BACKGROUND The regulatory factor X6 (RFX6), a member of regulatory factor X family, is known to play a key role in the development and differentiation of pancreatic beta cells as well as insulin production and secreti...BACKGROUND The regulatory factor X6 (RFX6), a member of regulatory factor X family, is known to play a key role in the development and differentiation of pancreatic beta cells as well as insulin production and secretion. However, the potential role of RFX6 in type 2 diabetes (T2D) is still unclear. AIM Recent studies have indicated that RFX6 binding to DNA could be disrupted in diabetes. Therefore, in this study we investigated whether genetic mutations are present in the DNA binding domain of RFX6 gene that could abrogate its function in T2D. METHODS A cohort of T2D patients was enrolled in this study, and the gene encoding the DNA binding domain of RFX6 was amplified by polymerase chain reaction and then analysed by direct DNA sequencing. RESULTS The DNA sequence analysis revealed the absence of any exonic mutation. However, we have identified a new heterozygous single nucleotide polymorphism (IVS6+31 C>T) in the intronic region of DNA binding domain gene that is present in 9.2% and 8.5% of diabetic and control people, respectively (P = 0.97).CONCLUSION We report the absence of any significant genetic variant that could affect the function of RFX6-DNA binding domain in T2D.展开更多
Background Proliferation, cell migration and phenotypic modulation of airway smooth muscle cells （ASMCs） are important features of airway remodelling in asthma. The precise cellular and molecular mechanisms that reg...Background Proliferation, cell migration and phenotypic modulation of airway smooth muscle cells （ASMCs） are important features of airway remodelling in asthma. The precise cellular and molecular mechanisms that regulate ASMCs proliferation, migration and phenotypic modulation in the lung remain unknown. Basic fibroblast growth factor （bFGF）, a highly specific chemotactic and mitogenic factor for many cell types, appears to be involved in the development of airway remodelling. Our study assessed whether bFGF directly stimulates the proliferation, migration and phenotypic modulation of ASMCs. Methods Confluent and growth arrested human ASMCs were treated with human recombinant FGF. Proliferation was measured by BrdU incorporation and cell counting. Migration was examined using Boyden chamber apparatus. Expressions of smooth muscle （sm）-α-actin and sm-myosin heavy chain （MHC） isoform 1 were determined by RT-PCR and Westem blot analysis. Results It was found that hrbFGF （10 ng/ml）, when added to ASMCs, induced a significant increase in BrdU uptake and cell number by ASMCs as compared to controls and a significant increase in ASMCs migration with respect to controls. The mRNA and protein expressions of sm-α-actin and sm-MHC in ASMCs that were stimulated with hrbFGF decreased with respect to controls. Conclusion It appears that bFGF can directly stimulate proliferation and migration of ASMCs, however, the expressions of cells＇ contractive phenotype decreased.展开更多
文摘BACKGROUND The regulatory factor X6 (RFX6), a member of regulatory factor X family, is known to play a key role in the development and differentiation of pancreatic beta cells as well as insulin production and secretion. However, the potential role of RFX6 in type 2 diabetes (T2D) is still unclear. AIM Recent studies have indicated that RFX6 binding to DNA could be disrupted in diabetes. Therefore, in this study we investigated whether genetic mutations are present in the DNA binding domain of RFX6 gene that could abrogate its function in T2D. METHODS A cohort of T2D patients was enrolled in this study, and the gene encoding the DNA binding domain of RFX6 was amplified by polymerase chain reaction and then analysed by direct DNA sequencing. RESULTS The DNA sequence analysis revealed the absence of any exonic mutation. However, we have identified a new heterozygous single nucleotide polymorphism (IVS6+31 C>T) in the intronic region of DNA binding domain gene that is present in 9.2% and 8.5% of diabetic and control people, respectively (P = 0.97).CONCLUSION We report the absence of any significant genetic variant that could affect the function of RFX6-DNA binding domain in T2D.
文摘Background Proliferation, cell migration and phenotypic modulation of airway smooth muscle cells （ASMCs） are important features of airway remodelling in asthma. The precise cellular and molecular mechanisms that regulate ASMCs proliferation, migration and phenotypic modulation in the lung remain unknown. Basic fibroblast growth factor （bFGF）, a highly specific chemotactic and mitogenic factor for many cell types, appears to be involved in the development of airway remodelling. Our study assessed whether bFGF directly stimulates the proliferation, migration and phenotypic modulation of ASMCs. Methods Confluent and growth arrested human ASMCs were treated with human recombinant FGF. Proliferation was measured by BrdU incorporation and cell counting. Migration was examined using Boyden chamber apparatus. Expressions of smooth muscle （sm）-α-actin and sm-myosin heavy chain （MHC） isoform 1 were determined by RT-PCR and Westem blot analysis. Results It was found that hrbFGF （10 ng/ml）, when added to ASMCs, induced a significant increase in BrdU uptake and cell number by ASMCs as compared to controls and a significant increase in ASMCs migration with respect to controls. The mRNA and protein expressions of sm-α-actin and sm-MHC in ASMCs that were stimulated with hrbFGF decreased with respect to controls. Conclusion It appears that bFGF can directly stimulate proliferation and migration of ASMCs, however, the expressions of cells＇ contractive phenotype decreased.
