Ovary: Immunolocalization of transforming growth factor-{beta}1 and transforming growth factor-{beta}2 in the mouse ovary during gonadotrophin-induced follicular maturation

An immunohistochemical approach was utilized to evaluate thecellular distribution of transforming growth factor-₁ (TGF₁)and transforming growth factor ₂ (TGF₂) at different stagesof follicle development in the prepubertal mouse ovary underthe following conditions: (i) after pregnant mare's serum gonadotrophin(PMSG) treatment; (ii) after PMSG and human chorionic gonadotrophin(HCG) treatment; (iii) after PMSG and HCG treatment plus mating.In the immature ovary, TGFF₁ and TGF₂ immunoreactivities arelocalized in theca and granulosa cells and in oocytes. AfterPMSG treatment, TGF₁ and TGF₂ immunoreactivities are localizedin granulosa cells; in addition, TGF₂ staining is noted in thematrix surrounding antral cells. Staining for both TGF₁ andTGF₂ drops in the theca but persists in the oocyte. PMSG plusHCG treatment results in a significant increase in TGF₁ andTGF₂ immunoreactivity in the theca and in the maintenance ofTGF₁ staining in both basal granulosa cells and cumulus cellswhereas TGF₂ immunoreactivity is essentially localized in thematrix surrounding cumulus cells. Staining for TGF₁ and TGF₂persists in the oocyte. Following PMSG plus HCG treatment andmating, TGF₁ immunoreactivity is localized in the luteal cellsof corpora lutea and TGF₂ shows a similar localization pattern.This study provides evidence that TGF₁ and TGF₂ peptides areexpressed in specific cell types during induced follicular maturationin the mouse ovary.     

Differential effect of transforming growth factor-{beta}1 on the activation of human naive and memory CD4+ T lymphocytes

Transforming growth factor-ß1 (TGF-ß1) canhave stimulatory or inhibitory effects on cell growth. For severalcell types, the effect of TGF-ß1 was found to correlatewith the differentiation stage of the cells and the presenceof other cytoklnes. We have studied here the influence of TGF-ß1on CD4⁺ T cell activation in relation to the differentiationstage of the cells by evaluating the effect of TGF-ß1on the prollferatlve responses of purified CD4⁺CD45RA⁺ (unprfmed)and CD4⁺CD45RO⁺ (primed) lymphocytes. Under certain conditions,TGF-ß1 exerted a co-stlmulatory effect on peripheralblood CD4⁺CD45RA⁺ T cells whereas the outgrowth of CD4⁺CD45RO⁺T cells was suppressed in any activation system tested. Theenhancement of prollferatlve responses by TGF-ß1 inTCR/CD3 or CD2 stimulated cultures of CD45RA⁺ cells involvedup-regulatlon of CD25 expression and was dependent on the presenceof exogenous IL-2 or CD28 mAbs; IL-7 driven proliferatlve responseswere suppressed by TGF-ß1. These observations wereconfirmed in experiments with purified cord blood (CB) CD4⁺T cells inasmuch as addition of TGF-ß1 caused a 2-to 7-fold increase in IL-2 driven proliferatlve responses ofthese cells. Finally we show that, in contrast to the effectof TGF-ß1 during primary stimulation of CB CD4⁺ Tcells, TGF-ß1 suppressed T cell proliferation for40% in secondary cultures of these cell. Our findings indicatethat TGF-ß1 Is a blfunctlonal regulator of CD4⁺ Tcell growth in vitro, with co-stimulatory capacities duringCD45RA⁺ T cell mediated primary responses and growth suppresslveeffects during secondary responses of CD45RO⁺ T cells.     

转化生长因子-β族信号转导与肿瘤

转化生长因子 β(ｔｒａｎｓｆｏｒｍｉｎｇｇｒｏｗｔｈｆａｃｔｏｒβ,ＴＧＦ- β)族细胞因子包括ＴＧＦ - β类、骨成形蛋白 (ｂｏｎｅｍｏｒｐｈｏｇｅｎｅｔｉｃｐｒｏｔｅｉｎ ,ＢＭＰ)类、活素 (ａｃｔｉｖｉｎ)类、抑素(ｉｎｈｉｂｉｎ)类、苗勒氏抑制物 (ｍｕｌｌｅｒｉａｎｉｎｈｉｂｉｔｏｒｙｓｕｂ ｓｔａｎｃｅ)及结节物 (ｎｏｄａｌ) ,胶质细胞源性促神经因子(ｇｌｉａｌ-ｄｅｒｉｖｅｄｎｅｕｒｏｔｒｏｐｉｃｆａｃｔｏｒ) ,Ｄｐｐ(果蝇Ｄｅｃａｐｅｎｔａ ｐｌｅｇｉｃ基因产物 ) ,Ｖｇｌ(蛙卵ｖｇｌＲＮＡ产物 )等 2 5多…     

石蜡包埋人胰腺癌组织中Smad4蛋白和转化生长因子β1及其Ⅱ型受体的表达

目的：探讨转化生长因子（TGF）－β通路中Smad4蛋白,TGFβ1和转化生长因子βⅡ型受体（TβRⅡ）的关系及它们在胰腺癌中的可能作用机制。方法：用EnVision免疫组织化学技术检测56份石蜡包埋人胰腺癌标本Smad4蛋白,TGFβ1和TβRⅡ蛋白表达的情况。结果：56份胰腺癌组织Smad4,TGFβ1和TβRII阳性率分别为58．93％（33）,66．07％（37）和60．71（34）,对应正常胰腺组织阳性率分别为89．29％（50）,25．00％（14）和25．00％（14）,TGFβ1的表达与临床分期,肿瘤的有无转移相关（P＜0．05）,TGFβ1和TβRII之间也有相关关系（P＜0．05）,结论：胰腺癌组织中Smad4表达降低,TGFβ1与TβRII则呈过表达,TGFβ1和TβRII对胰腺癌的发生可能有协同作用。Smad在TGF－β诱导基因表达调控和随后的生长抑制中是关键的转录因子,但TGFβ有时也可能以与Smad4无关的形式起作用。     

Interferon-{beta} inhibits bleomycin-induced lung fibrosis by decreasing transforming growth factor-{beta} and thrombospondin

Pulmonary fibrosis is the result of abnormal processes of repair that occur after lung injury. Transforming growth factor (TGF)-beta is a key molecule in the progression of pulmonary fibrosis. Although clinical use of interferon (IFN)-beta did not improve survival in patients with idiopathic pulmonary fibrosis, because some preclinical studies have suggested that IFN-beta is a potent inhibitor of fibrogenesis, beneficial effects of IFN-beta have been expected. We therefore attempted to determine effects of IFN-beta and investigated the mechanism of action of IFN-beta in bleomycin-induced pulmonary fibrosis. Bleomycin at Day 0 and IFN-beta for 4 wk were administered intravenously to ICR mice. At 28 d after bleomycin injection, histologic and chemical analysis was performed for evaluation of effects of IFN-beta. Tissue distribution and amounts of TGF-beta1 and thrombospondin (TSP)-1/2 were analyzed. IFN-beta attenuated prolylhydroxylase activity, resulting in inhibition of pulmonary fibrosis. Bleomycin-induced increase in TGF-beta1 in epithelial cells and extracellular matrix was attenuated by IFN-beta. TSP-1/2 was limited in platelets of control mice, but was present in foamy cells in fibrotic regions induced by bleomycin. These findings suggest that the antifibrotic effect of IFN-beta is inhibition of TGF-beta and its activation via decrease in TSP-1/2 in lung tissue and change in location of TSP-1/2 from platelets to foamy cells.     

Effect of ionizing radiation on the expression of transforming growth factor-β

Experiments demonstrate the stimulation of transforming growth factor-β expression in porcine skin soon after ψ-irradiation in a dose of 64 Gy and in mouse macrophages after whole body irradiation in a dose of 4 Gy, which suggests the involvement of macrophages that produce transforming growth factor-β during the early postirradiation period in the development of postirradiation fibrosis. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 126, No. 11, pp. 529–533, November, 1998     

香烟提取物和脂多糖对人胚肺成纤维细胞TGF-β1 mRNA及蛋白表达的影响

目的:探讨香烟提取物(CSE)和脂多糖(LPS)对体外培养的人胚肺成纤维细胞(HELF)转化生长因子-β₁(TGF-β₁)mRNA及其蛋白表达的影响。方法:应用不同浓度的CSE(1∶50、1∶25和1∶10)、LPS(0.1 mg/L、1 mg/L和10 mg/L)及CSE(1∶25)与LPS(1 mg/L)联合作用于HELF, 37℃作用24 h后, 提取细胞总RNA, 应用逆转录-多聚酶链反应(RT-PCR)及免疫细胞化学技术检测TGF-β₁ mRNA和蛋白表达的变化。结果:CSE低浓度(1∶50和1∶25)时可增加HELF TGF-β₁ mRNA及蛋白的表达(Ｐ＜0.05), 高浓度(1∶10)时未引起TGF-β₁ mRNA及蛋白表达增强(Ｐ＞0.05)。不同浓度的LPS均引起HELF TGF-β₁ mRNA及蛋白表达增强(Ｐ＜0.05)。CSE与LPS联合作用也可增加HELF TGF-β₁ mRNA及蛋白的表达(Ｐ＜0.05)。结论：一定浓度的CSE和LPS可上调肺成纤维细胞TGF-β₁ mRNA及蛋白表达。     

Embryonic expression of the transforming growth factor beta ligand and receptor genes in chicken

Results: Here we report the embryonic mRNA expression patterns in chicken embryos of the canonical TGFβ ligands (TGFB1, TGFB2, and TGFB3) and receptors (TGFBR1, TGFBR2, TGFBR3), plus the Activin A receptor, type 1 (ACVR1) and co receptor Endoglin (ENG) that also transduce TGFβ signaling. 相似文献   

转化生长因子3β在妊高征和正常妊娠胎盘组织中的差异表达

目的探讨转化生长因子3β(TGF-3β)蛋白及mRNA在妊高征和正常妊娠胎盘组织中表达的差异.方法取10例妊高征和10例年龄配对的正常妊娠的胎盘组织,应用Western blot方法,检测妊高征和正常妊娠胎盘组织中TGF-3β蛋白的表达水平;应用定量PCR方法,检测妊高征和正常妊娠胎盘组织中TGF-3βmRNA表达水平.结果与正常妊娠胎盘组织TGF-3β蛋白和mRNA表达水平相比,妊高征胎盘组织中的TGF-3βmRNA表达水平增加,妊高征胎盘组织中的TGF-3β蛋白表达水平也明显增加.结论 TGF-3β在妊高征胎盘组织中表达增加,妊高征胎盘中TGF-3β高表达可能与妊高征的病因有关.     

Two novel polymorphisms in the human transforming growth factor beta 2 gene

We have identified two novel polymorphisms in the transforming growth factor beta 2 (TGFbeta2) gene; an insertion in the 5'-untranslated region (5'UTR) and a single nucleotide polymorphism (SNP) in exon 1. A 895-bp fragment was analysed covering part of the 5'UTR and exon 1. Single-strand conformation polymorphism (SSCP) analysis of polymerase chain reaction (PCR) products was performed to detect sequence variations. This was followed by the sequencing of samples demonstrating distinct banding patterns. A 4-bp insertion (ACAA) in the 5'UTR and a SNP (G > A) within exon 1 was identified. The 5'UTR polymorphism was found to be common in three Caucasian populations from Spain, Turkey and the UK. Exon 1 polymorphism is rare and results in an R to H amino acid substitution in codon 91. Both polymorphisms may prove useful for investigating possible associations of TGFbeta2 with disease.     

Haemoglobin expression in human endometrium

BACKGROUND: The general concept that haemoglobin is only a carrier protein for oxygen and carbon dioxide is challenged since recent studies have shown haemoglobin expression in non-erythroid cells and the protection of haemoglobin against oxidative and nitrosative stress. Using microarrays, we previously showed expression of haemoglobins alpha, beta, delta and gamma and the haeme metabolizing enzyme, haeme oxygenase (HO)-1 in human endometrium. METHODS: Using real-time quantitative PCR, haemoglobin alpha, beta, delta and gamma, and HO-1 mRNA levels were assessed throughout the menstrual cycle (n = 30 women). Haemoglobin and HO-1 protein levels in the human endometrium were assessed with immunohistochemistry. For steroid responsiveness, menstrual and late proliferative-phase endometrial explants were cultured for 24 h in the presence of vehicle (0.1% ethanol), estradiol (17beta-E(2,) 1 nM), progestin (Org 2058, 1 nM) or 17beta-E(2)+Org 2058 (1 nM each). RESULTS: All haemoglobins and the HO-1 were expressed in normal human endometrium. Haemoglobin mRNA and protein expression did not vary significantly during the menstrual cycle. Explant culture with Org 2058 or 17beta-E(2)+Org 2058 increased haemoglobin gamma mRNA expression (P < 0.05). HO-1 mRNA levels, and not protein levels, were significantly higher during the menstrual (M)-phase of the cycle (P < 0.05), and were down-regulated by Org 2058 in M-phase explants and by 17beta-E(2)+Org 2058 in LP-phase explants, versus control (P < 0.05). CONCLUSIONS: The haemoglobin-HO-1 system may be required to ensure adequate regulation of the bioavailability of haeme, iron and oxygen in human endometrium.     

以Bacmid-杆状病毒-昆虫细胞系统表达人FGF-9①

目的在Bacmid-杆状病毒-昆虫细胞系统中表达人FGF-9。方法采用RT-PCR技术,自新鲜人脑胶质瘤组织获取人FGF-9全编码区cDNA,将其克隆入pCR