COL1A1and miR-29b show lower expression levels during osteoblast differentiation of bone marrow stromal cells from Osteogenesis Imperfecta patients

Abstract

BackgroundThe majority of Osteogenesis Imperfecta (OI) cases are caused by mutations in one of the two genes, COL1A1 and COL1A2 encoding for the two chains that trimerize to form the procollagen 1 molecule. However, alterations in gene expression and microRNAs (miRNAs) are responsible for the regulation of cell fate determination and may be evolved in OI phenotype.MethodsIn this work, we analyzed the coding region and intron/exon boundaries of COL1A1 and COL1A2 genes by sequence analysis using an ABI PRISM 3130 automated sequencer and Big Dye Terminator Sequencing protocol. COL1A1 and miR-29b expression were also evaluated during the osteoblastic differentiation of mesenchymal stem cell (MSC) by qRT-PCR using an ABI7500 Sequence Detection System.ResultsWe have identified eight novel mutations, where of four may be responsible for OI phenotype. COL1A1 and miR-29b showed lower expression values in OI type I and type III samples. Interestingly, one type III OI sample from a patient with Bruck Syndrome showed COL1A1 and miR-29b expressions alike those from normal samples.ConclusionsResults suggest that the miR-29b mechanism directed to regulate collagen protein accumulation during mineralization is dependent upon the amount of COL1A1 mRNA. Taken together, results indicate that the lower levels observed in OI samples were not sufficient for the induction of miR-29b.

Mir‐29b promotes human aortic valve interstitial cell calcification via inhibiting TGF‐β3 through activation of wnt3/β‐catenin/Smad3 signaling

“…MiR‐204, miR‐29b, and miR‐30b can block the differentiation of mesenchymal cells into osteoblasts and are regarded as new target for early intervention of CAVD . miR‐29b is reported to participate in the osteoblast differentiation of bone marrow stromal cells, osteogenic differentiation of somatic stem cells, and the calcification vascular smooth muscle cells through modulation of proteins such as BMPs, CDK6, and HDAC4 pathway . However, the role of miR‐29b in the CAVD has not been reported so far.…”

“…The calcification of aortic valve interstitial cells (VICs) is reported to be involved in the pathogenesis of CAVD. In addition, miR‐29b is involved in the osteoblastic differentiation of vascular smooth muscle cells and mesenchymal stem cells . Thus, we hypothesized that miR‐29b could be involved in the osteoblast differentiation of hAVICs and could be an important regulator of heterotopic ossification of the aortic valve.…”

Collagenase 1A2 (COL1A2) gene A/C polymorphism in relation to severity of dental fluorosis

“…Some genes associated with severe dental fluorosis are also associated with bone mineral content and density due to the similarities in the structure and formation of bones and teeth; others are involved in the formation of the protein matrix during tooth development. Some of these candidate genes include those for type 1 collagen, osteocalcin, osteonectin, and osteopontin.…”

“…It is possible that the polymorphisms in the COL1A2 gene are related to dental fluorosis and may influence the formation of teeth in children exposed to high concentrations of fluoride (31). Some genes associated with severe dental fluorosis are also associated with bone mineral content and density due to the similarities in the structure and formation of bones and teeth; (32) others are involved in the formation of the protein matrix during tooth development. Some of these candidate genes include those for type 1 collagen, osteocalcin, osteonectin, and osteopontin.…”

The Diagnostic Efficacy and Biological Effects of microRNA-29b for Colon Cancer

“…Downregulation of miR-29 family members has been observed in leukemia, melanoma, liver, cervical, and lung cancer. 12,13 Aberrant expression of miRNAs in CRC has been reported recently, suggesting a potential for their use as biomarkers for disease diagnosis. Imaging techniques are widely used for the diagnosis of CRC, and images of the tumor tissue may confirm the diagnosis of CRC via ophthalmoscopy, ultrasonography, computed tomography, and magnetic resonance imaging.…”