Abstract
This study aimed to analyze the expression of Musashi-1 (MSI1) in maxillary native bone and grafted bone after maxillary sinus floor elevation. To do so, fifty-seven bone biopsies from 45 participants were studied. Eighteen samples were collected from native bone while 39 were obtained 6 months after maxillary sinus grafting procedures. Musashi-1 was analyzed by immunohistochemistry and RT-PCR. MSI1 was detected in osteoblasts and osteocytes in 97.4% (38/39) of grafted areas. In native bone, MSI1 was detected in only 66.6% (12/18) of the biopsies, mainly in osteocytes. Detection of MSI1 was significantly higher in osteoprogenitor mesenchymal cells of grafted biopsies (p < 0.001) but minor in smooth muscle and endothelial cells; no expression was detected in adipocytes. The mesenchymal cells of the non-mineralized tissue of native bone showed very low nuclear expression of MSI1, in comparison to fusiform cells in grafted areas (0.28(0.13) vs. 2.10(0.14), respectively; p < 0.001). Additionally, the detection of MSI1 mRNA was significantly higher in biopsies from grafted areas than those from native bone (1.00(0.51) vs. 60.34(35.2), respectively; p = 0.029). Thus, our results regardig the significantly higher detection of Musashi-1 in grafted sites than in native bone reflects its importance in the remodeling/repair events that occur after maxillary sinus floor elevation in humans.
Highlights
The main function of MSI1 is to inhibit the translation of mRNA targets such as ttk[69] and m-numb that are key in the function of progenitor cells9,11. m-numb inhibits Notch signaling which is essential for maintaining self-renewal potential12. m-numb is silenced by MSI1 by binding to the 3′UTR of the mRNA encoding it[3]
According to previous studies from our group, bone grafted with a similar material as the one used in the current study showed an expression of MSI1 of 2.20 ± 0.8323
Our group has previously demonstrated a higher expression of MSI1 in mesenchymal stromal cells (MSCs) in biopsies collected from sites grafted with the same mix used in the current study (ACB + ABB: 2.20(0.83)) in comparison to those grafted with a different graft (ACB + freezed-dried bone allograft: 0.80(0.75))[23]
Summary
The main function of MSI1 is to inhibit the translation of mRNA targets such as ttk[69] and m-numb that are key in the function of progenitor cells9,11. m-numb inhibits Notch signaling which is essential for maintaining self-renewal potential12. m-numb is silenced by MSI1 by binding to the 3′UTR of the mRNA encoding it[3]. M-numb is silenced by MSI1 by binding to the 3′UTR of the mRNA encoding it[3] This occurs simultaneously to the translational inhibition of cyclin-dependent kinase inhibitor 1 (or p21WAF-1), a regulator of the cell cycle[13]. By both actions on m-numb and p21WAF-1, MSI1 un-inhibits Notch signaling, which in turn results in cell proliferation and differentiation[14]. MSCs can be obtained from adipose tissue, umbilical cord blood and bone marrow[21] They are known by other names, including marrow stromal cells, fibroblastoid colony forming units, stromal precursors or multi-potent adult progenitor cells (MAPCs). The aim of the current study was to analyze the expression of Musashi-1 in biopsies obtained from grafted posterior maxillary bone and to compare the results with those of native bone from non-grafted posterior maxillary bone
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