Sang-Uk Im

Cloning of BNIP3h, a member of proapoptotic BNIP3 family genes.

Apoptosis is regulated by interaction of antiapoptotic Bcl-2 family proteins with various proapoptotic proteins, several of which are also members of the Bcl-2 family. BNIP3 (formerly NIP3) is a proapoptotic mitochondrial protein classified in the Bcl-2 family based on limited sequence homology-3 (BH3) domain and COOH-terminal transmembrane domain. Sequence comparison of BNIP3 has indicated that there are several BNIP3 human homologs of this protein, like BNIP3L, Nix and BNIP3. We have cloned a new member of BNIP3 family from the cDNA library prepared from human dermal papilla cells and designated as BNIP3h. BNIP3h shows substantial homology with other BNIP3 family proteins. BNIP3h induced apoptosis from 24 hours after transfection in MCF7 cell lines and its apoptosis inducing activity is extended until 72 hours after transfection.

L-Ascorbic acid 2-phosphate promotes elongation of hair shafts via the secretion of insulin-like growth factor-1 from dermal papilla cells through phosphatidylinositol 3-kinase

Background  l‐Ascorbic acid 2‐phosphate (Asc 2‐P), a derivative of l‐ascorbic acid, promotes elongation of hair shafts in cultured human hair follicles and induces hair growth in mice.

Metabolic Syndrome Parameters in adolescents may be determinants for the future periodontal diseases

AIM The prevalence of metabolic syndrome (MetS) increases even in adolescents. The evidence that MetS is associated with the periodontal diseases in adolescents has been understudied. Therefore, our aim was to assess the association between MetS parameters and gingivitis in adolescents. MATERIAL AND METHODS A total of 941 participants (590 boys, 351 girls), aged 12-18 years was selected from the Fourth Korea National Health and Nutrition Examination Survey, a cross-sectional and nationally representative survey, which had had information on waist circumference, blood pressure, serum triglyceride, high-density lipoprotein (HDL) cholesterol, and the fasting blood sugar and community periodontal Index (CPI). RESULTS The number of positive parameters of MetS showed significant positive correlation with gingivitis; adjusted and crude ORs with one positive parameters of MetS were 1.92 (95% CI: 1.21-3.04) and 1.88(95% CI: 1.28-2.76), respectively. And adjusted OR with three or more positive parameters of MetS was 3.29 (95% CI: 1.24-8.71). Among five parameters of MetS, Low HDL-cholesterol showed significant association with gingivitis (crude OR 2.12, 95% CI 1.20-3.73; adjusted OR 1.96, 95% CI 1.24-3.12). CONCLUSIONS Having more positive parameters of MetS and low HDL-cholesterol parameter had an independent relationship with the prevalence of gingivitis, which may be determinants for the future periodontal diseases even in adolescents.

Conditioned media obtained from human outer root sheath follicular keratinocyte culture activates signalling pathways that contribute to maintenance of hair‐inducing capacity and increases trichogenicity of cultured dermal cells

Findings from recent studies have demonstrated that hair‐inducing capacity (trichogenicity) of cultured dermal cells can be maintained by addition of conditioned media obtained from culture of epidermal keratinocytes. In this study, we investigated the question of whether treatment with human follicular keratinocyte–conditioned media (FKCM) can result in activation of signalling pathways that contribute to trichogenicity and increase the trichogenicity of cultured dermal cells. Through conduct of hair reconstitution assays, we observed that treatment of cells with FKCM resulted in induction of a greater number of hair follicles, compared with control cells. Treatment of dermal cells with FKCM resulted in the activation of BMP and β‐catenin signalling pathways. In addition, higher levels of IGFBP‐7, IL‐8, OPG and uPA were observed in FKCM. Altogether, our data suggest that a patients own FKCM would be ideal for expansion of the patients own follicular dermal cells for cell therapy for treatment of hair loss.

Polycan suppresses osteoclast differentiation and titanium particle-induced osteolysis in mice

Particle-induced osteolysis is a major issue, and it is most likely the result of enhanced osteoclast activation in the pathogenesis of various skeletal diseases. This study investigated whether the inhibitory effect that Polycan has on osteoclast differentiation can be used to treat osteolysis induced by titanium (Ti) particles. To this end, the effects of Polycan were examined in terms of the cytotoxicity, osteoclast differentiation, cytokine expression, and Ti-induced calvarial osteolysis. Polycan had no significant cytotoxic effects on bone marrow macrophages (BMMs) but instead increased BMM proliferation. High levels of interleukin (IL)-6, IL-12, and macrophage colony-stimulating factor (M-CSF) were expressed in BMM cells in the presence of Polycan, suggesting that Polycan drives the differentiation of BMMs into M1 macrophages. Polycan significantly inhibited osteoclast differentiation induced by M-CSF and the receptor activator of nuclear factor kappa-B ligand (RANKL). The expression levels of the osteoclast marker genes significantly decreased, and Polycan induced and maintained the expression of IL-12, which suppressed osteoclast differentiation. In contrast, the RANKL signaling pathway was not inhibited by Polycan. An in vivo calvarial osteolysis model revealed that Polycan significantly decreased the osteoclast numbers and suppressed osteolysis. Our results suggest that the natural compound Polycan is a good candidate for therapeutic intervention against enhanced osteoclast differentiation and Ti particle-induced osteolysis.