1α,25-dihydroxyvitamin D3 increases TGF β1 binding to human osteoblasts

David Nagel, Rajiv Kumar

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

1β,25-Dihydroxyvitamin D3 (1α,25(OH)2D3) increases the binding of transforming growth factor β1(TGF β1) via TGF β receptors to the surface of human osteoblasts. The increase in TGF β receptors induced by 1α,25(OH)2D3 is dependent on increases in TGF β secretion induced by 1α,25(OH)2D3, since antibodies directed against TGF β block the increase in TGF β1 binding. The increase in TGF β type I and II receptors on cell surfaces following 1α,25(OH)2D3 treatment is associated with increases in receptor mRNA concentrations. Increases in receptor mRNA concentrations following 1α,25(OH)2D3 treatment are not due to changes in receptor gene transcription. The role of TGF β receptors, in mediating the growth responses to 1α,25(OH)2D3 is demonstrated by showing that osteoblasts which express dominant negative, kinase-deficient TGF β type II receptors, fail to respond to the growth-inhibitory effects of 1α,25(OH)2D3. An increase in TGF β receptor expression is important in mediating 1α,25(OH)2D3-associated changes in the growth rate of osteoblasts.

Original languageEnglish (US)
Pages (from-to)1558-1563
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume290
Issue number5
DOIs
StatePublished - 2002

Fingerprint

Calcitriol
Osteoblasts
Transforming Growth Factors
Growth
Messenger RNA
Cell Surface Receptors
Transcription
Phosphotransferases
Genes
Antibodies

Keywords

  • 1α,25-dihydroxyvitamin D
  • Cellular growth
  • Osteoblasts
  • TGF β receptors
  • Transforming growth factor β

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

1α,25-dihydroxyvitamin D3 increases TGF β1 binding to human osteoblasts. / Nagel, David; Kumar, Rajiv.

In: Biochemical and Biophysical Research Communications, Vol. 290, No. 5, 2002, p. 1558-1563.

Research output: Contribution to journalArticle

@article{63d8e2292dbd4b4f967cbb2c1030667c,
title = "1α,25-dihydroxyvitamin D3 increases TGF β1 binding to human osteoblasts",
abstract = "1β,25-Dihydroxyvitamin D3 (1α,25(OH)2D3) increases the binding of transforming growth factor β1(TGF β1) via TGF β receptors to the surface of human osteoblasts. The increase in TGF β receptors induced by 1α,25(OH)2D3 is dependent on increases in TGF β secretion induced by 1α,25(OH)2D3, since antibodies directed against TGF β block the increase in TGF β1 binding. The increase in TGF β type I and II receptors on cell surfaces following 1α,25(OH)2D3 treatment is associated with increases in receptor mRNA concentrations. Increases in receptor mRNA concentrations following 1α,25(OH)2D3 treatment are not due to changes in receptor gene transcription. The role of TGF β receptors, in mediating the growth responses to 1α,25(OH)2D3 is demonstrated by showing that osteoblasts which express dominant negative, kinase-deficient TGF β type II receptors, fail to respond to the growth-inhibitory effects of 1α,25(OH)2D3. An increase in TGF β receptor expression is important in mediating 1α,25(OH)2D3-associated changes in the growth rate of osteoblasts.",
keywords = "1α,25-dihydroxyvitamin D, Cellular growth, Osteoblasts, TGF β receptors, Transforming growth factor β",
author = "David Nagel and Rajiv Kumar",
year = "2002",
doi = "10.1006/bbrc.2002.6387",
language = "English (US)",
volume = "290",
pages = "1558--1563",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "5",

}

TY - JOUR

T1 - 1α,25-dihydroxyvitamin D3 increases TGF β1 binding to human osteoblasts

AU - Nagel, David

AU - Kumar, Rajiv

PY - 2002

Y1 - 2002

N2 - 1β,25-Dihydroxyvitamin D3 (1α,25(OH)2D3) increases the binding of transforming growth factor β1(TGF β1) via TGF β receptors to the surface of human osteoblasts. The increase in TGF β receptors induced by 1α,25(OH)2D3 is dependent on increases in TGF β secretion induced by 1α,25(OH)2D3, since antibodies directed against TGF β block the increase in TGF β1 binding. The increase in TGF β type I and II receptors on cell surfaces following 1α,25(OH)2D3 treatment is associated with increases in receptor mRNA concentrations. Increases in receptor mRNA concentrations following 1α,25(OH)2D3 treatment are not due to changes in receptor gene transcription. The role of TGF β receptors, in mediating the growth responses to 1α,25(OH)2D3 is demonstrated by showing that osteoblasts which express dominant negative, kinase-deficient TGF β type II receptors, fail to respond to the growth-inhibitory effects of 1α,25(OH)2D3. An increase in TGF β receptor expression is important in mediating 1α,25(OH)2D3-associated changes in the growth rate of osteoblasts.

AB - 1β,25-Dihydroxyvitamin D3 (1α,25(OH)2D3) increases the binding of transforming growth factor β1(TGF β1) via TGF β receptors to the surface of human osteoblasts. The increase in TGF β receptors induced by 1α,25(OH)2D3 is dependent on increases in TGF β secretion induced by 1α,25(OH)2D3, since antibodies directed against TGF β block the increase in TGF β1 binding. The increase in TGF β type I and II receptors on cell surfaces following 1α,25(OH)2D3 treatment is associated with increases in receptor mRNA concentrations. Increases in receptor mRNA concentrations following 1α,25(OH)2D3 treatment are not due to changes in receptor gene transcription. The role of TGF β receptors, in mediating the growth responses to 1α,25(OH)2D3 is demonstrated by showing that osteoblasts which express dominant negative, kinase-deficient TGF β type II receptors, fail to respond to the growth-inhibitory effects of 1α,25(OH)2D3. An increase in TGF β receptor expression is important in mediating 1α,25(OH)2D3-associated changes in the growth rate of osteoblasts.

KW - 1α,25-dihydroxyvitamin D

KW - Cellular growth

KW - Osteoblasts

KW - TGF β receptors

KW - Transforming growth factor β

UR - http://www.scopus.com/inward/record.url?scp=0036295959&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036295959&partnerID=8YFLogxK

U2 - 10.1006/bbrc.2002.6387

DO - 10.1006/bbrc.2002.6387

M3 - Article

VL - 290

SP - 1558

EP - 1563

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 5

ER -