Alpha1-adrenergic receptor stimulation induces the expression of receptor activator of nuclear factor kappaB ligand gene via protein kinase C and extracellular signal-regulated kinase pathways in MC3T3-E1 osteoblast-like cells.

Alpha1-adrenergic receptor stimulation induces the expression of receptor activator of nuclear factor kappaB ligand gene via protein kinase C and extracellular signal-regulated kinase pathways in MC3T3-E1 osteoblast-like cells. Research Abstract Details 

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Alpha1-adrenergic receptor stimulation induces the expression of receptor activator of nuclear factor kappaB ligand gene via protein kinase C and extracellular signal-regulated kinase pathways in MC3T3-E1 osteoblast-like cells. Abstract Text:

Toshihiro Nishiura,Kimio Abe,Toshihiro Nishiura,Kimio Abe,

The receptor activator of nuclear factor kappaB ligand (RANKL) produced by bone marrow stromal/osteoblast cells is a crucial regulator of osteoclastgenesis and bone resorption. Osteoblastic cells have been demonstrated to express alpha(1)-adrenergic receptors. OBJECTIVE: The purpose of this study was to test the hypothesis that alpha(1)-adrenergic receptor stimulation induces the expression of RANKL gene via protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) pathways in osteoblastic cells. DESIGN: The steady-state mRNA levels of RANKL and activation of ERK in mouse MC3T3-E1 osteoblast-like cells were analyzed by semi-quantitative RT-PCR and Western blotting, respectively. RESULTS: In three alpha(1)-adrenergic receptor subtype mRNAs, alpha(1b)- and alpha(1d)-subtypes were expressed in MC3T3-E1 cells. The mRNA levels of RANKL were increased by phenylephrine (alpha(1)-agonist) in time- and dose-dependent manners. Prazosin (alpha(1)-antagonist) suppressed the phenylephrine-induced RANKL mRNA expression, but yohimbine (alpha(2)-antagonist) and propranolol (beta-antagonist) did not. Phorbol 12-myristate 13-acetate (PMA, PKC activator) increased RANKL mRNA expression and GF109203X (PKC inhibitor) suppressed the phenylephrine-induced RANKL mRNA expression. Both phenylephrine and PMA stimulated the phosphorylation of ERK, while both prazosin and GF109203X inhibited phenylephrine-induced ERK activation. Pretreatment with PD98059 (ERK kinase inhibitor) inhibited both the phosphorylation of ERK and the expression of RANKL gene induced by phenylephrine in MC3T3-E1 cells. CONCLUSION: These results show that alpha(1b)- and alpha(1d)-adrenergic receptor subtype genes are expressed and the expression of RANKL mRNA may be regulated by alpha(1)-adrenergic receptor stimulation in osteoblastic cells. The induction of RANKL mRNA by activating the alpha(1)-adrenergic receptor is probably mediated via PKC and ERK signalling pathways in osteoblastic cells.

Alpha1-adrenergic receptor stimulation induces the expression of receptor activator of nuclear factor kappaB ligand gene via protein kinase C and extracellular signal-regulated kinase pathways in MC3T3-E1 osteoblast-like cells. Publishing Authors By Initials

T Nishiura,K Abe,T Nishiura,K Abe,

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Alpha1-adrenergic receptor stimulation induces the expression of receptor activator of nuclear factor kappaB ligand gene via protein kinase C and extracellular signal-regulated kinase pathways in MC3T3-E1 osteoblast-like cells. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Archives of oral biology

VOLUME: 52

Page Numbers: 778-85

Journal Abbreviation: Arch. Oral Biol.

ISSN: 0003-9969

DAY: 15

MONTH: 02

YEAR: 2007

Alpha1-adrenergic receptor stimulation induces the expression of receptor activator of nuclear factor kappaB ligand gene via protein kinase C and extracellular signal-regulated kinase pathways in MC3T3-E1 osteoblast-like cells. Information

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LANGUAGE: eng

NlmUniqueID: 116711

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Grant and Affiliation Information for Alpha1-adrenergic receptor stimulation induces the expression of receptor activator of nuclear factor kappaB ligand gene via protein kinase C and extracellular signal-regulated kinase pathways in MC3T3-E1 osteoblast-like cells.

AFFILIATION: Section of Biochemistry, Department of Functional Bioscience, Fukuoka Dental College, 2-15-1 Tamura, Sawara-ku, Fukuoka 814-0193, Japan. nishiura@college.fdcnet.ac.jp

Country: England

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MEDLINETA: Arch Oral Biol

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