8. Gene expression in osteoblast cells

Rodan, G.A.; Harada, Shun Ichi; Suva, Larry J.; Tanaka, Hirofumi; Rodan, SB

doi:10.1016/8756-3282(94)90719-6

Cited by 5 publications

(5 citation statements)

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“…The osteocalcin gene is expressed in progenitor-like cells after induction of osteoblast differentiation [Shalhoub et al, 1992;Katagiri et al, 1994;Rosen et al, 19941, in postproliferative osteoblasts in vitro and i n vivo, and is upregulated at the onset of mineralization of the bone extracellular matrix i n vitro and in vivo [reviewed in Stein and Lian, 19931. Osteocalcin is also expressed in several osteosarcoma or transformed cell lines exhibiting properties (e.g., hormone responsiveness and ability to form a mineralized matrix) of the mature osteoblast phenotype [Rodan and Noda, 1991;Rodan et al, 19931. This developmental regulation and tissue specificity provides an opportunity to search for factors which control transcription of osteocalcin that may also control osteoblast differentiation.…”

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confidence: 99%

Bone tissue-specific transcription of the osteocalcin gene: Role of an activator osteoblast-specific complex and suppressor hox proteins that bind the OC box

et al. 1996

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Bone-specific expression of the osteocalcin gene is transcriptionally controlled. Deletion analysis of osteocalcin promoter sequences by transient transfection of osseous (ROS 17/2.8) and nonosseous (R2 fibroblast) cells revealed that the most proximal 108 nucleotides are sufficient to confer tissue-specific expression. By gel mobility shift assays with wild-type and mutated oligonucleotides and nuclear extracts from several different cell lines we identified a novel transcription factor complex which exhibits sequence-specific interactions with the primary transcriptional element, the OC box (nt -99 to -76). This OC box binding protein (OCBP) is present only in osteoblast-like cells. Methylation interference demonstrated association of the factor with OC box sequences overlapping the Msx homeodomain consensus binding site. By assaying several mutations of the OC box, both in gel shift and transient transfection studies using ROS 17/2.8, we show the following. First, binding of OCBP correlates with osteocalcin promoter activity in ROS 17/2.8 cells. Increased binding leads to a 2-3-fold increase in transcription, while decreased binding results in transcription 30-40% of control. Second, homeodomain protein binding suppresses transcription. However, Msx expression is critical for full development of the bone phenotype as determined by antisense studies. Last, we show that one of the mutations of the OC box permits expression of osteocalcin in non-osseous cell lines. In summary, we demonstrate association of at least two classes of tissue-restricted transcription factors with the OC box element, the OCBP and Msx proteins, supporting the concept that these sequences contribute to defining tissue specificity.

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confidence: 99%

Bone tissue-specific transcription of the osteocalcin gene: Role of an activator osteoblast-specific complex and suppressor hox proteins that bind the OC box

et al. 1996

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“…Alkaline phosphatase activity and osteocalcin production. ALP activity and osteocalcin production, two parameters of osteoblast differentiation (39), were determined in confluent marrow stromal cells isolated from treated and untreated rats with rhTGF-,/2. Bone marrow stromal cells were plated at 5,000 cells/cm2 in six-well plates (Falcon), cultured until confluence in DME with 10% FCS, and then cultured for 2 d in serum-free medium.…”

Section: Introductionmentioning

confidence: 99%

Systemic administration of transforming growth factor-beta 2 prevents the impaired bone formation and osteopenia induced by unloading in rats.

Machwate¹,

Zérath²,

Holy³

et al. 1995

J. Clin. Invest.

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We investigated the effect of recombinant human transforming growth factor .82 (rhTGF-J32) administration on trabecular bone loss induced by unloading in rats. Hind limb suspension for 14 d inhibited bone formation and induced osteopenia as shown by decreased bone volume, calcium and protein contents in long bone metaphysis. Systemic infusion of rhTGF-P2 (2 jug/kg per day) maintained normal bone formation rate, and prevented the decrease in bone volume, bone mineral content, trabecular thickness and number induced by unloading. In vitro analysis of tibial marrow stromal cells showed that rhTGF-f32 infusion in unloaded rats increased the proliferation of osteoblast precursor cells, but did not affect alkaline phosphatase activity or osteocalcin production. Northern blot analysis of RNA extracted from the femoral metaphysis showed that rhTGF-fi2 infusion in unloaded rats increased steady-state levels of type I collagen mRNA but not alkaline phosphatase mRNA levels. rhTGF-P2 infusion at the dose used had no effect on metaphyseal bone volume and formation, osteoblast proliferation or collagen expression in control rats. The results show that systemic administration of rhTGF-l2 enhances osteoblast precursor cell proliferation and type I collagen expression by osteoblasts, and prevents the impaired bone formation and osteopenia induced by unloading. (J. Cln. Invest. 1995.

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“…В культуре ОБ in vitro было показано, что они имеют рецепторы к гормонам и регуляторным факторам (паратгормон, простагландины Е 2 -PGE 2 , 1,25(ОН) 2 D 3 ), которые стимулируют резорбцию. На этом основании была предложена гипотеза о том, что ОБ специализированы для восприятия и передачи специфических сигналов механичес-кой нагрузки или деформаций, которые модулируют процес-сы самообновления кости [44].…”

Section: клеточные аспектыunclassified

IZMENENIYa KOSTNOY TKANI ChELOVEKAV KOSMIChESKOM POLETE: O VOZMOZhNYKh MEKhANIZMAKh OSTEOPENII

Оганов¹,

Бакулин²,

Novikov³

et al. 2005

Osteopor Bone Dis

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Some results of possible participation of bone metabolism regulation different levels in the bone changes caused by microgravity are presented taking into account the body fluid redistribution which usually accompany the space flight. The primary starting changes associate with biomechanical factors and realize on the strictly bone level (osteocytic osteolysis, breach of «collagen-crystal» connection, slowing of osteoblastic histogenesis). There are calcium homeostasis distortion on the extrabone (tissue, organs) level: decrease of calcium intestinal absorption and renal reabsorption. Changes in the hierarchy of ion and fluid volume regulation systems may provoke the osteoclastic resorption, which intensify the bone loss.

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8. Gene expression in osteoblast cells

Cited by 5 publications

References 0 publications

Bone tissue-specific transcription of the osteocalcin gene: Role of an activator osteoblast-specific complex and suppressor hox proteins that bind the OC box

Bone tissue-specific transcription of the osteocalcin gene: Role of an activator osteoblast-specific complex and suppressor hox proteins that bind the OC box

Systemic administration of transforming growth factor-beta 2 prevents the impaired bone formation and osteopenia induced by unloading in rats.

IZMENENIYa KOSTNOY TKANI ChELOVEKAV KOSMIChESKOM POLETE: O VOZMOZhNYKh MEKhANIZMAKh OSTEOPENII

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