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Article ; Online: Oncostatin M enhances osteoprotegerin synthesis but reduces macrophage colony‑stimulating factor synthesis in bFGF‑stimulated osteoblast‑like cells.

Hioki, Tomoyuki / Tachi, Junko / Ueda, Kyohei / Matsushima-Nishiwaki, Rie / Iida, Hiroki / Kozawa, Osamu / Tokuda, Haruhiko

Experimental and therapeutic medicine

2023 Volume 27, Issue 1, Page(s) 34

Abstract: Bone remodeling is tightly controlled by various factors, including hormones, autacoids and cytokines. Among them, oncostatin M (OSM) is a multifunctional cytokine produced by osteal macrophages, which serves as an essential modulator of bone remodeling. ...

Abstract	Bone remodeling is tightly controlled by various factors, including hormones, autacoids and cytokines. Among them, oncostatin M (OSM) is a multifunctional cytokine produced by osteal macrophages, which serves as an essential modulator of bone remodeling. Macrophage colony-stimulating factor (M-CSF) and osteoprotegerin are secreted by osteoblasts, and also have pivotal roles in the regulation of the bone remodeling process. The binding of basic fibroblast growth factor (bFGF), a key regulator of bone remodeling, to the corresponding receptor [fibroblast growth factor receptor (FGFR)] triggers the dimerization and activation of FGFRs, which causes the phosphorylation of FGFR substrates and subsequent activation of downstream effectors, including mitogen-activated protein kinases (MAPKs), via Grb2. bFGF can activate MAPKs, resulting in the synthesis of osteoprotegerin and vascular endothelial growth factor in osteoblast-like MC3T3-E1 cells. In the present study, the effects of OSM on bFGF-induced osteoblast activation were investigated in the synthesis of osteoprotegerin and M-CSF in osteoblasts. The release of osteoprotegerin and M-CSF were analyzed using ELISA. The mRNA expression levels of osteoprotegerin and M-CSF were analyzed using reverse transcription-quantitative PCR. Phosphorylation of p38 MAPK, stress-activated protein kinase/c
Language	English
Publishing date	2023-11-24
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2683844-8
ISSN	1792-1015 ; 1792-0981
ISSN (online)	1792-1015
ISSN	1792-0981
DOI	10.3892/etm.2023.12322
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Article ; Online: Oncostatin M stimulates prostaglandin D

Kuroyanagi, Gen / Hioki, Tomoyuki / Tachi, Junko / Matsushima-Nishiwaki, Rie / Iida, Hiroki / Kozawa, Osamu / Tokuda, Haruhiko

Prostaglandins, leukotrienes, and essential fatty acids

2023 Volume 192, Page(s) 102575

Abstract: Oncostatin M produced by osteal macrophages plays a significant role in fracture healing. Osteoprotegerin (OPG) secreted by osteoblasts, binds to the receptor activator of nuclear factor-κB (RANK) ligand (RANKL) as a decoy receptor and prevents RANKL ... ...

Abstract	Oncostatin M produced by osteal macrophages plays a significant role in fracture healing. Osteoprotegerin (OPG) secreted by osteoblasts, binds to the receptor activator of nuclear factor-κB (RANK) ligand (RANKL) as a decoy receptor and prevents RANKL from binding to RANK, resulting in bone resorption suppression. Interleukin-6 (IL-6) is a pro-inflammatory cytokine and generally regulates bone resorption. However, accumulating evidence suggests that IL-6 plays pivotal roles in bone formation. We previously showed that prostaglandin D
MeSH term(s)	Humans ; Interleukin-6 ; Prostaglandins/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Osteoprotegerin/genetics ; Oncostatin M/pharmacology ; Oncostatin M/metabolism ; Phosphorylation ; p38 Mitogen-Activated Protein Kinases/metabolism ; Osteoblasts/metabolism
Chemical Substances	Interleukin-6 ; Prostaglandins ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Osteoprotegerin ; Oncostatin M (106956-32-5) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2023-04-13
Publishing country	Scotland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	286714-x
ISSN	1532-2823 ; 0952-3278
ISSN (online)	1532-2823
ISSN	0952-3278
DOI	10.1016/j.plefa.2023.102575
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Article ; Online: Resveratrol inhibits basic fibroblast growth factor-induced macrophage colony-stimulating factor synthesis via the PI3-kinase/Akt pathway in osteoblasts.

Kuroyanagi, Gen / Hioki, Tomoyuki / Tachi, Junko / Matsushima-Nishiwaki, Rie / Iida, Hiroki / Tokuda, Haruhiko / Kozawa, Osamu

Bioscience, biotechnology, and biochemistry

2023 Volume 87, Issue 12, Page(s) 1462–1469

Abstract: Resveratrol is a natural polyphenol found in grapes and beneficial for human health. Resveratrol regulates basic fibroblast growth factor (bFGF)-induced osteoprotegerin synthesis through Akt pathway in osteoblast-like MC3T3-E1 cells. In this study, we ... ...

Abstract	Resveratrol is a natural polyphenol found in grapes and beneficial for human health. Resveratrol regulates basic fibroblast growth factor (bFGF)-induced osteoprotegerin synthesis through Akt pathway in osteoblast-like MC3T3-E1 cells. In this study, we investigated resveratrol effects on bFGF-induced macrophage colony-stimulating factor (M-CSF) synthesis in MC3T3-E1 cells. bFGF significantly stimulated release and mRNA expression of M-CSF, which was reduced by resveratrol and SRT1720, sirtuin 1 (SIRT1) activator. Inauhzin, SIRT1 inhibitor, reversed inhibitory effects of resveratrol on bFGF-induced mRNA expression of M-CSF. Deguelin, Akt inhibitor, and LY294002, phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, reduced bFGF-induced M-CSF synthesis. Inauhzin reversed inhibitory effects of resveratrol on bFGF-induced Akt phosphorylation. Suppressive effect of resveratrol on bFGF-induced osteoprotegerin mRNA expression was confirmed in the identical samples using in experiment of M-CSF mRNA expression. Therefore, resveratrol reduces bFGF-induced M-CSF synthesis in addition to osteoprotegerin synthesis by inhibiting PI3-kinase/Akt pathway and suppressive effects are mediated through SIRT1 activation in osteoblasts.
MeSH term(s)	Fibroblast Growth Factor 2/drug effects ; Fibroblast Growth Factor 2/metabolism ; Macrophage Colony-Stimulating Factor/drug effects ; Macrophage Colony-Stimulating Factor/metabolism ; Osteoblasts/metabolism ; Osteoprotegerin/drug effects ; Osteoprotegerin/metabolism ; Phosphatidylinositol 3-Kinase/drug effects ; Phosphatidylinositol 3-Kinase/metabolism ; Phosphatidylinositol 3-Kinase/pharmacology ; Proto-Oncogene Proteins c-akt/metabolism ; Resveratrol/pharmacology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Sirtuin 1/genetics ; Sirtuin 1/metabolism ; Mice ; Animals
Chemical Substances	Fibroblast Growth Factor 2 (103107-01-3) ; inauzhin ; Macrophage Colony-Stimulating Factor (81627-83-0) ; Osteoprotegerin ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Resveratrol (Q369O8926L) ; RNA, Messenger ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2023-09-14
Publishing country	England
Document type	Journal Article
ZDB-ID	1106450-x
ISSN	1347-6947 ; 0916-8451
ISSN (online)	1347-6947
ISSN	0916-8451
DOI	10.1093/bbb/zbad121
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Article: GLP-1 reduces the migration of hepatocellular carcinoma cells via suppression of the stress-activated protein kinase/c-Jun N-terminal kinase pathway

Yamada, Noriko / Matsushima-Nishiwaki, Rie / Kobayashi, Kaido / Tachi, Junko / Kozawa, Osamu

Archives of biochemistry and biophysics. 2021 May 30, v. 703

2021

Abstract: Incretins, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are hormones secreted from small intestine accompanied with oral intake. We previously showed that transforming growth factor (TGF)-α stimulates the ... ...

Abstract	Incretins, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are hormones secreted from small intestine accompanied with oral intake. We previously showed that transforming growth factor (TGF)-α stimulates the migration of hepatocellular carcinoma (HCC) cells via mitogen-activated protein (MAP) kinases, AKT and Rho-kinase. However, it remains to be elucidated whether incretins affect HCC cell functions. In the present study, therefore, we investigated whether incretins affect the migration of HCC cells using human HCC-derived HuH7 cells. GLP-1, but not GIP, reduced both TGF-α- and hepatocyte growth factor (HGF)-induced cell migration. IBMX, an inhibitor of cyclic nucleotide phosphodiesterase, enhanced the suppressive effect of GLP-1. GLP-1 attenuated the phosphorylation of stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) by TGF-α and HGF. Our results strongly suggest that GLP-1 suppresses TGF-α- and HGF-induced migration of HCC cells through inhibiting the SAPK/JNK signaling pathway, and that the inhibition by GLP-1 is due to cAMP production.
Keywords	biophysics ; cell movement ; gastric inhibitory polypeptide ; glucagon-like peptide 1 ; hepatocyte growth factor ; hepatoma ; humans ; phosphorylation ; small intestine
Language	English
Dates of publication	2021-0530
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2021.108851
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Article ; Online: GLP-1 reduces the migration of hepatocellular carcinoma cells via suppression of the stress-activated protein kinase/c-Jun N-terminal kinase pathway.

Yamada, Noriko / Matsushima-Nishiwaki, Rie / Kobayashi, Kaido / Tachi, Junko / Kozawa, Osamu

Archives of biochemistry and biophysics

2021 Volume 703, Page(s) 108851

Abstract	Incretins, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are hormones secreted from small intestine accompanied with oral intake. We previously showed that transforming growth factor (TGF)-α stimulates the migration of hepatocellular carcinoma (HCC) cells via mitogen-activated protein (MAP) kinases, AKT and Rho-kinase. However, it remains to be elucidated whether incretins affect HCC cell functions. In the present study, therefore, we investigated whether incretins affect the migration of HCC cells using human HCC-derived HuH7 cells. GLP-1, but not GIP, reduced both TGF-α- and hepatocyte growth factor (HGF)-induced cell migration. IBMX, an inhibitor of cyclic nucleotide phosphodiesterase, enhanced the suppressive effect of GLP-1. GLP-1 attenuated the phosphorylation of stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) by TGF-α and HGF. Our results strongly suggest that GLP-1 suppresses TGF-α- and HGF-induced migration of HCC cells through inhibiting the SAPK/JNK signaling pathway, and that the inhibition by GLP-1 is due to cAMP production.
MeSH term(s)	Carcinoma, Hepatocellular/pathology ; Cell Line, Tumor ; Cell Movement/drug effects ; Cyclic AMP/biosynthesis ; Glucagon-Like Peptide 1/pharmacology ; Hepatocyte Growth Factor/pharmacology ; Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; Liver Neoplasms/pathology ; Mitogen-Activated Protein Kinases/metabolism ; Phosphorylation/drug effects ; Transforming Growth Factor alpha/pharmacology
Chemical Substances	Transforming Growth Factor alpha ; Hepatocyte Growth Factor (67256-21-7) ; Glucagon-Like Peptide 1 (89750-14-1) ; Cyclic AMP (E0399OZS9N) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2021-03-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2021.108851
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Article ; Online: SERMs (selective estrogen receptor modulator), acting as estrogen receptor β agonists in hepatocellular carcinoma cells, inhibit the transforming growth factor-α-induced migration via specific inhibition of AKT signaling pathway.

Matsushima-Nishiwaki, Rie / Yamada, Noriko / Hattori, Yuria / Hosokawa, Yui / Tachi, Junko / Hori, Takamitsu / Kozawa, Osamu

PloS one

2022 Volume 17, Issue 1, Page(s) e0262485

Abstract: Selective estrogen receptor modulator (SERM) interacts with estrogen receptors and acts as both an agonist or an antagonist, depending on the target tissue. SERM is widely used as a safer hormone replacement therapeutic medicine for postmenopausal ... ...

Abstract	Selective estrogen receptor modulator (SERM) interacts with estrogen receptors and acts as both an agonist or an antagonist, depending on the target tissue. SERM is widely used as a safer hormone replacement therapeutic medicine for postmenopausal osteoporosis. Regarding hepatocellular carcinoma (HCC), accumulating evidence indicates gender differences in the development, and that men are at higher morbidity risk than premenopausal women, suggesting that estrogen protects against HCC. However, it remains unclear whether SERM affects the HCC progression. Previously, we have shown that transforming growth factor (TGF)-α promotes the migration of HCC cells via p38 mitogen-activated protein kinases (MAPK), c-Jun N-terminal kinase and AKT. In the present study, we investigated whether SERM such as tamoxifen, raloxifene and bazedoxifene, affects the HCC cell migration using human HCC-derived HuH7 cells. Raloxifene and bazedoxifene but not tamoxifen, significantly suppressed the TGF-α-induced HuH7 cell migration. ERB041 and DPN, estrogen receptor (ER) β agonists, inhibited the TGF-α-induced cell migration whereas PPT, an ERα agonist, did not show the suppressive effect on the cell migration. ERB041 attenuated the TGF-α-induced phosphorylation of AKT without affecting the phosphorylation of p38 MAPK and c-Jun N-terminal kinase. Raloxifene and bazedoxifene also inhibited the phosphorylation of AKT by TGF-α. Furthermore, PHTPP, an ERβ antagonist, significantly reversed the suppression by both raloxifene and bazedoxifene of the TGF-α-induced cell migration. Taken together, our results strongly indicate that raloxifene and bazedoxifene, SERMs, suppress the TGF-α-induced migration of HCC cells through ERβ-mediated inhibition of the AKT signaling pathway.
MeSH term(s)	Apoptosis ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cell Movement ; Cell Proliferation ; Estrogen Receptor beta/agonists ; Estrogens/pharmacology ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Indoles/pharmacology ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Raloxifene Hydrochloride/pharmacology ; Selective Estrogen Receptor Modulators/pharmacology ; Tamoxifen/pharmacology ; Tumor Cells, Cultured
Chemical Substances	ESR2 protein, human ; Estrogen Receptor beta ; Estrogens ; Indoles ; Selective Estrogen Receptor Modulators ; Tamoxifen (094ZI81Y45) ; Raloxifene Hydrochloride (4F86W47BR6) ; AKT1 protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; bazedoxifene (Q16TT9C5BK)
Language	English
Publishing date	2022-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0262485
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Article ; Online: Oncostatin M reduces the synthesis of macrophage-colony stimulating factor stimulated by TGF-β via suppression of p44/p42 MAP kinase and JNK in osteoblasts.

Doi, Tomoaki / Hioki, Tomoyuki / Tachi, Junko / Ueda, Kyohei / Matsushima-Nishiwaki, Rie / Iida, Hiroki / Ogura, Shinji / Kozawa, Osamu / Tokuda, Haruhiko

Biomedical research (Tokyo, Japan)

2022 Volume 43, Issue 2, Page(s) 41–51

Abstract: Bone fracture is an important trauma frequently encountered into emergency medicine as well as orthopedics reflecting an aging society. Oncostatin M, an inflammatory cytokine produced by osteal macrophages, has been considered to play a crucial role in ... ...

Abstract	Bone fracture is an important trauma frequently encountered into emergency medicine as well as orthopedics reflecting an aging society. Oncostatin M, an inflammatory cytokine produced by osteal macrophages, has been considered to play a crucial role in fracture healing. Macrophage colony-stimulating factor (M-CSF) secreted from osteoblasts is essential in osteoclastgenesis, and the secretion is stimulated by transforming growth factor-β (TGF-β). The aim of this study is to elucidate the effects of oncostatin M on the TGF-β-induced M-CSF synthesis in osteoblast-like MC3T3-E1 cells and the underlying mechanisms. Oncostatin M attenuated the TGF-β-stimulated M-CSF release and the mRNA expressions. SMAD3 inhibitor SIS3, p38 MAP kinase inhibitor SB203580, MEK1/2 inhibitor PD98059, and SAPK/JNK inhibitor SP600125 significantly suppressed the M-CSF release. Oncostatin M suppressed the TGF-β-induced phosphorylation of p44/p42 MAP kinase and SAPK/JNK, but failed to affect the phosphorylation of SMAD3 and p38 MAP kinase. Oncostatin M attenuated the TGF-β-stimulated vascular endothelial growth factor (VEGF) release and the TGF-β-induced mRNA expressions of VEGF. These results strongly suggest that oncostatin M downregulates TGF-β signaling upstream of p44/p42 MAP kinase and SAPK/JNK, but not SMAD 2/3 and p38 MAP kinase, in osteoblasts, leading to the attenuation of M-CSF synthesis. Our findings might provide a new therapeutic strategy for the acceleration of fracture healing process.
MeSH term(s)	Macrophage Colony-Stimulating Factor/metabolism ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Oncostatin M/metabolism ; Oncostatin M/pharmacology ; Osteoblasts/metabolism ; Phosphorylation ; RNA, Messenger/metabolism ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/pharmacology ; Vascular Endothelial Growth Factor A/metabolism ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	RNA, Messenger ; Transforming Growth Factor beta ; Vascular Endothelial Growth Factor A ; Oncostatin M (106956-32-5) ; Macrophage Colony-Stimulating Factor (81627-83-0) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-03-24
Publishing country	Japan
Document type	Journal Article
ZDB-ID	604561-3
ISSN	1880-313X ; 0388-6107
ISSN (online)	1880-313X
ISSN	0388-6107
DOI	10.2220/biomedres.43.41
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Article ; Online: Acetaminophen reduces osteoprotegerin synthesis stimulated by PGE

Kim, Woo / Tokuda, Haruhiko / Tanabe, Kumiko / Yamaguchi, Shinobu / Hioki, Tomoyuki / Tachi, Junko / Matsushima-Nishiwaki, Rie / Kozawa, Osamu / Iida, Hiroki

Biomedical research (Tokyo, Japan)

2021 Volume 42, Issue 2, Page(s) 77–84

Abstract: Acetaminophen is one of the most widely used analgesic and antipyretic medicines, whose long-period use has reportedly been associated with an increased risk of bone fracture. However, the mechanism underlying this undesired effect remains to be ... ...

Abstract	Acetaminophen is one of the most widely used analgesic and antipyretic medicines, whose long-period use has reportedly been associated with an increased risk of bone fracture. However, the mechanism underlying this undesired effect remains to be investigated. The homeostatic control of bone tissue depends on the interaction between osteoblasts and osteoclasts. Osteoprotegerin produced by osteoblasts is known to play an essential role in suppressing osteoclast induction. We have previously reported that prostaglandin (PG) E
MeSH term(s)	3T3 Cells ; Acetaminophen/pharmacology ; Animals ; Anthracenes ; Bone Remodeling ; Bone and Bones/drug effects ; Densitometry ; Dinoprost/biosynthesis ; Dinoprostone/biosynthesis ; Down-Regulation ; MAP Kinase Kinase 4/metabolism ; Mice ; Mitogen-Activated Protein Kinase 3/metabolism ; Osteoblasts/drug effects ; Osteoblasts/metabolism ; Osteoprotegerin/biosynthesis ; Phosphorylation ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Anthracenes ; Osteoprotegerin ; pyrazolanthrone (1TW30Y2766) ; Acetaminophen (362O9ITL9D) ; Dinoprost (B7IN85G1HY) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2021-02-17
Publishing country	Japan
Document type	Journal Article
ZDB-ID	604561-3
ISSN	1880-313X ; 0388-6107
ISSN (online)	1880-313X
ISSN	0388-6107
DOI	10.2220/biomedres.42.77
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Article ; Online: Olive polyphenols attenuate TNF-α-stimulated M-CSF and IL-6 synthesis in osteoblasts: Suppression of Akt and p44/p42 MAP kinase signaling pathways.

Hioki, Tomoyuki / Tokuda, Haruhiko / Kuroyanagi, Gen / Kim, Woo / Tachi, Junko / Matsushima-Nishiwaki, Rie / Iida, Hiroki / Kozawa, Osamu

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2021 Volume 141, Page(s) 111816

Abstract: Background: Olive oil polyphenols, which possess cytoprotective activities like anti-oxidant and anti-inflammatory effects, could modulate osteoblast functions. The aim of this study is to elucidate the effects and the underlying mechanisms of ... ...

Abstract	Background: Olive oil polyphenols, which possess cytoprotective activities like anti-oxidant and anti-inflammatory effects, could modulate osteoblast functions. The aim of this study is to elucidate the effects and the underlying mechanisms of hydroxytyrosol and oleuropein on the tumor necrosis factor-α (TNF-α)-induced macrophage colony-stimulating factor (M-CSF) and interleukin-6 (IL-6) synthesis in osteoblasts. Methods: Osteoblast-like MC3T3-E1 cells were pretreated with hydroxytyrosol, oleuropein, deguelin, PD98059 or wedelolactone, and then stimulated by TNF-α. The levels of M-CSF and IL-6 in the conditioned medium were determined with ELISA. The mRNA expression levels of M-CSF or IL-6 were determined with real-time RT-PCR. The phosphorylation levels of Akt, p44/p42 mitogen-activated protein (MAP) kinase or NF-κB in the cell lysates were determined with Western blot analysis. Results: Hydroxytyrosol and oleuropein attenuated the TNF-α-stimulated M-CSF release. Deguelin, an inhibitor of Akt, significantly suppressed the TNF-α-stimulated M-CSF release, which failed to be affected by the MEK1/2 inhibitor PD98059 or the IκB inhibitor wedelolactone. Hydroxytyrosol and oleuropein suppressed the TNF-α-induced phosphorylation of Akt and p44/p42 MAP kinase. Hydroxytyrosol and oleuropein attenuated the TNF-α-stimulated IL-6 release. Hydroxytyrosol suppressed the TNF-α-induced mRNA expressions of M-CSF and IL-6. Hydroxytyrosol or oleuropein failed to affect the cell viability. Conclusion: Our present findings strongly suggest that olive oil polyphenols hydroxytyrosol and oleuropein down-regulates TNF-α signaling at the points upstream of Akt and p44/p42 MAP kinase in osteoblasts, leading to the attenuation of M-CSF and IL-6 synthesis.
MeSH term(s)	3T3 Cells ; Animals ; Culture Media, Conditioned ; Interleukin-6/biosynthesis ; Iridoid Glucosides/pharmacology ; MAP Kinase Signaling System/drug effects ; Macrophage Colony-Stimulating Factor/biosynthesis ; Mice ; Mitogen-Activated Protein Kinase 1/antagonists & inhibitors ; Olea/chemistry ; Oncogene Protein v-akt/antagonists & inhibitors ; Phenylethyl Alcohol/analogs & derivatives ; Phenylethyl Alcohol/pharmacology ; Polyphenols/pharmacology ; Rotenone/analogs & derivatives ; Rotenone/pharmacology ; Signal Transduction/drug effects ; Tumor Necrosis Factor-alpha/antagonists & inhibitors
Chemical Substances	Culture Media, Conditioned ; Interleukin-6 ; Iridoid Glucosides ; Polyphenols ; Tumor Necrosis Factor-alpha ; interleukin-6, mouse ; Rotenone (03L9OT429T) ; 3,4-dihydroxyphenylethanol (10597-60-1) ; oleuropein (2O4553545L) ; Macrophage Colony-Stimulating Factor (81627-83-0) ; Oncogene Protein v-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; deguelin (K5Z93K66IE) ; Phenylethyl Alcohol (ML9LGA7468)
Language	English
Publishing date	2021-06-11
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2021.111816
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Article ; Online: Amplification by tramadol of PGD

Hioki, Tomoyuki / Tokuda, Haruhiko / Tanabe, Kumiko / Kim, Woo / Tachi, Junko / Yamaguchi, Shinobu / Matsushima-Nishiwaki, Rie / Kozawa, Osamu / Iida, Hiroki

Prostaglandins, leukotrienes, and essential fatty acids

2021 Volume 172, Page(s) 102323

Abstract: Tramadol, a weak μ-opioid receptor (MOR) agonist with inhibitory effects on the reuptake of serotonin (5-hydroxytryptamine; 5-HT) and norepinephrine, is an effective analgesic to chronic pains. Osteoprotegerin produced by osteoblasts is essential for ... ...

Abstract	Tramadol, a weak μ-opioid receptor (MOR) agonist with inhibitory effects on the reuptake of serotonin (5-hydroxytryptamine; 5-HT) and norepinephrine, is an effective analgesic to chronic pains. Osteoprotegerin produced by osteoblasts is essential for bone remodeling to suppress osteoclastic bone resorption. We previously reported that prostaglandin D
MeSH term(s)	Analgesics, Opioid/pharmacology ; Animals ; Anthracenes/pharmacology ; Bone Remodeling/drug effects ; Enzyme Inhibitors/pharmacology ; Fluvoxamine/pharmacology ; Imidazoles/pharmacology ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mice ; Naloxone/pharmacology ; Narcotic Antagonists/pharmacology ; Osteoblasts/drug effects ; Osteoblasts/metabolism ; Osteoprotegerin/biosynthesis ; Osteoprotegerin/drug effects ; Prostaglandin D2/pharmacology ; Pyridines/pharmacology ; RNA, Messenger/drug effects ; RNA, Messenger/metabolism ; Receptors, Opioid, mu/agonists ; Serotonin Plasma Membrane Transport Proteins/metabolism ; Serotonin Uptake Inhibitors/pharmacology ; Sertraline/pharmacology ; Tramadol/pharmacology ; p38 Mitogen-Activated Protein Kinases/drug effects ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Analgesics, Opioid ; Anthracenes ; Enzyme Inhibitors ; Imidazoles ; Narcotic Antagonists ; Osteoprotegerin ; Pyridines ; RNA, Messenger ; Receptors, Opioid, mu ; Serotonin Plasma Membrane Transport Proteins ; Serotonin Uptake Inhibitors ; pyrazolanthrone (1TW30Y2766) ; Naloxone (36B82AMQ7N) ; Tramadol (39J1LGJ30J) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Fluvoxamine (O4L1XPO44W) ; SB 203580 (OU13V1EYWQ) ; Sertraline (QUC7NX6WMB) ; Prostaglandin D2 (RXY07S6CZ2)
Language	English
Publishing date	2021-08-08
Publishing country	Scotland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	286714-x
ISSN	1532-2823 ; 0952-3278
ISSN (online)	1532-2823
ISSN	0952-3278
DOI	10.1016/j.plefa.2021.102323
Database	MEDical Literature Analysis and Retrieval System OnLINE

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