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Passive sensitization increases histamine-stimulated calcium signaling and NF-κB transcription activity in bronchial epithelial cells

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Acta Pharmacologica Sinica 2006年第6期27卷 708-714页

作者： Si JIN~(2.5)Dan TIAN~3 Jian-guo CHEN~4 Li-ping ZHU~2.Sheng-yuan LIU~2.Di-xun WANG~2.2.department of pathophysiology,{2. medical college,huazhong university of science and technology Key Laboratory of Pulmonary Disease of Ministry of Health of China,wuhan 430030,China 3 department of Pathology,{2. medical college.huazhong university of science and technology.wuhan 430030,China 4 department of Pharmacology,{2. medical college,huazhong university of science and technology,wuhan 430030,China department of pathophysiology Tongji Medical College Huazhong University of Science and Technology Key Laboratory of Pulmonary Disease of Ministry of Health of China Wuhan China department of Pathology Tongji Medical College Huazhong University of Science and Technology Wuhan China department of Pharmacology Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:To find out if the two aspects of asthma（chronic airway inflammation andbronchial hyperresponsiveness）are related to hypersensitivity of calcium signal-ing in bronchial epithelial ***:Porcine bronchial epithelial cells（PBEC）were divided into sensitized（S）and nonsesitized（N）*** group S,the cellswere preincubated with serum from ovalbumin sensitized guinea *** group N,the cells were preincubated with serum from nonsensitized guinea *** calcium imaging and ELISA-based NF-κ3 activity were used to evaluate thehistamine-stimulated intracellular free calcium level and NF-κB activity,***:First,0.1μmol/L histamine could induce [Ca2.]ioscillationsin PBEC of group S,but not in group ***,1/Jmol/L histamine could induce[Ca2.]ioscillations of PBEC in both group S and group *** [Ca2.]ioscillationfrequency of PBEC was significantly higher in group S than in group N,thoughthe[Ca2.]ioscillation amplitude showed no difference between the two ***,when 10 μmol/L histamine was used to stimulate PBEC a transient initialincrease followed by a sustained elevation（FSE）of [Ca2.]iwas observed in PBECin both *** amplitude of the FSE of [Ca2.]iin PBEC was significantlyhigher in group S than in group *** subsequent NF-κB activity was in accor-dance to the calcium oscillation frequency evoked by histamine,but not to ***:It was suggested that the increased sensitivity of calciumsignaling in bronchial epithelial cells might contribute to the exorbitant inflamma-tion or increased susceptibility in asthmatic airway epithelial cells.

关键词： asthma histamine calcium signaling bronchi epithelial cell nuclear factor of kappaB

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Acta Pharmacologica Sinica 2006年第9期27卷 1159-1164页

作者： Jin QIN Zheng-xiang LIU~1 department of Cardiology,tongji Hospital,tongji medical college,huazhong university of science and technology,wuhan 430030,China department of Cardiology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:To examine the inhibitory effect of FAK-related nonkinase(FRNK)in cardiachypertrophy in vitro and investigate the possible ***:A func-tional fragment of FRNK cDNA was amplified by reverse transcription-polymerasechain reaction and cloned into the vector *** in neonatal ratcardiac myocytes was established with angiotensin-Ⅱ *** pcDNA3.1-FRNK or pcDNA3.1 was respectively transfected into cardiomyocytes byLipofectamine *** surface area and mRNA expression of atrial natriureticpeptide(ANP)of myocytes were employed to detect cardiac ***-κBp65 protein in nuclear extracts,phosphorylation levels of ERK1/2.p-ERK 1/2.andAKT(p-AKT),as well as total ERK1/2.and AKT in variant treated cardiomyocyteswere determined by Western ***:Under the stimulation of angiotensin Ⅱ,the surface area of myocytes and levels ofANP mRNA were significantly *** transient transfection with pcDNA3.1-FRNK in advance may reduce the sur-face area and expression of ANP mRNA of hypertrophic *** proteinlevels of NF-κB p65 in nuclear extracts and p-ERKI/2.p-AKT in FRNK treatedcardiomyocytes were significantly decreased compared with that in angiotensin-Ⅱ induced cardiomyocytes,while different treatments had little effect on totalERK1/2.and ***:FRNK may inhibit angiotensin-Ⅱ-inducedcardiomyocyte hypertrophy via decreasing phosphorylation levels at ERK1/2.andAKT,consequently downregulating nuclear translocation of NF-κB p65.

关键词： FAK-related nonkinase angiotensin Ⅱ cardiomyocyte hypertrophy extracellular signal-regulated kinase 1/2 protein kinase B NF-kappaB p65

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CD151 gene delivery increases eNOS activity and induces ECV304 migration, proliferation and tube formation

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Acta Pharmacologica Sinica 2007年第1期28卷 66-72页

作者： Zhen-zhong ZHENG Zheng-xiang LIU~2.department of Cardiology,tongji Hospital,tongji medical college,huazhong university of science and technology,wuhan 430030,China department of Cardiology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:To investigate the effects of CD 151 on the activity of endothelial NO syn-thase(eNOS),and ECV304 migration,proliferation and tube ***:pAAV-CD 151 and pAAV-anti-CD 151 were constructed and used to transientlytransfect ECV304 mediated with Lipofectamine *** transfection,the ex-pression of CD 151 was measured by Western *** migration assay wasperformed using Boyden transwell;proliferation assay was evaluated using the 3-[4,5-dimethylthiazol-2.yl]-2.5,diphenyltetrazolium bromide(MTT)method,andtube formation test was examined on matrigel,eNOS activity was assayed by L-[~3H]citrulline production from L-[~3H]*** involvement of eNOS was ex-plored using an eNOS inhibitor(L-NAME)and the effects in the process ***:CD 151 promotes cell migration,proliferation and tube *** addition,CD151 increases eNOS ***,cell migration,prolifera-tion and tube formation induced by CD 151 are inhibited when L-NAME is used,which indicates that there is an involvement of eNOS in CD151-induced cellmigration,cell proliferation and tube ***:CD 151 promotesECV304 migration,proliferation and tube *** mechanism is that CD151increases eNOS *** result also suggests that eNOS is involved in theangiogenic effects of CD151.

关键词： CDI51 endothelial NO synthase(eNOS) cell migration cell proliferation tube formation

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Deguelin regulates nuclear pore complex proteins Nup98 and Nup88 in U937 cells in vitro1

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Acta Pharmacologica Sinica 2005年第10期26卷 1265-1273页

作者： Hong-li LIU~2. Yan CHEN~(2.3), Guo-hui CUI~2. Qiu-ling WU~2. Jing HE~2. Wei-hua CHEN~2. Jian-feng ZHOU~4 ~2.department of Hematology, Union Hospital, tongji medical college,{2., wuhan 43002. ~4 department of Hematology, tongji Hospital, tongji medical college,{2., wuhan 430030, China department of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China department of Hematology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim: To investigate the anticancer effects and the molecular mechanisms of deguelin on human U937 leukemia cells, and to explore the underlying mechanism regulating nucleoporin 98 （Nup98） and nucleoporin 88 （Nup88） in vitro. Methods: The effects of deguelin on the growth of U937 cells were studied by MTT assay. The effect of deguelin on the cell cycle of U937 cells was studied by using a propidium iodide method. The localization of the nuclear pore complex proteins Nup98 and Nup88 was investigated by using immunofluorescence and immunoelectron microscopy. The expression of Nup98 and Nup88 in U937 cells was investigated by using flow cytometry and Western blot. Results: The prolif eration of U937 cells was inhibited in the deguelin-treated group, with a 2.-h IC50value of 2..61 nmol/L and a 36-h IC50value of 17.07 nmol/L. U937 cells treated with deguelin had reduced percentages of cells in the G0/G1phase, whereas cells accumulated in the S and G2.M phases. Nup88 and Nup98 were found on both the nuclar and cytoplasmic sides of the U937 cells by using immunofluorescence and immunoelectron microscopy. The expression of Nup98 was upregulated and that of the Nup88 protein was downregulated in U937 cells treated with deguelin. Conclusion: Deguelin is able to inhibit the proliferation of U937 cells by regulating the cell cycle such that cells are arrested at the S and G2.M phases, so that the proportion of cells in the G0/G1phase decreases. The antitumor effects of deguelin are related to upregulating the expression of Nup98 and downregulating the expression of Nup88 protein in U937 cells.

关键词： deguelin U937 cells nucleoporin Nup98 Nup88

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5-Hydroxydecanoate inhibits proliferation of hypoxic human pulmonary artery smooth muscle cells by blocking mitochondrial KATP channels

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Acta Pharmacologica Sinica 2007年第10期28卷 1531-1540页

作者： Tao WANG~2,Zhen-xiang ZHANG~(2,4),Yong-jian XU~2,Qing-hua HU~3~2 department of Respiratory Medicine,tongji Hospital,tongji medical college,huazhong university of science and technology,wuhan430030,China ~3 Key Laboratory of Pulmonary Diseases of the Ministry of Health of China and department of pathophysiology,tongjimedical college,huazhong university of science and technology{2.},China department of Respiratory Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China Key Laboratory of Pulmonary Diseases of the Ministry of Health of China and department of pathophysiology Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:To study the effect of 5-hydroxydecanoate （5-HD） on the proliferation of 2.h hypoxic human pulmonary artery smooth muscle cells （HPASMC） and to explorethe pharmacological mechanisms of 5-HD as an inhibitor of mitochondrial mem-brane ATP-sensitive potassium channel ***:Normoxic or hy-poxic HPASMC in culture were stimulated by either diazoxide or 5-HD for 2. *** proliferation of HPASMC was examined by 3-（4,5-dimethyl-2.thiazol-yl）-2.5-diphenyl-2.-tetrazolium bromide （MTT） assay and proliferating cell nuclear anti-gen （PCNA） immunohistochemistry *** apoptosis of HPASMC wasassessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end la-beling （TUNEL） assayand flow cytometric *** relative changes inmitochondrial membrane potential （ΔΨm） were measured using the rhodamine fluo-rescence （R-12.） ***:Both hypoxia and diazoxide stimulationincreased ΔΨmvalue measured by the absorbance of MTT,PCNA-positive stain-ing and decreased TUNEL-positive staining and apoptotic cells in *** and the concomitant stimulation of diazoxide obviously enhanced theeffects of hypoxia or diazoxide alone.5-HD significantly attenuated the effects ineach of the above ***,5-HD partially inhibited the effect ofhypoxia on R-12. fluorescence intensity in ***:5-HD caninhibit the proliferation of hypoxic HPASMC by blocking mitochondrial KATPchannels.

关键词： pulmonary artery smooth muscle cell hypoxia 5-hydroxydecanoate mitochondrial membrane ATP-sensitive potassium channel

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Prediction of Trend between Water Environment Pollution of D Lake and Death Rate of Malignancy in Population

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Journal of huazhong university of science and technology(medical {2.s) 2003年第4期23卷 420-422页

作者：李龙吴春松 Institute of Environmental Medicine department of Mathematics

Grey system analysis method was used to study the correlation between water pollution in D Lake area and death rate of malignancy with death rate of malignancy as effect sequence and a variety of water pollution index as factor sequence. On the basis of grey correlation analysis, grey system predication model was established for death rate of malignancy in population in D Lake area including GM (1, N) model for death rate of malignancy [ MR (t+1) =(9.9987E 1+5.0001E 2.+10.8994E 3+1.1114E 4+165.102.) ·e -0.0070t -9.9987E 1-5.0001E 2.10.8994E 3-1.1114E 4 ] and GM (1, 1) model for related factors [ E 1(t+1) =52.12.4-46.9468e -0.0058t , E 2.t+1) =4.6114-4.5664e 0.0015t, E 3(t+1) =1.1389-1.12.2. 0.0065t , E 4(t+1) = 554.5867-549.8006e 0.0016t ], and the trend of death rate of malignancy from 2.00 to 2.10 was predicted.

关键词： death rate of malignancy grey system water environment pollution

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Overexpression of dishevelled-1 attenuates wortmannin-induced hyperphosphorylation of cytoskeletal proteins in N2. cell

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Acta Pharmacologica Sinica 2005年第6期26卷 679-684页

作者： Hai-hong WANG, Ai-hong ZHANG, Ling-qiang ZHU, Qun WANG, Jian-zhi WANG~2.department of pathophysiology,{2., huazhong university of science and technology, wuhan 430030, China department of pathophysiology Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim: To investigate the effect of dishevelled-1 (DVL-1) on wortmannin-induced Alzheimer-like hyperphosphorylation of cytoskeletal proteins in mouse neuroblastoma 2. (N2.) cells. Methods: Cultured N2. cells were transitorily transfected with DVL-1 expression plasmid using Lipofectamine鈩?2.00. Western blot and immunofluorescence microscopy were used to measure the phosphorylation of neurofilament and tau. Results: Level of phosphorylated neurofilament at SMI31 epitope and phosphorylated tau determined by PHF-1 was increased at 1 h and 3 h and back to normal at 6 h after wortmannin 1 |imol/L treatment. The highest level of phosphorylated neurofilament and phosphorylated tau was seen at 1 h and 3 h after wortmannin treatment, respectively. When DVL-1 protein was overexpressed, the hyperphosphorylation of neurofilament at SMI31 and SMI32.epitopes and tau atPHF-l(Ser-396/404),M4(Thr-2.1/Ser-2.5),andTau-l(Ser-198/199/2.2.epitopes was attenuated. Conclusion: Overexpression of mouse DVL-1 protein inhibits wortmannin-induced hyperphosphorylation of neurofilament and tau in N2. cells.

关键词： Alzheimer disease tau proteins neurofilament wortmannin dishevelled-1

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Melatonin attenuatesβ-amyloid-induced inhibition of neurofilament expression

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Acta Pharmacologica Sinica 2004年第4期25卷 49-53页

作者： Ying-chun ZHANG, Ze-fen WANG, Qun WANG, Yi-pengWANG, Jian-zhi WANG2.department of pathophysiology,{2., huazhong university ofscience and technology, wuhan 430030, China department of pathophysiology Tongji Medical College Huazhong University of Science and Technology

AIM: To explore the effect of β-amyloid (Aβ) on metabolism of cytoskeletal protein neurofilament, and search for effective cure to the lesion. METHODS: Wild type murine neuroblastoma N2. (N2.wt) and N2. stably transfected with wild type amyloid precursor protein (N2.APP) were cultured. Sandwich ELISA, immunocytochemistry, and Western blot were used respectively to measure the level of Aβ, the expression and phosphorylation of neurofilament proteins. RESULTS: The immunoreactivity of neurofilament protein was almost abolished in N2.APP, which beard a significantly higher level of Aβ. Melatonin effectively decreased the level of Aβ, and restored partially the level of phosphorylated and non-phosphorylated neurofilament in N2.APP. CONCLUSION: Overproduction of Aβ inhibits neurofilament expression, and melatonin attenuates the Aβ-induced lesion in cytoskeletal protein.

关键词： Alzheimer disease amyloid beta-protein neurofilament proteins melatonin

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Effect of telmisartan on expression of protein kinase C-α in kidneys of diabetic mice

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Acta Pharmacologica Sinica 2007年第6期28卷 829-838页

作者： Li-jun YAO~(2.4),Jian-qing WANG~2.Hong ZHAO~3,Jian-she LIU~2.An-guo DENG~2.2.department of Nephrology,Union Hospital,tongji {2. college,huazhong university of science and technology wuhan 430030,China,~3 department of Trauma Surgery,tongji Hospital,tongji {2. college,huazhong university of science and technology,430030wuhan.China department of Nephrology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China department of Trauma Surgery Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:To investigate the effects of angiotensin receptor blocker (ARB) telmisartanon the expression and distribution of protein kinase C (PKC)-α in the kidneys ofdiabetic ***:Diabetic mice were induced with streptozotocin and agroup of them were randomly selected for treatment with *** 6weeks,the expression and localization of PKC-α in the renal cortex,and the outerand inner medulla were assessed by immunohistochemistry and semiquantitativeWestern *** addition,expressions of PKC-α,transforming growth factor-β1 (TGF-β1),and vascular endothelial growth factor (VEGF) in glomeruli weremeasured by semiquantitative ***:Diabetic and nor-mal mice showed similar distributions of PKC-α in the *** expression ofPKC-α was found in glomeruli,epithelial cells of proximal tubules,and medullary-collecting duct,while not in the medullary and cortical thick ascending limb,andwas different in the epithelial cells of proximal tubules of diabetic nephropathy(DN) mice,PKC-α was mostly translocated from the basement membrane to theapical membrane,whereas it was largely translocated from the apical membrane tothe basement membrane in epithelial cells of the inner medullary-collecting *** blotting detected increased expression of PKC-α in the renal cortex andouter medulla,but not in the inner medulla of DN *** expressions ofPKC-α,TGF-β1,and VEGF were shown in the glomeruli of DN mice,where PKC-αexhibited a correlation to VEGF,but no correlation to TGF-β*** telmisartanattenuated alterations of PKC-α as mentioned earlier in the DN ***:Our findings suggest that PKC-α may play a role in the pathogenesis of DN,andthat the nephroprotective effects of ARB telmisartan may be partly associatedwith its influence on PKC-α.

关键词： diabetic nephropathy protein kinases C-α telmisartan mouse kidney

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Sonic hedgehog protein promotes bone marrow-derived endothelial pro-genitor cell proliferation,migration and VEGF production via PI 3-kinase/Akt signaling pathways

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Acta Pharmacologica Sinica 2006年第6期27卷 685-693页

作者： Jin-rong FU~2.Wen-li LIU~(2.4)Jian-feng ZHOU~2.Han-ying SUN~2.Hui-zhen XU~2.Li LUO~2.Heng ZHANG~2.Yu-feng ZHOU~3 2.department of Hematology.tongji Hospital,tongji medical college,huazhong university of science and technology,wuhan 430030,China:3 department of Pediatrics,tongji Hospital,tongji medical college,huazhong university of science and technology,wuhan 430030,China department of Hematology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China department of Pediatrics Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:To investigate the effects of Sonic hedgehog(shh)protein on bone marrow-derived endothelial progenitor cells(BM-EPC)proliferation,migration and vascu-lar endothelial growth factor(VEGF)production,and the potential signaling path-ways involved in these ***:Bone marrow-derived Flk-1~+ cells wereenriched using the MACS system from adult Kunming mice and then BM-EPCwas cultured in gelatin-coated culture *** effects of shh N-terminal pep-tide on BM-EPC proliferation were evaluated using the MTT colorimetric *** migration was assayed using a modified Boyden chamber *** of VEGF was determined by ELISA and immunofluorescence *** potential involvement of PKC and PI3K signaling pathways was exploredusing selective inhibitor or Western ***:The proliferation,migrationand VEGF production in BM-EPC could be promoted by endogenous shh N-terminal peptide at concentrations of 0.1μg/mL to 10 μg/mL,and could be inhib-ited by anti-shh ***-mediated proliferation and migration in BM-EPCcould be partly attenuated by ***-PI3-kinase expression in newlyseparated BM-EPC was low,and it increased significantly when exogenous shhN-terminal peptide was added,but could be attenuated by anti-human/mouse shhN-terminal peptide ***,the inhibitor of the PI3-kinase,but notthe inhibitor of the PKC,significantly inhibited the shh-mediated proliferation,migration and VEGF ***:Shh protein can stimulate bonemarrow-derived BM-EPC proliferation,migration and VEGF production,whichmay promote neovascularization to ischemic *** results also suggeststhat the PI3-kinase/Akt signaling pathways are involved in the angiogenic effectsof shh.

关键词： mouse Sonic hedgehog protein endothelial cells stem cells protein kinase C 1-phosphatidylinositol 3-kinase vascular endothelial growth factor A cell proliferation emigration immigration

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