Osteoblast-specific deletion of Hrpt2/Cdc73 results in high bone mass and increased bone turnover

Droscha, Casey J.; Diegel, Cassandra R.; Ethen, Nicole J.; Burgers, Travis; McDonald, Mitchell; Maupin, Kevin A.; Naidu, Agni; Wang, Pengfei; Teh, Bin Tean; Williams, Bart O.

doi:10.1016/j.bone.2016.12.006

Cited by 11 publications

(10 citation statements)

References 42 publications

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“…Primary osteoblasts were isolated from calvaria of mice on postnatal day 1 as previously described . Briefly, calvaria was dissected and sequentially digested by digestion solution containing 0.1% type II collagenase (Invitrogen, CA, USA) and 0.2% neutral protease (Kehao) in hanks’ balanced salt solution for 15 minutes at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Deficiency of Macf1 in osterix expressing cells decreases bone formation by Bmp2/Smad/Runx2 pathway

Qiu

Lin

Zhao

et al. 2019

J Cellular Molecular Medi

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Microtubule actin cross‐linking factor 1 (Macf1) is a spectraplakin family member known to regulate cytoskeletal dynamics, cell migration, neuronal growth and cell signal transduction. We previously demonstrated that knockdown of Macf1 inhibited the differentiation of MC3T3‐E1 cell line. However, whether Macf1 could regulate bone formation in vivo is unclear. To study the function and mechanism of Macf1 in bone formation and osteogenic differentiation, we established osteoblast‐specific Osterix (Osx) promoter‐driven Macf1 conditional knockout mice (Macf1f/fOsx‐Cre). The Macf1f/fOsx‐Cre mice displayed delayed ossification and decreased bone mass. Morphological and mechanical studies showed deteriorated trabecular microarchitecture and impaired biomechanical strength of femur in Macf1f/fOsx‐Cre mice. In addition, the differentiation of primary osteoblasts isolated from calvaria was inhibited in Macf1f/fOsx‐Cre mice. Deficiency of Macf1 in primary osteoblasts inhibited the expression of osteogenic marker genes (Col1, Runx2 and Alp) and the number of mineralized nodules. Furthermore, deficiency of Macf1 attenuated Bmp2/Smad/Runx2 signalling in primary osteoblasts of Macf1f/fOsx‐Cre mice. Together, these results indicated that Macf1 plays a significant role in bone formation and osteoblast differentiation by regulating Bmp2/Smad/Runx2 pathway, suggesting that Macf1 might be a therapeutic target for bone disease.

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Section: Methodsmentioning

confidence: 99%

Deficiency of Macf1 in osterix expressing cells decreases bone formation by Bmp2/Smad/Runx2 pathway

Qiu

Lin

Zhao

et al. 2019

J Cellular Molecular Medi

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“…BGP, also known as osteocalcin, is synthesized specifically by osteoblasts and plays an important role in mineralization and calcium ion homeostasis . Additionally, Col 1 is the major structural component of the extracellular matrix of osteoblasts and supports maintenance of osteoblast phenotypic properties .…”

Section: Resultsmentioning

confidence: 99%

“…Osteoblasts are fundamentally characterized by their primary and exclusive function: the ability to form osseous tissue identifiable as bone . Mature osteoblasts synthesize and secrete collagen type 1 (Col 1) and various noncollagen proteins , which could control bone mineral deposition, regulate bone turnover, and bone cell activity . Additionally, osteoblasts have been employed for evaluation of the osteogenetic activities of natural products .…”

Section: Introductionmentioning

confidence: 99%

Osteoblast cell membrane chromatography coupled with liquid chromatography and time-of-flight mass spectrometry for screening specific active components from traditional Chinese medicines

et al. 2017

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A method using osteoblast membrane chromatography coupled with liquid chromatography and time-of-flight mass spectrometry was developed to recognize and identify the specific active components from traditional Chinese medicines. Primary rat osteoblasts were used for the preparation of the stationary phase in the cell chromatography method. Retention components from the cell chromatography were collected and analyzed by liquid chromatography with time-of-flight mass spectrometry. This method was applied in screening active components from extracts of four traditional Chinese medicines. In total, 24 potentially active components with different structures were retained by osteoblast cell chromatography. There were five phenolic glucosides and one triterpenoid saponin from Curculigo orchioides Gaertn, two organic acids and ten flavonoids from Epimedium sagittatum Maxim, one phthalide compound and one organic acid from Angelica sinensis Diels, and two flavonoids and two saponins from Anemarrhena asphodeloides Bunge. Among those, four components (icariin, curculigoside, ferulaic acid, and timosaponin BII) were used for in vitro pharmacodynamics validation. They significantly increased the osteoblast proliferation, alkaline phosphatase activity, levels of bone gla protein and collagen type 1, and promoted mineralized nodule formation. The developed method was an effective screening method for finding active components from complex medicines that act on bone diseases.

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“…Homozygous deletion of Cdc73 in MSCs resulted in embryos non-presenting mesenchymal development of the internal organs. The immunohistochemical staining of inactive and active caspase-3 revealed a high rate of apoptosis of MSCs [45]. Conversely, selective homozygous elimination of Cdc73 in mature osteoblasts and osteocytes generated mice with normal life span, but increased cortical and trabecular bone [45].…”

Section: Role Of the Cdc73 Gene In Bone Phenotypementioning

confidence: 99%

Bone tissue and mineral metabolism in hereditary endocrine tumors: clinical manifestations and genetic bases

Maraghelli

Giusti

Marini

et al. 2020

Orphanet J Rare Dis

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Inherited endocrine tumors are neoplasms of endocrine cells, transmitted via autosomal dominant germinal mutations. They present in two different forms: non-syndromic (patient has a single affected endocrine organ during his/her lifetime) or syndromic forms (multiple tumors in endocrine and non-endocrine organs during his/her lifetime).In addition to their common tumoral manifestations, many of these diseases present clinical affection of bone tissues and/or mineral metabolism, both as secondary complications of primary tumors and as primary defects due to genetic mutation. To date, few studies have documented these bone complications, and there are no systematic reviews in this area.We present a revision of medical literature about skeletal and mineral metabolism affections in inherited endocrine tumor syndromes, and studies, in cells and animal models, investigating the direct role of some genes, whose mutations are responsible for the development of endocrine tumors, in the regulation of bone and mineral metabolism.

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Osteoblast-specific deletion of Hrpt2/Cdc73 results in high bone mass and increased bone turnover

Cited by 11 publications

References 42 publications

Deficiency of Macf1 in osterix expressing cells decreases bone formation by Bmp2/Smad/Runx2 pathway

Deficiency of Macf1 in osterix expressing cells decreases bone formation by Bmp2/Smad/Runx2 pathway

Osteoblast cell membrane chromatography coupled with liquid chromatography and time-of-flight mass spectrometry for screening specific active components from traditional Chinese medicines

Bone tissue and mineral metabolism in hereditary endocrine tumors: clinical manifestations and genetic bases

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