Hormonal regulation of intercellular communication

Parathyroid hormone increases connexin 43 gene expression and gap-junctional communication in osteoblastic cells

Paul C. Schiller, Parmender P Mehta, Bernard A. Roos, Guy A. Howard

Research output: Contribution to journalArticle

118 Citations (Scopus)

Abstract

The presence of gap junctions between osteoblastic cells has been previously reported. For this study we used the rat osteosarcoma cell line UMR 106, which expresses the osteoblastic phenotype, as a model to characterize further the nature, physiology, and regulation of gap junctions. Northern blot analysis identified a 3.0-kilobase RNA species corresponding to the gap junction protein connexin 43. The presence of two other connexin RNA species (26 and 32) could not be detected by this method in these cells. The identified connexin RNA was amplified by reverse transcription coupled to polymerase chain reaction; the sequence of the amplified product appears identical to the sequence of a cloned rat heart connexin 43 gene. After treatment with PTH, forskolin, and 8-Br-cAMP (a cAMP analog), the levels of connexin 43 RNA in UMR 106 cells increased. Further evidence for the role of PTH and cAMP in the physiology of gap junctions in these cells was obtained with Lucifer yellow dye transfer experiments. Gap-junctional intercellular communication increased in response to PTH and forskolin (an inducer of adenylate cyclase activity). Expression of connexin 43 RNA increased severalfold in response to PTH in a concentration- and time-dependent fashion. Connexin 43 RNA and its PTH-mediated stimulation were also observed in several other osteoblastic cell lines. The roles of PTH and forskolin in regulating the physiological state of gap junctions were confirmed in primary cultures of rat calvaria osteoblasts.

Original languageEnglish (US)
Pages (from-to)1433-1440
Number of pages8
JournalMolecular Endocrinology
Volume6
Issue number9
DOIs
StatePublished - Jan 1 1992

Fingerprint

Connexin 43
Parathyroid Hormone
Gap Junctions
Communication
RNA
Gene Expression
Connexins
Colforsin
Cell Line
Osteosarcoma
Osteoblasts
Adenylyl Cyclases
Skull
Northern Blotting
Reverse Transcription
Coloring Agents
Phenotype
Polymerase Chain Reaction
Genes

ASJC Scopus subject areas

  • Molecular Biology
  • Endocrinology

Cite this

Hormonal regulation of intercellular communication : Parathyroid hormone increases connexin 43 gene expression and gap-junctional communication in osteoblastic cells. / Schiller, Paul C.; Mehta, Parmender P; Roos, Bernard A.; Howard, Guy A.

In: Molecular Endocrinology, Vol. 6, No. 9, 01.01.1992, p. 1433-1440.

Research output: Contribution to journalArticle

@article{d367054efa6342a38dea61f61cc46f50,
title = "Hormonal regulation of intercellular communication: Parathyroid hormone increases connexin 43 gene expression and gap-junctional communication in osteoblastic cells",
abstract = "The presence of gap junctions between osteoblastic cells has been previously reported. For this study we used the rat osteosarcoma cell line UMR 106, which expresses the osteoblastic phenotype, as a model to characterize further the nature, physiology, and regulation of gap junctions. Northern blot analysis identified a 3.0-kilobase RNA species corresponding to the gap junction protein connexin 43. The presence of two other connexin RNA species (26 and 32) could not be detected by this method in these cells. The identified connexin RNA was amplified by reverse transcription coupled to polymerase chain reaction; the sequence of the amplified product appears identical to the sequence of a cloned rat heart connexin 43 gene. After treatment with PTH, forskolin, and 8-Br-cAMP (a cAMP analog), the levels of connexin 43 RNA in UMR 106 cells increased. Further evidence for the role of PTH and cAMP in the physiology of gap junctions in these cells was obtained with Lucifer yellow dye transfer experiments. Gap-junctional intercellular communication increased in response to PTH and forskolin (an inducer of adenylate cyclase activity). Expression of connexin 43 RNA increased severalfold in response to PTH in a concentration- and time-dependent fashion. Connexin 43 RNA and its PTH-mediated stimulation were also observed in several other osteoblastic cell lines. The roles of PTH and forskolin in regulating the physiological state of gap junctions were confirmed in primary cultures of rat calvaria osteoblasts.",
author = "Schiller, {Paul C.} and Mehta, {Parmender P} and Roos, {Bernard A.} and Howard, {Guy A.}",
year = "1992",
month = "1",
day = "1",
doi = "10.1210/mend.6.9.1331776",
language = "English (US)",
volume = "6",
pages = "1433--1440",
journal = "Molecular Endocrinology",
issn = "0888-8809",
publisher = "The Endocrine Society",
number = "9",

}

TY - JOUR

T1 - Hormonal regulation of intercellular communication

T2 - Parathyroid hormone increases connexin 43 gene expression and gap-junctional communication in osteoblastic cells

AU - Schiller, Paul C.

AU - Mehta, Parmender P

AU - Roos, Bernard A.

AU - Howard, Guy A.

PY - 1992/1/1

Y1 - 1992/1/1

N2 - The presence of gap junctions between osteoblastic cells has been previously reported. For this study we used the rat osteosarcoma cell line UMR 106, which expresses the osteoblastic phenotype, as a model to characterize further the nature, physiology, and regulation of gap junctions. Northern blot analysis identified a 3.0-kilobase RNA species corresponding to the gap junction protein connexin 43. The presence of two other connexin RNA species (26 and 32) could not be detected by this method in these cells. The identified connexin RNA was amplified by reverse transcription coupled to polymerase chain reaction; the sequence of the amplified product appears identical to the sequence of a cloned rat heart connexin 43 gene. After treatment with PTH, forskolin, and 8-Br-cAMP (a cAMP analog), the levels of connexin 43 RNA in UMR 106 cells increased. Further evidence for the role of PTH and cAMP in the physiology of gap junctions in these cells was obtained with Lucifer yellow dye transfer experiments. Gap-junctional intercellular communication increased in response to PTH and forskolin (an inducer of adenylate cyclase activity). Expression of connexin 43 RNA increased severalfold in response to PTH in a concentration- and time-dependent fashion. Connexin 43 RNA and its PTH-mediated stimulation were also observed in several other osteoblastic cell lines. The roles of PTH and forskolin in regulating the physiological state of gap junctions were confirmed in primary cultures of rat calvaria osteoblasts.

AB - The presence of gap junctions between osteoblastic cells has been previously reported. For this study we used the rat osteosarcoma cell line UMR 106, which expresses the osteoblastic phenotype, as a model to characterize further the nature, physiology, and regulation of gap junctions. Northern blot analysis identified a 3.0-kilobase RNA species corresponding to the gap junction protein connexin 43. The presence of two other connexin RNA species (26 and 32) could not be detected by this method in these cells. The identified connexin RNA was amplified by reverse transcription coupled to polymerase chain reaction; the sequence of the amplified product appears identical to the sequence of a cloned rat heart connexin 43 gene. After treatment with PTH, forskolin, and 8-Br-cAMP (a cAMP analog), the levels of connexin 43 RNA in UMR 106 cells increased. Further evidence for the role of PTH and cAMP in the physiology of gap junctions in these cells was obtained with Lucifer yellow dye transfer experiments. Gap-junctional intercellular communication increased in response to PTH and forskolin (an inducer of adenylate cyclase activity). Expression of connexin 43 RNA increased severalfold in response to PTH in a concentration- and time-dependent fashion. Connexin 43 RNA and its PTH-mediated stimulation were also observed in several other osteoblastic cell lines. The roles of PTH and forskolin in regulating the physiological state of gap junctions were confirmed in primary cultures of rat calvaria osteoblasts.

UR - http://www.scopus.com/inward/record.url?scp=0026746159&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026746159&partnerID=8YFLogxK

U2 - 10.1210/mend.6.9.1331776

DO - 10.1210/mend.6.9.1331776

M3 - Article

VL - 6

SP - 1433

EP - 1440

JO - Molecular Endocrinology

JF - Molecular Endocrinology

SN - 0888-8809

IS - 9

ER -