Osteoclast activation and sickle bone disease

Gordeuk, Victor R.

doi:10.1182/blood-2015-09-669333

Cited by 1 publication

(1 citation statement)

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“…They are critical for normal skeletal growth and the maintenance of bone integrity throughout life. Overactive osteoclasts may cause several bone diseases including Paget’s disease in bone, juvenile Paget’s disease, expansile skeletal hyperphosphatasia, and familial expansile osteolysis [ 35 – 39 ]. Dental problems resulting from osteoclast activation have long been recognized.…”

Section: Discussionmentioning

confidence: 99%

HDAC6 regulates dental mesenchymal stem cells and osteoclast differentiation

et al. 2018

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BackgroundDental and periodontal tissue development is a complicated process involving a finely regulated network of communication among various cell types. Understanding the mechanisms involved in regulating dental mesenchymal stem cells (MSCs) and osteoclast cell differentiation is critical. However, it is still unclear whether histone deacetylase HDAC6 is involved in dental MSCs fate determination and osteoclast differentiation.MethodsWe used shRNA and siRNA knockdown to explore the role of HDAC6 in dental MSCs odontogenic differentiation and osteoclasts maturation.ResultsBased on HDAC6 knockdown dental MSCs, our data suggest that HDAC6 knockdown significantly increases alkaline phosphate activity and mineralized nodules formation. Additionally, mRNA expression of odontogenic marker genes (OSX, OCN, and OPN) was induced by HDAC6 knockdown. By using HDAC6 siRNA, we knocked down HDAC6 in osteoclast precursor RAW 264.7 cells. Our data suggests that HDAC6 knockdown significantly inhibited osteoclasts differentiation. Additionally, mRNA expression of osteoclast marker genes Trap, Mmp9, and Ctsk was decreased by HDAC6 knockdown.ConclusionsOur study demonstrated that HDAC6 plays an important role in regulating dental MSCs and osteoclasts differentiation.

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Section: Discussionmentioning

confidence: 99%