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Last update 08 May 2025

SP7

Last update 08 May 2025

Basic Info

Synonyms

osterix, OSX, SP7

+ [3]

Introduction

Transcriptional activator essential for osteoblast differentiation (PubMed:23457570). Binds to SP1 and EKLF consensus sequences and to other G/C-rich sequences (By similarity).

Drugs associated with SP7

CN115287263

Patent Mining

Target

SP7

Mechanism-

Active Org.

The Naval Medical University of PLA

Originator Org.

The Naval Medical University of PLA

Active Indication

Other Diseases [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SP7

100 Translational Medicine associated with SP7

0 Patents (Medical) associated with SP7

3,290

Literatures (Medical) associated with SP7

01 Dec 2025·Histochemistry and Cell Biology

Polycomb protein Bmi1 promotes odontoblast differentiation by accelerating Wnt and BMP signaling pathways

Article

Author: Ninomiya, Tadashi ; Kitamura, Chiaki ; Hosoya, Akihiro ; Seki-Kishimoto, Yuri ; Yukita, Akira ; Nakamura, Hiroaki ; Takebe, Hiroaki ; Iijima, Masahiro ; Noguchi, Yukiko ; Yoshiba, Nagako ; Washio, Ayako ; Morotomi, Takahiko

Bmi1 is a polycomb protein localized in stem cells and maintains their stemness. This protein is also reported to regulate the expression of various differentiation genes. In this study, to analyze the role of Bmi1 during dentinogenesis, we examined the immunohistochemical localization of Bmi1 during rat tooth development as well as after cavity preparation. Bmi1 localization was hardly detected in the dental mesenchyme at the bud and cap stages. After the bell stage, however, this protein became detectable in preodontoblasts and early odontoblasts just beginning dentin matrix secretion. As dentin formation progressed, Bmi1 immunoreactivity in the odontoblasts decreased in intensity. After cavity preparation, cells lining the dentin and some pulp cells under the cavity were immunopositive for Bmi1 at 4 days. Odontoblast-like cells forming reparative dentin were immunopositive for Bmi1 at 1 week, whereas their immunoreactivity was not detected after 8 weeks. We further analyzed the function of Bmi1 using KN-3 cells, a dental mesenchymal cell line. Overexpression of Bmi1 in KN-3 cells promoted mineralized tissue formation. In contrast, siRNA knockdown of Bmi1 in KN-3 cells reduced alkaline phosphatase activity and the expression of odontoblast differentiation marker genes such as Runx2, osterix, and osteocalcin. Additionally, KN-3 cells transfected with siRNA against Bmi1 showed reduced nuclear transition of β-catenin and expression of phosphorylated-Smad1/5/8. Taken together, these findings suggest that Bmi1 was localized in the odontoblast-lineage cells in their early differentiation stages. Bmi1 might positively regulate their differentiation by accelerating Wnt and BMP signaling pathways.

01 Jun 2025·Phytomedicine

Kaempferol combats the osteogenic differentiation damage of periodontal ligament stem cells in periodontitis via regulating EphrinB2-mediated PI3K/Akt and P38 pathways

Article

Author: Cao, Jiao ; Liu, Jin ; Shi, Anbang ; Li, Yue ; Li, Meng ; Ma, Shaoyang ; Li, Ang ; Si, Mengying

BACKGROUNDThe osteogenic differentiation of periodontal ligament stem cells (PDLSCs) plays a fundamental role in endogenous bone regeneration during periodontitis treatment, yet achieving consistent differentiation under inflammatory conditions remains clinically challenging. Kaempferol, a phytochemical flavonol, has demonstrated osteoprotective efficacy in osteoporosis and bone repair models. However, whether kaempferol exerts pro-osteogenic effects on PDLSCs within the pathologically complex microenvironment of periodontitis, and through what molecular mechanisms, remains unexplored.PURPOSEThis study aimed to systematically characterize the therapeutic efficacy of kaempferol in restoring osteogenic differentiation of human PDLSCs under inflammatory stress, and promoting bone regeneration in a mice periodontitis model, and elucidate novel molecular targets and downstream mechanisms mediating these regenerative actions.METHODSAn in vitro inflammatory microenvironment was established using lipopolysaccharide (LPS)-stimulated human PDLSCs to mimic periodontitis-induced osteogenic impairment. Osteogenic recovery was assessed through alkaline phosphatase (ALP), alizarin red S staining, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot analysis of osteogenesis-related markers (ALP, RUNX2, OSX, OPN). The bioinformatics, network pharmacology and siRNA transfection were performed to identify EphrinB2 as kaempferol's putative cellular target. Downstream PI3K/Akt and p38 MAPK pathway activation was evaluated through phosphoprotein analysis. In vivo validation employed micro-CT quantification of alveolar bone loss and immunohistochemical profiling of pathways key proteins in a mice periodontitis model.RESULTSKaempferol dose-dependently rescued LPS-impaired osteogenic differentiation in human PDLSCs, especially at 10 μM, where kaempferol significantly reversed suppressed ALP activity, mineralized nodule formation, and transcriptional and protein expression of osteogenic markers (ALP, RUNX2, OSX, OPN). Mechanistically, kaempferol upregulated the key target EphrinB2 under inflammatory stress, thereby reactivating the downstream PI3K/Akt and p38 pathways. In periodontitis mice, kaempferol administration (10 mg/kg) significantly promoted the periodontal expression of OPN and EphrinB2, restored the phosphorylation of PI3K, AKT, and P38, attenuating alveolar bone loss by 63.8 % (BV/TV: 72.4 % ± 2.07 vs. 44.2 % ± 3.19 in CON).CONCLUSIONKaempferol could rescue PDLSCs' osteogenic differentiation and mitigates bone loss in periodontitis microenvironments by targeting EphrinB2 to activate PI3K/Akt and P38 pathways. This work underscores kaempferol's potential as a natural therapeutic for reversing pathological bone resorption and promoting periodontal regeneration.

01 Jun 2025·Bone Reports

Intake of eggshell membrane enhances bone mass and suppresses bone marrow adiposity in normal growing rats

Article

Author: Matsunaga, Hiroya ; Nakai, Shingo ; Yashima, Nao ; Lyu, Jiazheng ; Ohsako, Masafumi ; Fujikawa, Kaoru ; Okunuki, Takumi ; Minamizono, Wataru ; Suito, Hirai

Eggshell membrane intake is considered to have beneficial effects on bone health; however, relevant evidence remains scant. Therefore, we aimed to explore the direct effects of eggshell membrane intake on osteogenic function in normal growing rats. Six-week-old male Wistar rats were divided into control (CO) and eggshell membrane (EM) groups. The experiment was conducted over 8 weeks. Visual observation and micro-computed tomography analysis revealed a significant increase in bone mass in the EM group compared with that in the CO group. Histological analysis showed thick and long trabeculae in the EM group, accompanied by an increase in the number of osteoblasts and suppression of adipocyte accumulation. Furthermore, Col1a1 expression was significantly higher in the EM group than in the CO group, although no significant differences were found in the number of TRAP-positive osteoclasts or Ctsk expression. Immunohistochemical analysis demonstrated a notable increase in the number of Col1-positive osteoblasts but a significant decrease in the number of Dlk1-positive adipocytes in the EM group. Gene expression analysis revealed no difference in the expression of Runx2 (the master regulator of osteoblast differentiation) between the groups. However, the expression of Sp7, which functions downstream of Runx2, was significantly upregulated, whereas that of Pparg, the master regulator of adipocyte differentiation, was significantly downregulated in the EM group compared with those in the CO group. Overall, the intake of eggshell membranes may enhance osteogenic function and suppress bone marrow adiposity. These findings support the beneficial effects of eggshell membrane intake on bone health.

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SP7

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