http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Arang Kwon,Hyun-Jung Park,Jeong-Hwa Baek 대한구강생물학회 2018 International Journal of Oral Biology Vol.43 No.3
We previously demonstrated that epidermal growth factor (EGF) enhances cell migration and invasion of breast cancer cells in a SMAD ubiquitination regulatory factor 1 (SMURF1)-dependent manner and that SMURF1 induces degradation of β-catenin in CC1 cells. However, the relationship between EGF-induced SMURF1 and β-catenin expression in breast cancer cells remains unclear. So, we investigated if EGF and SMURF1 regulate β-catenin expression in MDAMB31 human breast cancer cells. When MDAMB31 cells were incubated with EGF for 4, 48, and 7 hours, EGF significantly increased expression levels of SMURF1 mRNA and protein while suppressing expression levels of β-catenin mRNA and protein. Overexpression of SMURF1 downregulated β-catenin mRNA and protein, whereas knockdown of SMURF1 increased β-catenin expression and blocked EGF-induced β-catenin downregulation. Knockdown of β-catenin enhanced cell migration and invasion of MDAMB31 cells, while β-catenin overexpression suppressed EGF-induced cell migration and invasion. Furthermore, knockdown of β-catenin enhanced vimentin expression and decreased cytokeratin expression, whereas β -catenin overexpression decreased vimentin expression and increased cytokeratin expression. These results suggest that EGF downregulates β-catenin in a SMURF1-dependent manner and that β-catenin downregulation contributes to EGF-induced cell migration and invasion in MDAMB breast cancer cells.
( Kyung Hwa Baek ),( Hyo Rin Hwang ),( Hyun Jung Park ),( Arang Kwon ),( Abdul S. Qadir ),( Jeong Hwa Baek ) 생화학분자생물학회(구 한국생화학분자생물학회) 2014 BMB Reports Vol.47 No.9
We investigated the effects of high calorie and low caloriediets on skeletal integrity, and whether β adrenergic blockade(BB) attenuates bone loss induced by dietary calorie alteration. Male 6-week old C57BL/6 mice were assigned to either anad-lib fed control diet (CON), a high calorie diet (HIGH), or alow calorie diet (LOW) group. In each diet group, mice weretreated with either vehicle (VEH) or propranolol, a β-adrenergicantagonist. Over 12-weeks, β-blockade mitigated bodyweight and fat mass increases induced by the high calorie diet. Femoral trabecular bone mineral density and the expressionlevels of osteogenic marker genes in bone marrow cells were reduced in HIGHVEH and LOWVEH mice, and BB significantly attenuated this decline only in HIGH mice. In summary, the magnitude of bone loss induced by low calorie diet was greater than that caused by high calorie diet in growing mice, and β-blockade mitigated high calorie diet-induced bone loss.
TNFα Increases the Expression of β2 Adrenergic Receptors in Osteoblasts
Kyunghwa Baek,Hye-Lim Lee,Hyo Rin Hwang,Hyun-Jung Park,Arang Kwon,Abdul S. Qadir,Jeong-Hwa Baek KOREAN ACADAMY OF ORAL BIOLOGY 2011 International Journal of Oral Biology Vol.36 No.4
Tumor necrosis factor alpha (TNFα) is a multifunctional cytokine that is elevated in inflammatory diseases such as atherosclerosis, diabetes and rheumatoid arthritis. Recent evidence has suggested that β2 adrenergic receptor (β2AR) activation in osteoblasts suppresses osteogenic activity. In the present study, we explored whether TNFα modulates βAR expression in osteoblastic cells and whether this regulation is associated with the inhibition of osteoblast differentiation by TNFα. In the experiments, we used C2C12 cells, MC3T3-E1 cells and primary cultured mouse bone marrow stromal cells. Among the three subtypes of βAR, β2 and β3AR were found in our analysis to be upregulated by TNFα. Moreover, isoproterenol-induced cAMP production was observed to be significantly enhanced in TNFα-primed C2C12 cells, indicating that TNFα enhances β2AR signaling in osteoblasts. TNFα was further found in C2C12 cells to suppress bone morphogenetic protein 2-induced alkaline phosphatase (ALP) activity and the expression of osteogenic marker genes including Runx2, ALP and osteocalcin. Propranolol, a β2AR antagonist, attenuated this TNFα suppression of osteogenic differentiation. TNFα increased the expression of receptor activator of NF-κB ligand (RANKL), an essential osteoclastogenic factor, in C2C12 cells which was again blocked by propranolol. In summary, our data show that TNFα increases β2AR expression in osteoblasts and that a blockade of β2AR attenuates the suppression of osteogenic differentiation and stimulation of RANKL expression by TNFα. These findings imply that a crosstalk between TNFα and β2AR signaling pathways might occur in osteoblasts to modulate their function.