK1/2. In conclusion, these results indicate that PI3K-dependent HSP27 and p53 induction and PI3K-and ERK1/2-dependent inhibition of the GD-induced increase in RIPA-insoluble HSP27 and p53 protein levels by heat play a key role(s) in heat shock-mediated switch of GD-induced necrosis to apoptosis.

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Mild Heat Shock Induces Proliferation, Alkaline Phosphatase Activity, and Mineralization in Human Bone Marrow Stromal Cells and Mg-63 Cells In Vitro

Abstract: Bone formation has been shown to be stimulated by local diathermy in vivo; however, the mechanisms involved in this heat-induced osteogenesis are unclear. In this study, we investigated the direct effect of temperature on human bone marrow-derived stromal cells (

Cited by 134 publications

References 42 publications

Heat-shock-induced cellular responses to temperature elevations occurring during orthopaedic cutting

Heat-shock-induced cellular responses to temperature elevations occurring during orthopaedic cutting

Mild Heat Stress Enhances Angiogenesis in a Co-culture System Consisting of Primary Human Osteoblasts and Outgrowth Endothelial Cells

Implication of PI3K-dependent HSP27 and p53 expression in mild heat shock-triggered switch of metabolic stress-induced necrosis to apoptosis in A549 cells

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