Serial passage of MC3T3-E1 cells alters osteoblastic function and responsiveness to transforming growth factor-beta1 and bone morphogenetic protein-2.

Serial passage of MC3T3-E1 cells alters osteoblastic function and responsiveness to transforming growth factor-beta1 and bone morphogenetic protein-2. Research Abstract Details 

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Serial passage of MC3T3-E1 cells alters osteoblastic function and responsiveness to transforming growth factor-beta1 and bone morphogenetic protein-2. Abstract Text:

C Y Chung,A Iida-Klein,L E Wyatt,G H Rudkin,K Ishida,D T Yamaguchi,T A Miller,

The murine-derived clonal MC3T3-E1 cell is a well-studied osteoblast-like cell line. To understand the effects of serial passages on its cellular function, we examined changes in cell morphology, gap junctional intercellular communication (GJIC), proliferation, and osteoblastic function between early passage (<20) and late passage (>65) cells. MC3T3-E1 cells developed an elongated, spindle shape after multiple passages. Intercellular communication decreased significantly (33%) in late vs. early passage cells. Transforming growth factor-beta1 (TGF-beta1) stimulated cell proliferation in early passage cells and induced c-fos expression, while it inhibited proliferation in late passage cells. Using alkaline phosphatase (ALP) activity and osteocalcin (OC) secretion as markers for osteoblastic function and differentiation, we demonstrated that both markers were significantly reduced after multiple cell passages. Bone morphogenetic protein-2 (BMP-2) significantly enhanced ALP activity and OC secretion in early passage cells while TGF-beta1 exerted an opposite effect. Both BMP-2 and TGF-beta1 had minimal effects on late passage cells. We conclude that serial passage alters MC3T3-E1 cell morphology, and significantly diminishes GJIC, osteoblastic function, TGF-beta1-mediated cell proliferation, and responsiveness to TGF-beta1 and BMP-2. Cell passage numbers should be clearly defined in functional studies involving MC3T3-E1 cells.

Serial passage of MC3T3-E1 cells alters osteoblastic function and responsiveness to transforming growth factor-beta1 and bone morphogenetic protein-2. Publishing Authors By Initials

CY Chung,A Iida-Klein,LE Wyatt,GH Rudkin,K Ishida,DT Yamaguchi,TA Miller,

For similar peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta research

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Serial passage of MC3T3-E1 cells alters osteoblastic function and responsiveness to transforming growth factor-beta1 and bone morphogenetic protein-2. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Biochemical and biophysical research communication

VOLUME: 265

Page Numbers: 246-51

Journal Abbreviation: Biochem. Biophys. Res. Commun.

ISSN: 0006-291X

DAY: 19

MONTH: Nov

YEAR: 1999

Serial passage of MC3T3-E1 cells alters osteoblastic function and responsiveness to transforming growth factor-beta1 and bone morphogenetic protein-2. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 372516

Serial passage of MC3T3-E1 cells alters osteoblastic function and responsiveness to transforming growth factor-beta1 and bone morphogenetic protein-2. Keywords Mesh Terms:

KEYWORDS: Transforming Growth Factor beta

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Serial passage of MC3T3-E1 cells alters osteoblastic function and responsiveness to transforming growth factor-beta1 and bone morphogenetic protein-2. Information

Substance Name: Alkaline Phosphatase

Registry Number: EC 3.1.3.1

Grant and Affiliation Information for Serial passage of MC3T3-E1 cells alters osteoblastic function and responsiveness to transforming growth factor-beta1 and bone morphogenetic protein-2.

AFFILIATION: Plastic Surgery Section, West Los Angeles VA Medical Center, Los Angeles, California, 90073, USA.

Country: UNITED STATES

AGENCY: United States NIA

GRANT: F32AG05708-01

ACRONYM: AG

MEDLINETA: Biochem Biophys Res Commun

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