Bone as an ion exchange organ: Evidence for instantaneous cell-dependent calcium efflux from bone not due to resorption

Marenzana, Massimo; Shipley, Alan; Squitiero, P.; Kunkel, Joseph G.; Rubinacci, Alessandro

doi:10.1016/j.bone.2005.04.036

Cited by 61 publications

(72 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The long bones of Mmp2 Ϫ/Ϫ mice, however, were not fully mineralized (pQCT analysis). The canalicular space is a site where mineral ions are exchanged between bone and extracellular fluid in the processes of resorption and mineralization of the organic matrix (39). The canalicular space is also a site for extracellular phosphorylation of matrix proteins that bind mineral ions (40,41).…”

Section: Mmp2mentioning

confidence: 99%

A Crucial Role for Matrix Metalloproteinase 2 in Osteocytic Canalicular Formation and Bone Metabolism

Inoue

Mikuni-Takagaki

Oikawa

et al. 2006

Journal of Biological Chemistry

177

168

View full text Add to dashboard Cite

Bone is continuously remodeled to adopt a volume appropriate for the local environment; the amount of bone deposited depends on the balance between bone formation and resorption by bone cells, osteoblasts, osteoclasts, and osteocytes (1). Osteoblasts are bone-forming cells that differentiate from mesenchymal stem cells and secrete extracellular matrix (ECM) 4 proteins, which are subsequently mineralized. Osteoclasts are bone-resorbing cells that differentiate from hematopoietic stem cells and degrade bone ECM proteins after demineralization in the extracellular space (Howship's lacunae) adjacent to the ruffled borders. In contrast to osteoblasts and osteoclasts, which act at bone surfaces, osteocytes, cells of osteoblastic lineage, are embedded in bone and are terminally differentiated. Osteocytes extend their dendritic processes into the bone matrix to constitute a well developed canalicular network with other cells. Although osteocytes are the most abundant cell type in bone tissue, their role in bone metabolism is not firmly established.ECM production and degradation by bone cells are critical steps in bone metabolism (1), and disturbed ECM turnover leads to bone disease. Type I collagen is a major ECM component. Secreted type I collagen molecules are processed by propeptidases and cross-linked by lysyl oxidases into mature collagen. Mutations of genes encoding type I collagen cause the bone disease osteogenesis imperfecta (2). Type I collagens are mainly degraded by matrix metalloproteinases (MMPs), which exert their enzymatic activity at a neutral pH in a zinc ion-dependent manner (3, 4). Several MMPs are expressed in bone tissue (5-9). MMPs may play a role in osteoclastic bone resorption (4, 5). Osteoblasts and osteocytes also produce MMPs such as MMP-2 and MMP-13 (7-9). Recent linkage analysis suggests that a loss of function mutation of MMP2 causes a human autosomal recessive disorder with multicentric nodulosis, arthropathy with joint erosion, and osteolysis, termed NAO syndrome (10, 11). This syndrome also includes facial abnormalities and generalized * This work was supported in part by a grant from the Ministry for Welfare and Health of Japan (to S. I.), by a Sasagawa Scientific Research Grant from the Japan Science Society (to K. I.), by a grant from the Japan Space Forum, National Space Development Agency of Japan (NASDA) (to N. M.), and by a research grant from the National Institutes of Health (to S. M. K.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. 4 The abbreviations used are: ECM, extracellular matrix; DMP-1, dentin matrix protein 1; DMEM, Dulbecco's modified Eagle's medium; MMP, matrix metalloproteinase; NAO, nodulosis, arthropathy, and osteolysis; BMD, bone mineral density; pQCT, peripheral quantitative computed tomography; MAR, mineral apposition rate; BFR/BS, ratio of bone formation rate to bone surface.

show abstract

Section: Mmp2mentioning

confidence: 99%

A Crucial Role for Matrix Metalloproteinase 2 in Osteocytic Canalicular Formation and Bone Metabolism

Inoue

Mikuni-Takagaki

Oikawa

et al. 2006

Journal of Biological Chemistry

177

168

View full text Add to dashboard Cite

show abstract

“…2+ ion-selective electrode measurements The scanning ion-selective electrode technique (SIET; Kühtreiber and Jaffe, 1990;Marenzana et al, 2005) was used to measure the Ca 2+ flux and the local [Ca 2+ ] around embryos. Glass micropipettes were pulled from TW150-4 glass capillaries with an outer diameter of 1.5 mm (World Precision Instruments, Sarasota, FL, USA) using a P-97 Flaming/Brown pipette puller (Sutter instruments, San Rafael, CA, USA).…”

Section: Scanning Camentioning

confidence: 99%

Inhibition of SOCE disrupts cytokinesis in zebrafish embryos via inhibition of cleavage furrow deepening

Chan

Chen²,

Hung³

et al. 2015

Int. J. Dev. Biol.

View full text Add to dashboard Cite

During the first few cell division cycles in zebrafish, distinct Ca 2+ transients are localized to the early embryonic cleavage furrows, where they accompany (and are required for) furrow positioning, propagation, deepening and apposition. It has previously been shown that the endoplasmic reticulum (ER) acts as the primary store for generating these Ca 2+ transients via release through inositol 1,4,5-trisphosphate receptors (IP 3 Rs). We hypothesised that maintaining the elevated levels of intracellular Ca 2+ required for deepening and apposition of the cleavage furrows in these large eggs might result in the depletion of the available ER Ca 2+ store, thus the role of store-operated Ca 2+ entry (SOCE) was examined. Newly fertilized, dechorionated embryos were incubated with various SOCE inhibitors, starting just prior to the onset of the first cell division cycle. The effect of these inhibitors on mitosis, furrow positioning, propagation, deepening and apposition, and the generation of the cytokinetic Ca 2+ transients was determined. Treatment with 2-APB or SKF 96365 had no major effect on mitosis, furrow positioning or propagation, but inhibited furrow deepening resulting in regression of the cleavage furrow. Both of these inhibitors also blocked the furrowing Ca 2+ transient, with SKF 96365 having a more profound inhibitory effect than 2-APB. In zebrafish, SOCE does not appear to be required for mitosis or the early stages of cytokinesis during the early embryonic cell division cycles, but it does appear to be essential for maintaining the elevated levels of [Ca 2+ ] i for the extended periods that are required during furrow deepening and daughter cell apposition.

show abstract

“…24 The canalicular spaces are locations in which mineral ion exchanges occur during the resorption and mineralization of the bone matrix. 25 Thus, disruption to these canalicular networks could possibly inhibit the mineralization and hardening of bone. An increase in MMP-2 protein expression has also been detected in fracture callus, and bone mineralization may be one aspect by which MMP-2 mediates bone remodeling during fracture repair.…”

mentioning

confidence: 99%

Matrix metalloproteinases in bone development and pathology: current knowledge and potential clinical utility

Liang¹,

Xu²,

Xue³

et al. 2016

MNM

View full text Add to dashboard Cite

Matrix metalloproteinases (MMPs) are degrading enzymes that have a pivotal function in extracellular matrix remodeling. More than half of the MMP members are expressed by bone and cartilage cells under physiological or pathological conditions such as rheumatoid arthritis, osteoarthritis, and osteoporosis. Through studies on the various bone diseases and on genetically modified mouse models in which one or more of the MMPs or their associated proteins and downstream signaling molecules have been targeted, it is becoming increasingly evident that MMPs and other players in their cellular pathway play a pivotal role in bone development and remodeling. This review details the latest findings related to MMPs and bone development and pathology.

show abstract

Bone as an ion exchange organ: Evidence for instantaneous cell-dependent calcium efflux from bone not due to resorption

Cited by 61 publications

References 42 publications

A Crucial Role for Matrix Metalloproteinase 2 in Osteocytic Canalicular Formation and Bone Metabolism

A Crucial Role for Matrix Metalloproteinase 2 in Osteocytic Canalicular Formation and Bone Metabolism

Inhibition of SOCE disrupts cytokinesis in zebrafish embryos via inhibition of cleavage furrow deepening

Matrix metalloproteinases in bone development and pathology: current knowledge and potential clinical utility

Contact Info

Product

Resources

About