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1.
AIM:To investigate the effect of HMGA2 down-regulation on apoptosis and Notch signaling pathway in renal tubular epithelial cells exposed to high glucose (HG). METHODS:D-glucose at 5, 10, 20 and 30 mmol/L was used to stimulate human renal tubular epithelial HK-2 cells for 2 h, and D-glucose at 30 mmol/L was used to stimulate the HK-2 cells for 10 min, 60 min and 120 min. The protein expression of HMGA2 was determined by Western blot. The HK-2 cells were divided into normal glucose (NG) group, HG group, HG+si-HMGA2 group and HG+NC group, in which siRNA was transfected by LipofectamineTM 2000 for 48 h. Flow cytometry was used to analyze the apoptotic rate, reactive oxygen species (ROS) assay kit was used to detect ROS content, and Western blot was used to detect the protein levels of Notch1, Hes1 and Bcl-2. The HK-2 cells were treated with the Notch signaling pathway inhibitor DAPT, and then the cells were divided into HG group, HG+DAPT group and HG+si-HMGA2+DAPT group. The apoptotic rate was analyzed by flow cytometry. RESULTS:Exposure of the HK-2 cells to D-glucose at different concentrations for different time significantly increased the expression of HMGA2 (P<0.05). Compared with NG group, the protein expression of HMGA2, Notch1 and Hes1 in HG group was increased, the expression of Bcl-2/Bax was decreased, the apoptotic rate was increased, and the content of ROS was increased obviously (P<0.05). Compared with HG group, the protein expression of HMGA2, Notch1 and Hes1 of HG+si-HMGA2 group was decreased, the expression of Bcl-2/Bax was increased, the apoptotic rate was decreased, and the content of ROS was decreased significantly (P<0.05). The apoptotic rate in HG+DAPT group was significantly lower than that in HG group, while the apoptotic rate in HG+si-HMGA2+DAPT group was significantly lower than that in HG+DAPT group (P<0.05). CONCLUSION:Down-regulation of HMGA2 expression inhibits the apoptosis of renal tubular epithelial cells by regulating Notch signaling pathway and decreasing ROS production.  相似文献   
2.
AIM: To observe the changes of Notch1 expression and autophagy in the renal tissues of diabetic mice, and to explore the regulatory effect of Notch1 on tubulointerstitial fibrosis by inhibiting autophagy in diabetic nephro-pathy. METHODS: The mice were randomly divided into normal control group (db/m mice) and diabetes group (db/db mice), with 8 rats in each group. After 12 weeks of feeding, the mice were sacrificed and the corresponding biochemical indexes were measured. The protein expression of Notch1 in the renal tubular epithelial cells was observed by immunohistochemical staining. The protein levels of Notch1, PTEN, p-Akt (Thr308), Akt, p-mTOR (Ser2448), mTOR, LC3, P62, collagen type Ⅰ (Col-Ⅰ) and collagen type Ⅲ (Col-Ⅲ) were determined by Western blot. RESULTS: Compared with the db/m mice, the blood glucose, glycosylated hemoglobin, serum creatinine, triglyceride and total cholesterol were increased in the db/db mice (P<0.01). Renal tubular epithelial cell vacuolar degeneration, renal tubular expansion and interstitial inflammatory cell infiltration in db/db mouse renal tissues with HE staining were observed. The images of Masson staining showed collagenous fiber-like substance deposition in the glomerular capillaries and renal interstitium, and disarrangement of tubular structure in the renal tissues of db/db mice. The protein expression levels of PTEN and LC3-Ⅱ were decreased (P<0.01 or P<0.05), while the protein levels of Notch1, P62, p-mTOR (Ser2448), p-Akt (Thr308), Col-I and Col-III were increased in the db/db mice as compared with the db/m mice (P<0.01). However, no significant change of total mTOR and Akt proteins between the 2 groups was found. CONCLUSION: Notch1 protein expression was increased, PTEN expression was significantly reduced, Akt/mTOR pathway was activated, autophagy was inhibited, and fibrosis was aggravated in the renal tissues of the diabetic mice.  相似文献   
3.
AIM: To study the expression of Jagged2/Notch3 signaling molecules in pulmonary vascular wall of pulmonary hypertensive rats induced by monocrotaline. METHODS: SD rats were randomly divided into normal control group (C group,n=15), solvent control group (S group,n=15) and monocrotaline model groups (M group,n=15). The model of pulmonary hypertension was established by a single subcutaneous injection of monocrotaline (50 mg/kg). The rats in S group were given a single subcutaneous injection of the same dose of solvent. After 4 weeks, the pulmonary vascular remodeling was assessed by HE staining, and the mean pulmonary artery pressure (mPAP) and right ventricular systolic pressure (RVSP) were determined by right heart catheterization. The expression of Jagged2/Notch3/Hes5 molecules in the pulmonary vascular wall was detected by immunohistochemical method and real-time PCR. RESULTS: Compared with S group and C group, the percentage of medial wall thickness of smaller arteries in model group increased significantly (P<0.01). The levels of mPAP and RVSP in M group were significantly higher than those in S group and C groups (P<0.01). The results of real-time PCR showed that the expression of Jagged2, Notch3 and Hes5 was significantly increased in M group compared with S group and C group. The data from immunohistochemical detection indicated that Jagged2 mainly expressed in the intima of small lung artery, Notch3 and Hes5 mainly expressed in the medial smooth muscle cells. Compared with S group and C group, the expression of Jagged2 and Notch3 was significantly increased in the lung small arteries of M group. CONCLUSION: The activation of Jagged2/Notch3 signaling pathway might play an important role in the formation of pulmonary hypertension.  相似文献   
4.
目的 从Notch1信号通路探讨姜黄素诱导结肠癌SW480细胞株凋亡的分子机制。方法 (1)利用流式细胞技术检测不同浓度姜黄素(0,7.5,15,30,60 μmol/L)处理结肠癌SW480株24 h和48 h后的细胞凋亡情况。(2)通过RT-PCR检测不同浓度姜黄素(0,7.5,15,30,60 μmol/L)处理结肠癌SW480细胞株24 h和48 h后,Notch1信号通路中膜受体基因Notch1及下游靶基因Hes-1 mRNA表达情况,观察姜黄素对Notch1信号通路中Notch1及Hes-1基因mRNA表达的影响。结果 (1)姜黄素能诱导结肠癌SW480细胞株凋亡;(2)姜黄素能一定程度上下调Notch1信号通路中Notch1及Hes-1基因mRNA的表达(P<0.05)。结论 姜黄素能一定程度上诱导结肠癌SW480细胞株凋亡,这种对结肠癌SW480细胞毒性作用可能与调控Notch1信号通路中膜受体基因Notch1及下游靶基因Hes-1转录有关。  相似文献   
5.
卵泡从原始卵泡发育为成熟卵泡,直至排卵、黄体发育等过程都受到精密的调控,产生大量的优势卵泡是绵羊产多羔及实现快速扩繁的关键因素。研究发现,相关信号通路和转录因子通过影响绵羊卵泡中卵母细胞、颗粒细胞的生长,进而调控卵泡的发育成熟,对这些信号通路进行深入了解,有助于探索卵泡发育的调控机制,早日实现绵羊高效繁育。Notch是卵泡发育过程中发挥重要作用的高度保守信号通路,PI3K/AKT/mTOR信号通路各成员都是广泛存在于细胞内的信号转导分子,在卵泡发育早期发挥了主要作用,还有间隙连接(gap junction,GJ)和跨带突触(transzonal projections,TZPs)等物理连接方式,在细胞间的交流通讯起到重要作用。作者详细介绍了Notch信号通路、PI3K/AKT/mTOR信号通路、间隙连接及跨带突触的结构功能在绵羊卵泡发育中的调控作用,为进一步探明绵羊卵泡发育的调控机制提供参考。  相似文献   
6.
目的 探讨丹龙醒脑方对脑缺血再灌注模型大鼠海马区Notch信号通路相关蛋白Notch1、Notch2及Hes1表达的影响。方法 将80只雄性SD大鼠随机分为假手术组、模型组、丹龙醒脑方小剂量组(丹小组7.4 g/kg)、大剂量组(丹大组14.8 g/kg),线栓法建立局灶性脑缺血再灌注大鼠模型,再灌注7 d取缺血侧海马组织。采用免疫组织化学法、免疫印迹法检测大鼠海马区Notch1、Notch2及Hes1蛋白表达。结果 与假手术组比较,各组Notch1、Notch2及Hes1蛋白表达显著升高(P<0.05,P<0.01);与模型组比较,丹小组、丹大组Notch1、Notch2及Hes1蛋白表达显著升高(P<0.05,P<0.01)。结论 丹龙醒脑方能通过上调海马区Notch1、Notch2及Hes1蛋白表达水平,调节Notch信号转导通路,这可能是其促进脑缺血损伤后神经功能修复的机制之一。  相似文献   
7.
Notch信号通路是一条进化上十分保守的信号转导系统,在调节干细胞增殖、分化和凋亡方面起到重要作用。研究表明,鹿生茸区骨膜和角柄骨膜分别含有鹿茸发生和再生的干细胞。应用RT-PCR的方法对离体培养生茸区骨膜和角柄骨膜细胞进行检测,得出Notch信号通路各信号因子在2种细胞中的表达情况。结果:Notch-1、Notch-2、Notch-4、Dll-4J、agged-1J、agged-2、Hes-1等信号因子在这2种干细胞中均有不同程度的表达,说明Notch信号通路可能参与了他们的增殖、分化的调控。  相似文献   
8.
Notch信号通路可以与TLR信号通路相互作用,协作调控炎性因子的产生以及巨噬细胞的激活。然而,在猪巨噬细胞上,Notch信号通路是如何调控炎性反应的还不清楚。本研究以LPS/TLR4诱导炎性反应为模型,利用猪肺泡巨噬细胞来研究LPS处理对Notch信号通路的影响及Notch信号通路对LPS诱导炎性反应的调控作用。结果显示:LPS处理增加配体Jagged1、Jagged2和Dll4的表达,并上调下游靶基因Hey1的表达;Notch信号通路调控LPS诱导的炎性反应。本研究结果不仅明确了在猪巨噬细胞上Notch信号通路调控LPS诱导的炎性反应,而且为将来揭示Notch信号通路在猪相关细菌感染中的作用奠定基础。  相似文献   
9.
骨骼系统对机体的生命活动至关重要,它为生物体提供了造血微环境、机械支撑、保护脏器等功能,同时也是钙和其他矿物质等的储存库。家鸡尾骨的表型多样性是研究骨骼系统发育及形成机制的良好资源。Notch、Wnt信号通路的靶基因及其相互作用可以形成周期性表达的特点,是调节体节形成及尾部骨骼终止延伸的分子通路。为了解无尾鸡骨骼发育终止的分子机制,作者分别总结了骨骼发育、无尾鸡骨骼研究进展,并重点讨论影响无尾性状的关键信号通路Notch、Wnt及其在无尾鸡研究中的进展。但是,受体和配体之间相互作用的精确调节以及信号通路中的核心元素仍不清楚,需要通过更多的功能基因组和蛋白质组等方法进行深入研究。  相似文献   
10.
AIM: To investigate the effect of Notch1 on the activation of pancreatic stellate cells (PSCs). METHODS: The expression of Notch1 in pancreatic duct adenocarcinoma (PDAC) tissues was detected by the immunohistochemical and immunofluorescence double staining. The PSCs were isolated, cultured, and identified by oil red O staining, Western blot and RT-qPCR. The expression of Notch1 and HES1 was detected by Western blot and RT-qPCR. After transfection of Notch1 siRNA to PSCs, Western blot was used to detect the protein expression of α-smooth muscle actin (α-SMA), fibronectin and collagen type Ⅰ (ColⅠ) in activated PSCs. The expression of Notch1 and HES1 was also detected by Western blot. The effects of Notch1 siRNA on migration ability and viability of PSCs were determine by scratch test and CCK-8 assay. RESULTS: The results of immunohistochemical and immunofluorescence double staining showed that Notch1 expressed in α-SMA positive cells in PDAC stroma. The mouse PSCs were successfully cultured, and the expression of α-SMA, fibronectin, ColⅠ, Notch1 and HES1 in activated PSCs were significantly increased compared with unactivated PSCs (P<0.01). After transfection of Notch1 siRNA to mouse PSCs, the expression of α-SMA and ColⅠ was significantly reduced compared with negative groups, but the expression of fibronectin and HES1 did not change significantly. After knock-down of Notch1 expression in activated PSCs, the migration ability and viability of PSCs were significantly reduced compared with negative group. CONCLUSION: Notch1 is involved in regulating the activation of PSCs. Knock-down of Notch1 expression inhibits the expression of the markers of activated PSCs, α-SMA and ColⅠ, reduces the activation of PSCs, and attenuates the migration capacity and viability of PSCs. Notch1 regulates the activation of PSCs without relying on the classic Notch signaling pathway.  相似文献   
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