Intracellular Ca2+ stores and extracellular Ca2+ are required in the real-time Ca2+ response of bone cells experiencing fluid flow

Hung, Clark T.; Allen, F.D.; Pollack, Solomon R.; Brighton, C.T.

doi:10.1016/0021-9290(96)84536-2

Cited by 167 publications

(129 citation statements)

References 30 publications

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“…Osteoblasts are highly specialized cells that are responsible for the development of bone, production of bone matrix proteins, maintenance of bone density, and formation of hydroxyapatite mineral (Marks and Hermey, 1996). Osteoblasts employ intracellular Ca 2+ as a second messenger modulating fluid shear stress or hormonal responses and also a cofactor for bone mineralization (Lieberherr et al, 1993;Heaney, 1996;Hung et al, 1996;Chen et al, 2000;Nesti et al, 2002). When sufficient amounts of calcium and phosphate are supplied, osteoblasts synthesize and secret a collagenous extracellular matrix that nucleates the formation of hydroxyapatite crystal, in response to diverse extracellular stimuli such as steroid hormones, growth factors, cytokines, biochemical signals and extracellular Ca 2+ concentration (Yamaguchi et al, 1998;McAllister and Frangos, 1999;De Jong et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…When sufficient amounts of calcium and phosphate are supplied, osteoblasts synthesize and secret a collagenous extracellular matrix that nucleates the formation of hydroxyapatite crystal, in response to diverse extracellular stimuli such as steroid hormones, growth factors, cytokines, biochemical signals and extracellular Ca 2+ concentration (Yamaguchi et al, 1998;McAllister and Frangos, 1999;De Jong et al, 2002). These stimuli elicit a transient rise of intracellular Ca 2+ concentration ( [Ca 2+ ] i ) which is triggered both by Ca 2+ release from intracellular Ca 2+ stores and Ca 2+ entry from extracellular fluid (Lieberherr et al, 1993;Hung et al, 1996;Chen et al, 2000;Nesti et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Na+-Ca2+ exchanger modulates Ca2+ content in intracellular Ca2+ stores in rat osteoblasts

Jung

Park²,

Park³

et al. 2007

Exp Mol Med

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Abstract]i. In AS-pretreated cells, the expression and activity of alkaline phosphatase (ALP), an osteogenic marker, were decreased. However, the cell viability was not affected by AS-pretreatment. Suppression of NCX activity by the AS-pretreatment decreased ATP-activated Ca 2+ release from intracellular stores and significantly enhanced Ca 2+ influx via store operated calcium influx (SOCI), compared to those of S-pretreated or control cells. These results strongly suggest that NCX has a regulatory role in cellular Ca 2+ pathways in osteoblasts by modulating intracellular Ca 2+ content.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Na+-Ca2+ exchanger modulates Ca2+ content in intracellular Ca2+ stores in rat osteoblasts

Jung

Park²,

Park³

et al. 2007

Exp Mol Med

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“…77 As mentioned above, osteoblasts and osteocytes express a number of calcium-conducting channels, including Land T-type calcium channels and an unidentified mechanosensitive cation channel, 37,78,79 that are activated by fluid flow. Exposing cells to fluid flow in calciumfree media or pharmacological inhibition of these channels dampens the elevation of intracellular calcium in response to fluid flow.…”

Section: Mechanotransduction Pathwaysmentioning

confidence: 99%

“…Exposing cells to fluid flow in calciumfree media or pharmacological inhibition of these channels dampens the elevation of intracellular calcium in response to fluid flow. 21,77,80 Calcium signaling is similarly affected when intracellular calcium stores are emptied or phospholipase C activity is inhibited. 21,77,80 The increase in intracellular calcium concentration is reported to contribute to the enhanced expression of osteopontin, 21 c-fos, cyclooxygenase-2, 80 and transforming growth factor-b, 81 but there is little data on how this change in ion concentration results in altered gene expression.…”

Section: Mechanotransduction Pathwaysmentioning

confidence: 99%

“…21,77,80 Calcium signaling is similarly affected when intracellular calcium stores are emptied or phospholipase C activity is inhibited. 21,77,80 The increase in intracellular calcium concentration is reported to contribute to the enhanced expression of osteopontin, 21 c-fos, cyclooxygenase-2, 80 and transforming growth factor-b, 81 but there is little data on how this change in ion concentration results in altered gene expression. While there is evidence that calcineurin 82,83 and calmodulin-dependent kinase 84,85 regulate osteoblast proliferation and differentiation, it has only recently been demonstrated that fluid flow activates the transcription factor NFAT (nuclear factor of activated T cells).…”

Section: Mechanotransduction Pathwaysmentioning

confidence: 99%

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From streaming-potentials to shear stress: 25 years of bone cell mechanotransduction

2009

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Mechanical loads are vital regulators of skeletal mass and architecture as evidenced by the increase in bone formation following the addition of exogenous loads and loss of bone mass following their removal. While our understanding of the molecular mechanisms by which bone cells perceive changes in their mechanical environment has increased rapidly in recent years, much remains to be learned. Here, we outline the effects of interstitial fluid flow, a potent biophysical signal induced by the deformation of skeletal tissue in response to applied loads, on bone cell behavior. We focus on the molecular mechanisms by which bone cells are hypothesized to perceive interstitial fluid flow, the cell signaling cascades activated by fluid flow, and the use of this signal in tissue engineering protocols. ß

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Intracellular Ca2+ stores and extracellular Ca2+ are required in the real-time Ca2+ response of bone cells experiencing fluid flow

Cited by 167 publications

References 30 publications

Na+-Ca2+ exchanger modulates Ca2+ content in intracellular Ca2+ stores in rat osteoblasts

Na+-Ca2+ exchanger modulates Ca2+ content in intracellular Ca2+ stores in rat osteoblasts

From streaming-potentials to shear stress: 25 years of bone cell mechanotransduction

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