AIM： To study the expression levels of E-selectin, integrin β1 and immunoglobulin supperfamily memberintercellular adhesion molecule-1 （ICAM-1） in human gastric carcinoma cells, and to explore the relationship bet...AIM： To study the expression levels of E-selectin, integrin β1 and immunoglobulin supperfamily memberintercellular adhesion molecule-1 （ICAM-1） in human gastric carcinoma cells, and to explore the relationship between these three kinds of cell adhesion molecules and gastric carcinoma. METHODS： The serum contents of E-selectin, integrin β1 and ICAM-1 were detected by enzyme-linked immunosorbent assay （ELISA）, in 47 healthy individuals （control group） and in 57 patients with gastric carcinoma （gastric carcinoma group） respectively prior to operation and 7 d after operation. RESULTS： The serum E-selectin, ECAM-1 and integrin β1 were found to be expressed in both control and gastric carcinoma groups. However, they were highly expressed in patients with gastric carcinoma patients before operation or with unresectable tumours. The expression levels of ICAM-1 and integrin β1 were significantly higher in gastric carcinoma patients than in controls （P 〈 0.01）. A comparison of the E-selectin levels between the two groups showed statistically insignificant differnce （P = 0.64）. In addition, the expression levels were all decreased substantially in the postoperative patients subjected to radical resection of the tumours, indicating that the high level expressions of these compounds might be the important factor for predicting the prognosis of these patients. CONCLUSION： Serum E-selectin, ICAM-1 and integrin β1 expression levels are probably related to the metastasis and relapse of gastric cancer.展开更多
AIM:To investigate the expressions of type I collagen, α2 integrin and β1 integrin in the posterior sclera of guinea pigs with defocus myopia and whether basic fibroblast growth factor (bFGF) injection inhibits the ...AIM:To investigate the expressions of type I collagen, α2 integrin and β1 integrin in the posterior sclera of guinea pigs with defocus myopia and whether basic fibroblast growth factor (bFGF) injection inhibits the formation and development of myopia by upregulating the expression of type I collagen, α2 integrin and β1 integrin. METHODS:After 14 days of treatment, the refractive state and axial length were measured and the levels of type I collagen, α2 integrin and β1 integrin were assayed in the posterior sclerae of groups of guinea pigs that wore a monocular-7D polymethylmethacrylate (PMMA) lens or had -7D lens wear followed by the peribulbar injection of Phosphate Buffer Solution (PBS) or bFGF. The untreated fellow eye served as a control. Guinea pigs with no treatment served as normal group. ·RESULTS:The results showed that 14 days of monocular defocus increased axial eye length and refraction, while bFGF delivery inhibited them markedly. Further, it was also found that the monocular-7D lens could decrease the levels of type I collagen, α2 integrin and β1 integrin expressions, while, unlike PBS, bFGF increased them significantly in comparison to contralateral control eyes and normal eyes. CONCLUSION:bFGF can prevent the formation anddevelopment of defocus myopia by upregulating the expressions of type I collagen, α2 integrin and β1 integrin. Taken together, our results demonstrate that bFGF promotes sclera remodeling to prevent myopia in guinea pigs.展开更多
Objective:To observe the expression changes of inflammatory markers TGF-β1,Smad3 and IL-6 in patients with atrial fibrillation(AF),and to explore the significance of TGF-β1 signaling pathway in the structural remode...Objective:To observe the expression changes of inflammatory markers TGF-β1,Smad3 and IL-6 in patients with atrial fibrillation(AF),and to explore the significance of TGF-β1 signaling pathway in the structural remodeling of AF.Methods:The expression of TGF-β1,Smad3 and IL-6 in 50 cases with AF and 30 normal cases were detected by RT-PCR and ELISA.Results:The TGF-β1,Smad3 and IL-6 mRNA and protein expression levels in patients with AF were significantly higher than that in the control group(P<0.05),but there was no significantly different between the paroxysmal AF group and the persistent AF group(P>0.05).The TGF-β1mRNA expression in the≥50 years subgroup was significantly higher than that in the<50years subgroups,and it was higher in the NYHAⅢsubgroup than in theⅠ/Ⅱgrade subgroup.It was also higher in the left ventricular ejection fraction(LVEF)<50%subgroup than in LVEF≥50%group,and it was significantly higher in the AF time≥36 months subgroup than that in<36months subgroup(P<0.05).The Smad3 and IL-6 expressions in the in the LVEF<50%subgroup were both high that than that in LVEF≥50%group,and higher in the AF time≥36 months subgroup than that in<36 months subgroup(P<0.05).There were a positive correlation between TGF-β1,Smad3 and IL-6(r=0.687,r=0.547).There were also a positive correlation between Smad3 and IL-6 mRNA(r=0.823).Conclusions:AF is associated with inflammation,and the inflammation is also involved in the fibrillation and sustain of AF.The TGF-β1 signal pathway may be involved in the process of atrial structural remodeling in patients with AF,and iss related with the occurrence and maintenance of AF.展开更多
Hepatocellular carcinoma(HCC) is one of the most lethal malignancies in the world. Several signaling pathways,including the wingless/int-1(Wnt) signaling pathway,have been shown to be commonly activated in HCC. The Wn...Hepatocellular carcinoma(HCC) is one of the most lethal malignancies in the world. Several signaling pathways,including the wingless/int-1(Wnt) signaling pathway,have been shown to be commonly activated in HCC. The Wnt signaling pathway can be triggered via both catenin β1(CTNNB1)-dependent(also known as "canonical") and CTNNB1-independent(often referred to as "non-canonical") pathways. Specifically,the canonical Wnt pathway is one of those most frequently reported in HCC. Aberrant regulation from three complexes(the cell-surface receptor complex,the cytoplasmic destruction complex and the nuclear CTNNB1/T-cell-specific transcription factor/lymphoid enhancer binding factor transcriptional complex) are all involved in HCC. Although the non-canonical Wnt pathway is rarely reported,two main non-canonical pathways,Wnt/planar cell polarity pathway and Wnt/Ca2+ pathway,participate in the regulation of hepatocarcinogenesis. Interestingly,the canonical Wnt pathway is antagonized by non-canonical Wnt signaling in HCC. Moreover,other signaling cascades have also been demonstrated to regulate the Wnt pathway through crosstalk in HCC pathogenesis. This review provides a perspective on the emerging evidence that the aberrant regulation of Wnt signaling is a critical mechanism for the development of HCC. Furthermore,crosstalk between different signaling pathways might be conducive to the development of novel molecular targets of HCC.展开更多
In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investi...In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investigate how hydrogen sulfide （HzS） sup- presses TGF-~l-induced differentiation of human cardiac fibroblasts to myofibroblasts. Human cardiac fibroblasts were se- rum-starved in fibroblast medium for 16 h before exposure to TGF-β1 （10 ng mL-1） for 24 h with or without sodium hydrosul- fide （NariS, 100 μmol L-1, 30 min pretreatment） treatment. NariS, an exogenous HzS donor, potently inhibited the prolifera- tion and migration of TGF-β1-induced human cardiac fibroblasts and regulated their cell cycle progression. Furthermore, NariS treatment led to suppression of fibroblast differentiation into myofibroblasts, and reduced the levels of collagen, TGF-β1, and activated Smad3 in TGF-β1-induced human cardiac fibroblasts in vitro. We therefore conclude that H2S sup- presses TGF-β1-stimulated conversion of fibroblasts to myofibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway, as well as by inhibiting the proliferation, migration, and cell cycle progression of human cardiac myofibroblasts. These effects of H2S may play significant roles in cardiac remodeling associated with heart failure.展开更多
基金the Science and Technology Key Project of Zhejiang Province, No. 2002c33015
文摘AIM： To study the expression levels of E-selectin, integrin β1 and immunoglobulin supperfamily memberintercellular adhesion molecule-1 （ICAM-1） in human gastric carcinoma cells, and to explore the relationship between these three kinds of cell adhesion molecules and gastric carcinoma. METHODS： The serum contents of E-selectin, integrin β1 and ICAM-1 were detected by enzyme-linked immunosorbent assay （ELISA）, in 47 healthy individuals （control group） and in 57 patients with gastric carcinoma （gastric carcinoma group） respectively prior to operation and 7 d after operation. RESULTS： The serum E-selectin, ECAM-1 and integrin β1 were found to be expressed in both control and gastric carcinoma groups. However, they were highly expressed in patients with gastric carcinoma patients before operation or with unresectable tumours. The expression levels of ICAM-1 and integrin β1 were significantly higher in gastric carcinoma patients than in controls （P 〈 0.01）. A comparison of the E-selectin levels between the two groups showed statistically insignificant differnce （P = 0.64）. In addition, the expression levels were all decreased substantially in the postoperative patients subjected to radical resection of the tumours, indicating that the high level expressions of these compounds might be the important factor for predicting the prognosis of these patients. CONCLUSION： Serum E-selectin, ICAM-1 and integrin β1 expression levels are probably related to the metastasis and relapse of gastric cancer.
文摘AIM:To investigate the expressions of type I collagen, α2 integrin and β1 integrin in the posterior sclera of guinea pigs with defocus myopia and whether basic fibroblast growth factor (bFGF) injection inhibits the formation and development of myopia by upregulating the expression of type I collagen, α2 integrin and β1 integrin. METHODS:After 14 days of treatment, the refractive state and axial length were measured and the levels of type I collagen, α2 integrin and β1 integrin were assayed in the posterior sclerae of groups of guinea pigs that wore a monocular-7D polymethylmethacrylate (PMMA) lens or had -7D lens wear followed by the peribulbar injection of Phosphate Buffer Solution (PBS) or bFGF. The untreated fellow eye served as a control. Guinea pigs with no treatment served as normal group. ·RESULTS:The results showed that 14 days of monocular defocus increased axial eye length and refraction, while bFGF delivery inhibited them markedly. Further, it was also found that the monocular-7D lens could decrease the levels of type I collagen, α2 integrin and β1 integrin expressions, while, unlike PBS, bFGF increased them significantly in comparison to contralateral control eyes and normal eyes. CONCLUSION:bFGF can prevent the formation anddevelopment of defocus myopia by upregulating the expressions of type I collagen, α2 integrin and β1 integrin. Taken together, our results demonstrate that bFGF promotes sclera remodeling to prevent myopia in guinea pigs.
基金supported by National Science Funded Project(81060017)
文摘Objective:To observe the expression changes of inflammatory markers TGF-β1,Smad3 and IL-6 in patients with atrial fibrillation(AF),and to explore the significance of TGF-β1 signaling pathway in the structural remodeling of AF.Methods:The expression of TGF-β1,Smad3 and IL-6 in 50 cases with AF and 30 normal cases were detected by RT-PCR and ELISA.Results:The TGF-β1,Smad3 and IL-6 mRNA and protein expression levels in patients with AF were significantly higher than that in the control group(P<0.05),but there was no significantly different between the paroxysmal AF group and the persistent AF group(P>0.05).The TGF-β1mRNA expression in the≥50 years subgroup was significantly higher than that in the<50years subgroups,and it was higher in the NYHAⅢsubgroup than in theⅠ/Ⅱgrade subgroup.It was also higher in the left ventricular ejection fraction(LVEF)<50%subgroup than in LVEF≥50%group,and it was significantly higher in the AF time≥36 months subgroup than that in<36months subgroup(P<0.05).The Smad3 and IL-6 expressions in the in the LVEF<50%subgroup were both high that than that in LVEF≥50%group,and higher in the AF time≥36 months subgroup than that in<36 months subgroup(P<0.05).There were a positive correlation between TGF-β1,Smad3 and IL-6(r=0.687,r=0.547).There were also a positive correlation between Smad3 and IL-6 mRNA(r=0.823).Conclusions:AF is associated with inflammation,and the inflammation is also involved in the fibrillation and sustain of AF.The TGF-β1 signal pathway may be involved in the process of atrial structural remodeling in patients with AF,and iss related with the occurrence and maintenance of AF.
基金Supported by National Natural Science Foundation of China,No.31470264 and No.81502418the Key Program of Natural Science Foundation of Hubei Province of China,No.2014CFA078+7 种基金the Hubei Provincial Natural Science Foundation of China,No.2015CFB168 and No.2012FFB04304the Scientific research Innovation Team in Hubei,No.2015CFA009the General Financial Grant from the China Postdoctoral Science Foundation,No.2014M550411the Fundamental research Funds for the Central Universities,No.2042014kf0029the Tianqing Liver Disease research Fund of the China Foundation for Hepatitis Prevention and Control,No.TQGB20140250the Innovation Seed Fund of Wuhan University School of Medicinethe Science and Technology Department Supported Program of Jiangxi Province of China,No.2010BSA13500the Science and Technology Project of Education Department of Jiangxi Province of China,No.GJJ11570
文摘Hepatocellular carcinoma(HCC) is one of the most lethal malignancies in the world. Several signaling pathways,including the wingless/int-1(Wnt) signaling pathway,have been shown to be commonly activated in HCC. The Wnt signaling pathway can be triggered via both catenin β1(CTNNB1)-dependent(also known as "canonical") and CTNNB1-independent(often referred to as "non-canonical") pathways. Specifically,the canonical Wnt pathway is one of those most frequently reported in HCC. Aberrant regulation from three complexes(the cell-surface receptor complex,the cytoplasmic destruction complex and the nuclear CTNNB1/T-cell-specific transcription factor/lymphoid enhancer binding factor transcriptional complex) are all involved in HCC. Although the non-canonical Wnt pathway is rarely reported,two main non-canonical pathways,Wnt/planar cell polarity pathway and Wnt/Ca2+ pathway,participate in the regulation of hepatocarcinogenesis. Interestingly,the canonical Wnt pathway is antagonized by non-canonical Wnt signaling in HCC. Moreover,other signaling cascades have also been demonstrated to regulate the Wnt pathway through crosstalk in HCC pathogenesis. This review provides a perspective on the emerging evidence that the aberrant regulation of Wnt signaling is a critical mechanism for the development of HCC. Furthermore,crosstalk between different signaling pathways might be conducive to the development of novel molecular targets of HCC.
基金supported by the State Key Program of National Natural Science of China(81230007)
文摘In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investigate how hydrogen sulfide （HzS） sup- presses TGF-~l-induced differentiation of human cardiac fibroblasts to myofibroblasts. Human cardiac fibroblasts were se- rum-starved in fibroblast medium for 16 h before exposure to TGF-β1 （10 ng mL-1） for 24 h with or without sodium hydrosul- fide （NariS, 100 μmol L-1, 30 min pretreatment） treatment. NariS, an exogenous HzS donor, potently inhibited the prolifera- tion and migration of TGF-β1-induced human cardiac fibroblasts and regulated their cell cycle progression. Furthermore, NariS treatment led to suppression of fibroblast differentiation into myofibroblasts, and reduced the levels of collagen, TGF-β1, and activated Smad3 in TGF-β1-induced human cardiac fibroblasts in vitro. We therefore conclude that H2S sup- presses TGF-β1-stimulated conversion of fibroblasts to myofibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway, as well as by inhibiting the proliferation, migration, and cell cycle progression of human cardiac myofibroblasts. These effects of H2S may play significant roles in cardiac remodeling associated with heart failure.
