Involvement of p38MAP kinase in bone morphogenetic protein-4-induced osteoprotegerin in mouse bone-marrow-derived stromal cells

Tazoe, Michiko; Mogi, Makio; Goto, Shigemi; Togari, Akifumi

doi:10.1016/s0003-9969(03)00100-6

Cited by 16 publications

(13 citation statements)

References 23 publications

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“…Furthermore, Delhanty et al [30] recently showed that ghrelin and unacylated ghrelin stimulate human osteoblast growth via mitogen-activated protein kinase (MAPK)/phosphoinositide 3-kinase (PI3K) pathways in the absence of GHS-R1a. The regulation of cytokine-induced OPG gene expression and protein secretion by specific MAPK signal transduction pathways have also been shown previously [31, 32]. Tazoe et al [32] reported that activation of the p38-MAP kinase pathway is necessary for BMP-4-induced OPG induction in mouse bone-marrow-derived stromal cells.…”

Section: Discussionmentioning

confidence: 55%

“…The regulation of cytokine-induced OPG gene expression and protein secretion by specific MAPK signal transduction pathways have also been shown previously [31, 32]. Tazoe et al [32] reported that activation of the p38-MAP kinase pathway is necessary for BMP-4-induced OPG induction in mouse bone-marrow-derived stromal cells. Taking all these data into consideration, the relation between ghrelin and OPG might be explained by MAPK signal transduction pathways; that stimulatory effects of ghrelin on osteoblast proliferation via MAPK signal transduction pathways might mediate OPG production, which mostly occurs in osteoblasts.…”

Section: Discussionmentioning

confidence: 55%

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Osteoprotegerin and RANKL Serum Levels and Their Relationship with Serum Ghrelin in Children with Chronic Renal Failure and on Dialysis

Özkaya

Buyan

Bıdecı³

et al. 2007

Nephron Clin Pract

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Background: Osteoprotegerin (OPG) and receptor activator of the nuclear factor ĸB ligand (RANKL) constitute a complex system of mediators involved in the regulation of bone resorption process. Ghrelin, a growth hormone secretagogue, has been shown to modulate proliferation and differentiation of osteoblasts. The present study was carried out to evaluate the serum concentrations of OPG and sRANKL in children with chronic renal impairment (CRI) and on dialysis, and to establish a possible relationship between their serum levels and that of ghrelin. Methods: 33 patients including 10 patients with CRI, 12 peritoneal dialysis (PD) and 11 hemodialysis (HD) patients and 22 healthy controls were enrolled into the study. OPG, sRANKL and ghrelin levels were studied with radioimmunoassay. Results: Serum OPG levels in CRI, PD and HD groups were significantly higher than the healthy controls (p = 0.002, p < 0.001, p < 0.001, respectively) whereas sRANKL levels were significantly lower than the healthy controls (p = 0.03, p = 0.01, p = 0.001, respectively). Ghrelin levels were significantly higher in CRI, PD and HD groups compared to healthy controls (p = 0.001, p < 0.001, p < 0.001, respectively). We observed a negative correlation between the sRANKL and OPG levels (r = –0.27, p = 0.04) as well as between sRANKL and ghrelin levels (r = –0.31, p = 0.02). OPG levels showed a positive correlation with ghrelin levels (r = 0.63, p < 0.001). Conclusion: We found a lower RANKL bioactivity index in children with CRI and on dialysis. The mechanism and the role of elevated OPG and low sRANKL in uremia are unclear, but they might partly represent a compensatory mechanism to the negative balance of bone remodeling in renal bone disease in children. Additionally, we demonstrated for the first time that ghrelin and the RANKL/OPG system have a close relationship in CRF. Therefore, ghrelin may be of importance in mediating the effects of the RANKL/OPG system in renal bone disease.

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 55%

Osteoprotegerin and RANKL Serum Levels and Their Relationship with Serum Ghrelin in Children with Chronic Renal Failure and on Dialysis

Özkaya

Buyan

Bıdecı³

et al. 2007

Nephron Clin Pract

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“…Expression of the cellular inhibitor of the apoptosis protein 2 gene is regulated by tumor necrosis factor (TNF) and other stimuli that activate NFB (Pryhuber et al, 2000). The Apo-2L/TRAIL gene is a well-known member of the TNF family and osteoprotegerin is a decoy receptor for the TNF receptor family member RANK, which is a target for p38 and TCF/␤-catenin (Wang and El Deiry, 2003;Glass et al, 2005;Tazoe et al, 2003). JUN, FOSL1, laminin ␥2 and MDR1 are targets of MAPK-JNK as well as ␤-catenin/TCF pathways (Olsen et al, 2000;Kang et al, 2000).…”

Section: Journal Of Cell Science 120 (15)mentioning

confidence: 99%

Mechanical force modulates global gene expression and β-catenin signaling in colon cancer cells

Avvisato

Xiang

Shah

et al. 2007

Journal of Cell Science

111

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At various stages during embryogenesis and cancer cells are exposed to tension, compression and shear stress; forces that can regulate cell proliferation and differentiation. In the present study, we show that shear stress blocks cell cycle progression in colon cancer cells and regulates the expression of genes linked to the Wnt/β-catenin, mitogen-activated protein kinase (MAPK) and NFκB pathways. The shear stress-induced increase of the secreted Wnt inhibitor DKK1 requires p38 and activation of NFκB requires IκB kinase-β. Activation of β-catenin, important in Wnt signaling and the cause of most colon cancers, is inhibited by shear stress through a pathway involving laminin-5, α6β4 integrin, phosphoinositide 3-kinase (PI 3-kinase) and Rac1 coupled with changes in the distribution of dephosphorylated β-catenin. These data show that colon cancer cells respond to fluid shear stress by activation of specific signal transduction pathways and genetic regulatory circuits to affect cell proliferation, and indicate that the response of colon cancers to mechanical forces such as fluid shear stress should be taken into account in the management of the disease.

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“…10,35 Although many cell signaling studies have been performed with BMP2 stimulation, inhibitors such as PD98059, SB203580, or Ly294002 have been also studied using BMP4. 20,21,28,[36][37][38] It has been shown that BMP4-stimulated osteocalcin synthesis is negatively regulated by ERK1/2, whereas p38 MAPK is a positive regulator of its synthesis in MC3T3-E1 cells.…”

mentioning

confidence: 99%

Effect of Phosphatidyl Inositol 3-Kinase, Extracellular Signal-Regulated Kinases 1/2, and p38 Mitogen-Activated Protein Kinase Inhibition on Osteogenic Differentiation of Muscle-Derived Stem Cells

Payne

Meszaros

Phillippi

et al. 2010

Tissue Engineering Part A

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Involvement of p38MAP kinase in bone morphogenetic protein-4-induced osteoprotegerin in mouse bone-marrow-derived stromal cells

Cited by 16 publications

References 23 publications

Osteoprotegerin and RANKL Serum Levels and Their Relationship with Serum Ghrelin in Children with Chronic Renal Failure and on Dialysis

Osteoprotegerin and RANKL Serum Levels and Their Relationship with Serum Ghrelin in Children with Chronic Renal Failure and on Dialysis

Mechanical force modulates global gene expression and β-catenin signaling in colon cancer cells

Effect of Phosphatidyl Inositol 3-Kinase, Extracellular Signal-Regulated Kinases 1/2, and p38 Mitogen-Activated Protein Kinase Inhibition on Osteogenic Differentiation of Muscle-Derived Stem Cells

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