Overexpression of the granulocyte colony-stimulating factor gene impairs bone morphogenetic protein responsiveness in mice.

Overexpression of the granulocyte colony-stimulating factor gene impairs bone morphogenetic protein responsiveness in mice. Research Abstract Details 

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Overexpression of the granulocyte colony-stimulating factor gene impairs bone morphogenetic protein responsiveness in mice. Abstract Text:

H Kuwabara,T Wada,T Oda,H Yoshikawa,N Sawada,Y Kokai,S Ishii,

Granulocyte colony-stimulating factor (G-CSF) is the major hematopoietic growth factor regulating the production and differentiation of neutrophils. We previously demonstrated that permanent overexpression of G-CSF in transgenic mice produces a dramatic enlargement of the bone cavity and reduction of bone mass. This phenotype was shown to be associated with an increase of osteoclast-mediated bone resorption. As a way of determining the role of G-CSF in bone formation in vivo, an ectopic bone was induced subcutaneously into G-CSF transgenic mice by bone morphogenetic protein (BMP)-2, a potent initiator of bone and cartilage from undifferentiated mesenchymal cells. A BMP-2/atelocollagen pellet containing recombinant human BMP-2 was implanted into a dorsal subfascial pocket. At one week after implantation, proliferation of mesenchymal cells around the implant was significantly decreased in transgenic mice compared with control mice. At three weeks, an ectopic bone containing bone marrow was formed both in transgenic and control mice. However, the ectopic bones of the transgenic mice were smaller and less consistent than those of control mice, and the calcium contents were reduced to 56.2% of those of controls. The ectopic bone in the G-CSF mice showed poor development of both lamellar and trabecular bone. Semiquantitative reverse transcription-polymerase chain reaction analysis of the ectopic bone at 3 weeks disclosed no significant differences in the mRNA levels of type I collagen, osteopontin, and osteocalcin between G-CSF mice and control mice. Immunohistochemical study in G-CSF mice showed reduced staining of osteocalcin in the bone matrix surrounding the reduced number of osteoblasts. The half-life of BMP in the implants was prolonged to 7 to 9 days in the G-CSF mice, whereas it was 5 days in the control mice. Collectively, the permanent expression of G-CSF may retard the differentiation process of osteoblasts by impairing the initial induction of mesenchymal cells, resulting in reduction of bone mass, suggesting that G-CSF regulates the bone metabolism by modulating both osteoclast and osteoblast function. Furthermore, it is suggested that G-CSF is a potent modulator of the BMP-2 signal pathway in vivo.

Overexpression of the granulocyte colony-stimulating factor gene impairs bone morphogenetic protein responsiveness in mice. Publishing Authors By Initials

H Kuwabara,T Wada,T Oda,H Yoshikawa,N Sawada,Y Kokai,S Ishii,

For similar genetic structures: genome: genome components: genes: transgenes research abstracts see: genetic structures: genome: genome components: genes: transgenes research

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Overexpression of the granulocyte colony-stimulating factor gene impairs bone morphogenetic protein responsiveness in mice. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Laboratory investigation; a journal of technical m

VOLUME: 81

Page Numbers: 1133-41

Journal Abbreviation: Lab. Invest.

ISSN: 0023-6837

DAY: 19

MONTH: Aug

YEAR: 2001

Overexpression of the granulocyte colony-stimulating factor gene impairs bone morphogenetic protein responsiveness in mice. Information

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LANGUAGE: eng

NlmUniqueID: 376617

Overexpression of the granulocyte colony-stimulating factor gene impairs bone morphogenetic protein responsiveness in mice. Keywords Mesh Terms:

KEYWORDS: Transgenes

MESH TERMS: metabolism

Chemical & Substance for Abstract: Overexpression of the granulocyte colony-stimulating factor gene impairs bone morphogenetic protein responsiveness in mice. Information

Substance Name: Collagen

Registry Number: 9007-34-5

Grant and Affiliation Information for Overexpression of the granulocyte colony-stimulating factor gene impairs bone morphogenetic protein responsiveness in mice.

AFFILIATION: Department of Orthopedic Surgery, Sapporo Medical University, Sapporo, Japan.

Country: United States

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MEDLINETA: Lab Invest

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