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Flagellin is a strong vaginal adjuvant of a therapeutic vaccine for genital cancer
Lee, Shee Eun,Hong, Seol Hee,Verma, Vivek,Lee, Youn Suhk,Duong, Tra-My Nu,Jeong, Kwangjoon,Uthaman, Saji,Sung, Young Chul,Lee, Jae-Tae,Park, In-Kyu,Min, Jung-Joon,Rhee, Joon Haeng TaylorFrancis 2016 Oncoimmunology Vol.5 No.2
<P><B>ABSTRACT</B></P><P>Cervical cancer is a high-incidence female cancer most commonly caused by human papilloma virus (HPV) infection of the genital mucosa. Immunotherapy targeting HPV-derived tumor antigens (TAs) has been widely studied in animal models and in patients. Because the female genital tract is a portal for the entry of HPV and a highly compartmentalized system, the development of topical vaginal immunotherapy in an orthotopic cancer model would provide an ideal therapeutic. Thus, we examined whether flagellin, a potent mucosal immunomodulator, could be used as an adjuvant for a topical therapeutic vaccine for female genital cancer. Intravaginal (IVAG) co-administration of the E6/E7 peptides with flagellin resulted in tumor suppression and long-term survival of tumor-bearing mice. In contrast to IVAG vaccination, intranasal (IN) or subcutaneous (SC) immunization did not induce significant tumor suppression in the same model. The vaginal adjuvant effect of the flagellin was completely abolished in Toll-like receptor-5 (TLR5) knock-out mice. IVAG immunization with the E6/E7 peptides plus flagellin induced the accumulation of CD4<SUP>+</SUP> and CD8<SUP>+</SUP> cells and the expression of T cell activation-related genes in the draining genital lymph nodes (gLNs). The co-administered flagellin elicited antigen-specific IFNγ production in the gLNs and spleen. The intravaginally administered flagellin was found in association with CD11c<SUP>+</SUP> cells in the gLNs. Moreover, after immunization with a flagellin and the E6/E7 peptides, the TLR5 expression in gLN cells was significantly upregulated. These results suggest that flagellin serves as a potent vaginal adjuvant for a therapeutic peptide cancer vaccine through the activation of TLR5 signaling.</P>
( Nu-ri Jun ),( Sun-kyung Lee ),( Sang-im Lee ) 한국치위생과학회 2021 치위생과학회지 Vol.21 No.4
Background: Endodontic sealers or their toxic components may become inflamed and lead to delayed wound healing when in direct contact with periapical tissues over an extended period. Moreover, an overfilled sealer can directly interact with adjacent tissues and may cause immediate necrosis or further resorption. Therefore, the treatment outcome conceivably depends on the endodontic sealer’s biocompatibility and osteogenic potential. This study aimed to evaluate the cell viability and osteogenic effects of four different sealers in osteoblastic cells. Methods: AH Plus (resin-based sealer), Pulp Canal Sealer EWT (zinc oxide-eugenol sealer), BioRoot RCS (calcium silicate-based sealer), and Well-Root ST (MTA-based calcium silicate sealer) were mixed strictly according to the manufacturer’s instructions, and dilutions of sealer extracts (1/2, 1/5 and 1/10) were determined. Cell viability was measured using the water-soluble tetrazolium-8 (WST-8) assay. Differentiation was assessed by alkaline phosphatase (ALP) activity and mineralized nodule formation by Alizarin Red S staining. Results: The cell viability of the extracts derived from the sealers excluding Well-Root ST was concentration dependent, with sealer extracts having the least viability at a 1/2 dilution. At sealer extract dilution of 1/10, the test groups showed the same survival rate as that control group, with the exception of BioRoot RCS. Among all experimental groups, BioRoot RCS showed the highest cell viability after 48 hours. The ALP activity was significantly higher in a concentration-dependent manner. Furthemore, all four materials promoted ALP activity and mineralized nodule formation compared to the control at 1/10 dilutions. Conclusion: This is the first study to highlight the differences in biological activity of these four materials. These results suggest that the composition of root canal sealers appears to alter the form of biocompatibility and osteoblastic differentiation.
Lee, Ji-Eun,Kim, Hyun-Jee,Lee, So-Young,Lee, Jai-Young,Jin, Yong-Nu,Lee, Shim-Sung Korean Chemical Society 2007 Bulletin of the Korean Chemical Society Vol.28 No.11
The reactions of mercury(II) chloride with O3S2-donor macrocyclic ligands with (L1) and without (L2) dibenzosubunit afforded respective exo- (1) and endo-coordinated (2) complexes depending on the ring rigidity of the ligands. From the X-ray crystal structures and comparative NMR studies for the complexes 1 and 2, it is confirmed that the resulting species with different coordination modes exist not only in solid state but also in solution state.
Autophagy May Mediate Cellular Senescence by Nicotine Stimulation in Gingival Fibroblasts
( Nu-ri Jun ),( Jong-hwa Jang ),( Jae-young Lee ),( Sang-im Lee ) 한국치위생과학회 2022 치위생과학회지 Vol.22 No.3
Background: When cells are damaged by nicotine, cellular senescence due to oxidative stress accelerates. In addition, stress-induced inflammatory response and cellular senescence cause the accumulation of damaged organelles in cells, and autophagy appears to remove them. Conversely, when autophagy is reduced, harmful cell components accumulate, and aging is accelerated. This study aimed to determine the association between nicotine-induced cellular senescence and autophagy expression patterns in human gingival fibroblasts. Methods: Cells were treated with various concentrations of nicotine (0, 0.1, 0.5, 1, 2, and 5 mM) and 10 nM rapamycin was added to 1 mM nicotine to investigate the relationship between autophagy and cellular senescence. Cell viability was confirmed using WST-8 and the degree of cellular senescence was measured by SA-β-gal staining. The expression of the inflammatory proteins (COX-2 and iNOS) and autophagy markers (LC3-II, p62, and Beclin-1) was analyzed by western blotting. Results: The cell viability tended to decrease in a concentration-dependent manner. COX-2 showed no concentration-dependent expression and iNOS increased in the 0.5 mM nicotine treated group. The degree of cellular senescence was the highest in the 1 mM nicotine treatment group. In the group treated with rapamycin and nicotine, the conversion ratio of LC3-II to LC3-I was the highest, that of p62 was the lowest, and the level of Beclin-1 proteins was significantly increased. Furthermore, the degree of cellular senescence was reduced in the group in which rapamycin was added to nicotine compared to that in the group treated with nicotine alone. Conclusion: This study provides evidence that autophagy activated in an aging environment reduces cellular senescence to a certain some extent.
Lee, Young-Rae,Yu, Hong-Nu,Noh, Eun-Mi,Kim, Jong-Suk,Song, Eun-Kyung,Han, Myung-Kwan,Kim, Byeong-Soo,Lee, Sung-Ho,Park, Jinny Elsevier Science Publishers 2007 INTERNATIONAL JOURNAL OF HEMATOLOGY Vol.85 No.3
<P>Peroxisome proliferator-activated receptor gamma (PPARgamma) and retinoic acid receptors (RARs) have been a focus in chemotherapy for human cancers. The tumor suppressor PTEN plays a pivotal role in the growth of human cancer cells. We investigated whether costimulation of PPARgamma and RAR could synergistically up-regulate PTEN in human leukemia cells and consequently potentiate the inhibition of growth and cell cycle progression of these cells. We found that overexpression of PTEN with the adenoviral vector Ad/PTEN caused growth arrest at the G1 phase of the cell cycle of HL-60 cells. HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand (all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. The 2 compounds in combination showed synergistic effects on PTEN expression at the protein and messenger RNA levels. Moreover, the combination of ciglitazone and ATRA synergistically reduced cell growth rates and cell cycle arrest at the G1 phase. Our results suggest that, PPARgamma and RAR play an important role in controlling the growth of leukemia cells via the up-regulation of PTEN.</P>
Lee Eunhyeong,Lee Eun-Ah,Kong Eunji,Chon Haemin,Llaiqui-Condori Melissa,Park Cheon Ho,Park Beom Yong,Kang Nu Ri,Yoo Jin-San,Lee Hyun-Soo,Kim Hyung Seok,Park Sung-Hong,Choi Seung-Won,Vestweber Dietmar 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Tumor progression is intimately associated with the vasculature, as tumor proliferation induces angiogenesis and tumor cells metastasize to distant organs via blood vessels. However, whether tumor invasion is associated with blood vessels remains unknown. As glioblastoma (GBM) is featured by aggressive invasion and vascular abnormalities, we characterized the onset of vascular remodeling in the diffuse tumor infiltrating zone by establishing new spontaneous GBM models with robust invasion capacity. Normal brain vessels underwent a gradual transition to severely impaired tumor vessels at the GBM periphery over several days. Increasing vasodilation from the tumor periphery to the tumor core was also found in human GBM. The levels of vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2) showed a spatial correlation with the extent of vascular abnormalities spanning the tumor-invading zone. Blockade of VEGFR2 suppressed vascular remodeling at the tumor periphery, confirming the role of VEGF-VEGFR2 signaling in the invasion-associated vascular transition. As angiopoietin-2 (ANGPT2) was expressed in only a portion of the central tumor vessels, we developed a ligand-independent tunica interna endothelial cell kinase 2 (Tie2)-activating antibody that can result in Tie2 phosphorylation in vivo. This agonistic anti-Tie2 antibody effectively normalized the vasculature in both the tumor periphery and tumor center, similar to the effects of VEGFR2 blockade. Mechanistically, this antibody-based Tie2 activation induced VE-PTP-mediated VEGFR2 dephosphorylation in vivo. Thus, our study reveals that the normal-to-tumor vascular transition is spatiotemporally associated with GBM invasion and may be controlled by Tie2 activation via a novel mechanism of action.