Редактирование: DMP1

Dentin matrix acidic phosphoprotein 1 precursor (DMP-1) (Dentin matrix protein 1)

==Publications==

{{medline-entry
|title=[[GREM1]] inhibits osteogenic differentiation, senescence and BMP transcription of adipose-derived stem cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32151168
|abstract=: Adipose-derived stem cells (ADSCs) are ideal for cell-based therapies to support bone regeneration. It is vital to understand the critical genes and molecular mechanisms involved in the functional regulation of ADSCs for enhancing bone regeneration. In the present study, we investigated the Gremlin 1 ([[GREM1]]) effect on ADSCs osteogenic differentiation and senescence. : The [i]in vitro[/i] ADSCs osteogenic differentiation potential was evaluated by determining alkaline phosphatase (ALP) activity, mineralization ability, and the expression of osteogenic markers. Cell senescence is determined by SA-β-gal staining, telomerase assay, and the expression of aging markers. : [[GREM1]] overexpression in ADSCs reduced ALP activity and mineralization, inhibited the expression of osteogenic related genes [i]OCN, OPN, [[DSPP]], [[DMP1]][/i], and [i]BSP[/i], and key transcription factors, [i]RUNX2[/i] and [i]OSX[/i]. [[GREM1]] knockdown in ADSCs enhanced ALP activity and mineralization, promoted the expression of [i]OCN, OPN, [[DSPP]], [[DMP1]], BSP, RUNX2[/i], and [i]OSX[/i]. [[GREM1]] overexpression in ADSCs reduced the percent SA-β-Gal positive cells, [i]P16[/i] and [i]P53[/i] expressions, and increased telomerase activity. [[GREM1]] knockdown in ADSCs increased the percentage of SA-β-Gal positive cells, [i]P16[/i] and [i]P53[/i] expressions, and reduced telomerase activity. Furthermore, [[GREM1]] reduced the mRNA expression levels of [[BMP2]], [[BMP6]], and [[BMP7]]. : In summary, our findings suggested that [[GREM1]] inhibited ADSCs senescence and osteogenic differentiation and antagonized BMP transcription.

|keywords=* BMP
* GREM1
* adipose-derived stem cells (ADSCs)
* osteogenic differentiation
* senescence
|full-text-url=https://sci-hub.do/10.1080/03008207.2020.1736054
}}
{{medline-entry
|title=Cx43 overexpression in osteocytes prevents osteocyte apoptosis and preserves cortical bone quality in aging mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29978155
|abstract=Young, skeletally mature mice lacking Cx43 in osteocytes exhibit increased osteocyte apoptosis and decreased bone strength, resembling the phenotype of old mice. Further, the expression of Cx43 in bone decreases with age, suggesting a contribution of reduced Cx43 levels to the age-related changes in the skeleton. We report herein that Cx43 overexpression in osteocytes achieved by using the [[DMP1]]-8kb promoter (Cx43  mice) attenuates the skeletal cortical, but not trabecular bone phenotype of aged, 14-month-old mice. The percentage of Cx43-expressing osteocytes was higher in Cx43  mice, whereas the percentage of Cx43 positive osteoblasts remained similar to wild type (WT) littermate control mice. The percentage of apoptotic osteocytes and osteoblasts was increased in aged WT mice compared to skeletally mature, 6-month-old WT mice, and the percentage of apoptotic osteocytes, but not osteoblasts, was decreased in age-matched Cx43  mice. Aged WT mice exhibited decreased bone formation and increased bone resorption as quantified by histomorphometric analysis and circulating markers, compared to skeletally mature mice. Further, aged WT mice exhibited the expected decrease in bone biomechanical structural and material properties compared to young mice. Cx43 overexpression prevented the increase in osteoclasts and decrease in bone formation on the endocortical surfaces, and the changes in circulating markers in the aged mice. Moreover, the ability of bone to resist damage was preserved in aged Cx43  mice both at the structural and material level. All together, these findings suggest that increased Cx43 expression in osteocytes ameliorates age-induced cortical bone changes by preserving osteocyte viability and maintaining bone formation, leading to improved bone strength.

|keywords=* aging
* apoptosis
* connexin 43
* genetic animal models
* osteocyte
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6029870
}}
{{medline-entry
|title=[i]Dmp1[/i] Null Mice Develop a Unique Osteoarthritis-like Phenotype.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27766035
|abstract=Patients with hypophosphatemia rickets (including [i][[DMP1]][/i] mutations) develop severe osteoarthritis (OA), although the mechanism is largely unknown. In this study, we first identified the expression of [[DMP1]] in hypertrophic chondrocytes using immunohistochemistry (IHC) and X-gal analysis of [i]Dmp1-[/i]knockout-[i]lacZ[/i]-knockin heterozygous mice. Next, we characterized the OA-like phenotype in [i]Dmp1[/i] null mice from 7-week-old to one-year-old using multiple techniques, including X-ray, micro-CT, H