• Parasites, Hosts and Diseases
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• v.49 no.3
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• pp.295-298
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• 2011

Lactobacillus species in the female genital tract are thought to act as a barrier to infection. Several studies have demonstrated that lactobacilli can adhere to vaginal epithelial cells. However, little is known about how the adherence of lactobacilli to vaginal epithelial cells affects the acidity, cell viability, or proliferation of the lactobacilli themselves or those of vaginal epithelial cells. Lactobacillus acidophilus was co-cultured with immortalized human vaginal epithelial cells (MS74 cell line), and the growth of L. acidophilus and the acidity of the culture medium were measured. MS74 cell density and viability were also assessed by counting cell numbers and observing the cell attachment state. L. acidophilus showed exponential growth for the first 6 hr until 9 hr, and the pH was maintained close to 4.0-5.0 at 24 hr after culture, consistent with previous studies. The growth curve of L. acidophilus or the pH values were relatively unaffected by co-culture with MS74 cells, confirming that L. acidophilus maintains a low pH in the presence of MS74 cells. This co-culture model could therefore potentially be used to mimic vaginal conditions for future in vitro studies. On the other hand, MS74 cells co-cultured with L. acidophilus more firmly attached to the culture plate, and a higher number of cells were present compared to cells cultured in the absence of L. acidophilus. These results indicate that L. acidophilus increases MS74 cell proliferation and viability, suggesting that lactobacilli may contribute to the healthy environment for vaginal epithelial cells.

• Archives of Pharmacal Research
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• v.15 no.4
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• pp.275-282
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• 1992

The present work was designed to investigate the effects of barzilin on ConAinducedd TCGF release, responsiveness to standardd IL-2, and mitogens-induced proliferation of splenocyte when administered intraperitoneally to 8 week-old C57BL/6 mice for 2 consecutive days. Immunological tests were performed 72 hours after the treatment of brailin. The administration of 50 mg/kg brazilin caused a noticeable increase in TCGF release and responsiveness to standard II-2 but inhibited mitogens-induced proliferation of splenocyte. These results that brazilin is able to modular immunological functions despite of its inhibitory effect on mitogen induced cell proliferation.

• Biomedical Science Letters
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• v.23 no.2
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• pp.49-56
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• 2017

Fibroblast growth factor (FGF)-2 is one of the most effective growth factors to increase the growth rate of mesenchymal stem cells (MSCs). Previously, we reported that low dose of FGF-2 (1 ng/ml) induced proliferation of bone marrow-derived mesenchymal stem cells (BMSCs) through AKT and ERK activation resulting in reduction of autophagy and senescence, but not at a high dose. In this study, we investigated the effects of high dose FGF-2 (10 ng/ml) on proliferation, autophagy and senescence of BMSCs for long term cultures (i.e., 2 months). FGF-2 increased the growth rate of BMSCs in a dose dependent manner for a short term (3 days), while during long term cultures (2 months), population doubling time was increased and accumulated cell number was lower than control in BMSCs when cultured with 10 ng/ml of FGF-2. 10 ng/ml of FGF-2 induced immediate de-phosphorylation of ERK1/2, expression of LC3-II, and increase of senescence associated ${\beta}$-galactosidase (SA-${\beta}$-Gal, senescence marker) expression. In conclusion, we showed that 10 ng/ml of FGF-2 was inadequate for ex vivo expansion of BMSCs because 10 ng/ml of FGF-2 induced growth retardation via ERK1/2 de-phosphorylation and induction of autophagy and senescence in BMSCs.

• Molecules and Cells
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• v.43 no.8
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• pp.739-748
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• 2020

Stringent regulation of the chondrocyte cell cycle is required for endochondral bone formation. During the longitudinal growth of long bones, mesenchymal stem cells condense and differentiate into chondrocytes. Epiphyseal chondrocytes sequentially differentiate to form growth-plate cartilage, which is subsequently replaced with bone. Although the importance of nuclear factor 1C (Nfic) in hard tissue formation has been extensively studied, knowledge regarding its biological roles and molecular mechanisms in this process remains insufficient. Herein, we demonstrated that Nfic deficiency affects femoral growth-plate formation. Chondrocyte proliferation was downregulated and the number of apoptotic cell was increased in the growth plates of Nfic^-/- mice. Further, the expression of the cell cycle inhibitor p21 was upregulated in the primary chondrocytes of Nfic^-/- mice, whereas that of cyclin D1 was downregulated. Our findings suggest that Nfic may contribute to postnatal chondrocyte proliferation by inhibiting p21 expression and by increasing the stability of cyclin D1 protein.

• Clinical and Experimental Reproductive Medicine
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• v.24 no.3
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• pp.355-359
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• 1997

Leiomyomas, which are the commonest pelvic tumors in women, are originated from myometrial cells. Although the exact initial pathophysiologic event of the leiomyoma is not known, recent evidences suggested that the effects of sex steroid hormones in the process of tumor growth are mediated by local production of growth factors including epidermal growth factor (EGF), insulin-like growth factor-I (IGF-I) and insulin-like growth factor-II (IGF-II). If we look at the effects of other cytokines, it was suggested that basic fibroblast growth factor (bFGF) may stimulate the proliferation of myometrial and leiomyomas cells. And it was reported that interferon-${\alpha}$ inhibit the action of bFGF. Therefore, we examined the effect of bFGF and interferon-${\alpha}$ on the proliferation of leiomyoma and myometrial cells. bFGF stimulated the myometrial and leiomyoma cells significantly at the concentration of 1ng/ml (p<0.05) and 5ng/ml (p<0.05). However, Interferon-${\alpha}$ inhibited the cell proliferation of myometrial and leiomyoma cells significantly at the concentration of 100U/ml (p<0.05) and 1000U/ml (p<0.05). And the stimulated effects of bFGF with the various concentration on the myometrial and leiomyoma cells ware inhibited by interferon-${\alpha}$ with 100U/ml. Therefore, we concluded that bFGF may stimulate the myometrial and leiomyoma cell proliferation and interferon-${\alpha}$ may inhibit the myometrial and leiomyoma cell proliferation through blocking the effect of basic fibroblast growth factor.

• Korean Journal of Plant Resources
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• v.30 no.3
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• pp.265-271
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• 2017

In this study, we elucidated the molecular mechanism of silymarin by which silymarin may inhibits cell proliferation in human colorectal cancer cells in order to search the new potential anti-cancer target associated with the cell growth arrest. Silymarin reduced the level of c-Myc protein but not mRNA level indicating that silymarin-mediated downregulation of c-Myc may result from the proteasomal degradation. In the confirmation of silymarin-mediated c-Myc degradation, MG132 as a proteasome inhibitor attenuated c-Myc degradation by silymarin. In addition, silymarin phosphorylated the threonine-58 (Thr58) of c-Myc and the point mutation of Thr58 to alanine blocked its degradation by silymarin, which indicates that Thr58 phosphorylation may be an important modification for silymarin-mediated c-Myc degradation. We observed that the inhibition of ERK1/2, p38 and $GSK3{\beta}$ blocked the Thr58 phosphorylation and subsequent c-Myc degradation by silymarin. Finally, the point mutation of Thr58 to alanine attenuated silymarin-mediated inhibition of the cell growth. The results suggest that silymarin induces the cell growth arrest through c-Myc proteasomal degradation via ERK1/2, p38 and $GSK3{\beta}-dependent$ Thr58 phosphorylation.

• The Korea Journal of Herbology
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• v.36 no.3
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• pp.47-53
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• 2021

Objectives : Currently, the alopecia is one of the most emotionally stressful syndromes in human life. Human hair dermal papilla cells (HDPCs) play an essential role in controlling hair growth and in regulating hair cycle. We performed MTT assay, cell cycle, and western blot to determine the effects of essential oil from Coicis Semen (ECS) on hair growth in HDPCs. Methods : We monitored cell proliferations by MTT assay in HDPCs. After setting up the safe and effective concentration range to be treated ECS, cell cycle analysis was performed using flow cytometry. Also, the protein expression of hair growth-related factors such as insulin like growth factor-1 (IGF-1), Wnt, extracellular signal-regulated kinase (ERK), serine/threonine-specific protein kinase (Akt) in HDPCs was determined by western blot. Results : As results, cell proliferation was increased in ECS group compared to dimethyl sulfoxide (DMSO) group and minoxidil (MNXD) group. Cell number of ECS group was more decrease in sub G1 phase than cell number of DMSO group. Also, cell number of ECS group increased compared to cell number of DMSO group in G1 phase. Protein expression of ECS group was higher than protein expression of DMSO group on related hair growth factors (IGF-1, Wnt, ERK, Akt). Conclusion : As mentioned above, ECS increased cell proliferation and the protein expression of IGF-1, Wnt, ERK, and Akt. These results suggest that ECS could be used as a potential material for the treatment of alopecia by increasing the proliferation of HDPCs.

• Korean Journal of Pharmacognosy
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• v.45 no.4
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• pp.288-293
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• 2014

The present study was conducted to evaluate the hair growth-promoting effect of Clitocybin A from mushroom Clitocybe aurantiaca with dermal papilla cells (DPCs), which play important roles in the regulation of hair cycle. Clitocybin A significantly increased the proliferation of immortalized rat vibrissa DPCs. Flow cytometry analysis revealed that Clitocybin A promoted cell-cycle progression through G0/G1 to S phase in immortalized rat vibrissa DPCs. In addition, Clitocybin A increased the level of cell cycle proteins such as cyclin D1, phospho-pRB, and phospho-CDK2. To elucidate the molecular mechanisms of Clitocybin A on the proliferation of DPCs, we examined the activation of wnt/${\beta}$-catenin signaling which is known to regulate hair follicle development, differentiation and hair growth. Clitocybin A activated wnt/${\beta}$-catenin signaling via the increase of phospho(ser552)-${\beta}$-catenin, phospho(ser675)-${\beta}$-catenin and phospho(ser9)-$GSK3{\beta}$. Furthermore, Clitocybin A markedly increased the activation of extracellular signal-regulated kinase (ERK). These results suggest that the Clitocybin A may induce hair growth by proliferation of DPCs via cell-cycle progression as well as the activation of Wnt/${\beta}$-catenin signaling and ERK pathway.

• Archives of Pharmacal Research
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• v.28 no.11
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• pp.1263-1269
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• 2005

Recently, it was reported that reduction in serum adiponectin levels is correlated with the incidence of breast cancer. As an effort to explain this, we screened various human breast cancer cell lines to identify those in which proliferation is directly controlled by adiponectin. Among the five tested cell lines, proliferation of MDA-MB-231 cancer cell was significantly suppressed by adiponectin within the range of physiological concentration. Furthermore, prolonged adiponectin treatment caused cell growth arrest and even apoptosis of MDA-MB-231. This result is the first to show that adiponectin can directly control cancer cell growth and provides a rationale for the theory that reduction in plasma adiponectin levels could be a risk factor for breast cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1431-1437
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• 2012

The growth of many breast tumors is stimulated by IGF-1, which activates signal transduction pathways inducing cell proliferation. $ER{\alpha}$ is important in this process. The aim of the study was to investigate relationships in vitro among inhibitory effects of luteolin on the growth of MCF-7 cells, IGF-1 pathway and $ER{\alpha}$. Our results showed that luteolin could effectively block IGF-l-stimulated MCF-7 cell proliferation in a dose- and time-dependent manner and block cell cycle progression and induce apoptosis evidenced by the flow cytometric detection of sub-G1DNA content. Luteolin markedly decreased IGF-l-dependent IGF-IR and Akt phosphorylation without affecting Erk1/2 phosphorylation. Further experiments pointed out that $ER{\alpha}$ was directly involved in IGF-l induced cell growth inhibitory effects of luteolin, which significantly decreased $ER{\alpha}$ expression. Knockdown of $ER{\alpha}$ in MCF-7 cells by an $ER{\alpha}$-specific siRNA decreased the IGF-l induced cell growth inhibitory effects of luteolin. $ER{\alpha}$ is thus a possible target of luteolin. These findings indicate that the inhibitory effect of luteolin on the growth of MCF-7 cells is via inhibiting IGF-l mediated PI3K-Akt pathway dependent of $ER{\alpha}$ expression.