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1.
Lipopolysaccharide (LPS) and endothelin-1 (ET-1) are critical pathogenic factors in sepsis-induced pulmonary hypertension; however it is unknown whether they have a coordinated action in the pathogenesis of this disease. Here we found that although LPS did not change the contractility of rat pulmonary arterial smooth muscle cells (PASMCs) in response to ET-1, it significantly promoted ET-1-induced PASMC proliferation. Measurement of ET-1-evoked Ca2+ transients in PASMCs showed that LPS dramatically enhanced Ca2+ influx mediated by transient receptor potential canonical (TRPC) channels. LPS did not directly activate TRPC channels, instead it selectively upregulated the expression of TRPC3 and TRPC4 in pulmonary arteries. Small interfering RNA (siRNA) and chemical blockers against TRPC channels abolished LPS-induced PASMC proliferation. LPS-induced cell proliferation and TRPC expression was mediated by the Ca2+-dependent calcineurin/NFAT signaling pathway. We suggest that blocking TRPC channels could be an effective strategy in controlling pulmonary arterial remodeling after endotoxin exposure.  相似文献   
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目的探讨NHE-1反义RNA对大鼠肺动脉平滑肌细胞(PASMC)凋亡的影响.方法构建NHE-1反义RNA逆转录病毒载体,转染体外培养的大鼠PASMC,应用半定量RT-PCR法(sqRT-PCR)测定细胞内NHE-1 mRNA的表达、BCECF法测定pHi、流式细胞仪测细胞周期、电镜及原位细胞凋亡检测(TUNEL法)观察细胞凋亡情况.结果转染NHE-1反义RNA逆转录病毒载体的细胞,NHE-1 mRNA表达量及pHi较空载体转染细胞及未转染细胞显著降低,细胞凋亡率显著增加,电镜示细胞凋亡,凋亡小体形成.结论抑制NHE-1可通过引起细胞内酸化,诱导肺动脉平滑肌细胞凋亡.  相似文献   
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Cytochrome P450 (CYP) epoxygenases metabolize arachidonic acid to biologically active eicosanoids. The primary epoxidation products are four regioisomers of cis-epoxyeicosatrienoic acid (EET): 5,6-, 8,9-, 11,12-, and 14,15-EET. CYP2J2, CYP2C8, and CYP2C9 are the predominant epoxygenase isoforms involved in EET formation. CYP2J and CYP2C gene families in humans are abundantly expressed in the endothelium, myocardium, and kidney. The cardiovascular effects of CYP epoxygenases and EETs range from vasodilation, anti-hypertension, pro-angiogenesis, anti-atherosclerosis, and anti-inflammation to anti-injury caused by ischemia-reperfusion. Using transgenic animals for in vivo analyses of CYP epoxygenases revealed comprehensive and marked cardiovascular protective effects. In contrast, CYP epoxygenases and their metabolites, EETs, are upregulated in human tumors and promote tumor progression and metastasis. These biological effects result from the anti-apoptosis, pro-mitogenesis, and anti-migration roles of CYP epoxygenases and EETs at the cellular level. Importantly, soluble epoxide hydrolase (sEH) inhibitors are anti-hypertensive and anti-inflammatory and, therefore, protect the heart from damage, whereas the terfenadine-related, specific inhibitors of CYP2J2 exhibit strong anti-tumor activity in vitro and in vivo. Thus, CYP2J2 and arachidonic acid-derived metabolites likely play important roles in regulating cardiovascular functions and malignancy under physiological and/or pathological conditions. Moreover, although challenges remain to improving the drug-like properties of sEH inhibitors and identifying efficient ways to deliver sEH inhibitors, sEH will likely become an important therapeutic target for cardiovascular diseases. In addition, CYP2J2 may be a therapeutic target for treating human cancers and leukemia.  相似文献   
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Objective:To explore the effects of Iptakalim on intracellular free calcium concentration and on the proliferation of cultured rabbit pulmonary arterial smooth muscle cells induced by endothelin-1(ET-1) in vitro. Methods:A cell culture model, [3H]-thymidine([3H]-TdR) incorporation test and confocal microscope were used to observe proliferation and intracellular free calcium concentration([Ca2 ]i) of rabbit PASMC induced by ET-1 in vitro. Results:The value of [3H]-TdR incorporation in ET-1 group was increased 1.468 times higher than that in control group. Iptakalim at the concentration of 10-7mol/L,10-6 mol/L,10-5 mol/L lowered [3H]-TdR incorporation by (19.8±4.6)%, (41.2±9.5)%, (54.7±10.1)%, respectively, compared with the value of the cells treated with ET-1(P<0.01); The intracellular fluorescence intensity of PASMC in ET-1 group was increased from 73.70±10.12 to 143.84±28.23, significantly higher than that in control group(P<0.01); whereas with Iptakalim,the fluorescence intensity(FI) was only increased from 74.30±10.20 to 86.03±9.82, significantly lower than that in ET-1 group(P<0.01). Conclusion:Iptakalim inhibited proliferation of PASMC and decreased intracellular free calcium concentration of cultured rabbit PASMC induced by ET-1.  相似文献   
7.
徐粟  丁志山  楼兰花  高承贤  宋红 《中草药》2007,38(9):1379-1381
目的研究血府逐瘀汤(XFZYD)对缺氧条件下肺动脉平滑肌细胞(PASMC)增殖及培养液中NO水平的影响。方法通过建立新生牛PASMC的原代和传代培养及缺氧细胞增殖模型,采用MTT法、光镜计数观察缺氧对PASMC增殖的影响;Griss试剂法测定PASMC培养液中NO的量。结果血府逐瘀汤能显著抑制缺氧条件下PASMC增殖,高、中、低剂量组与对照组比较差异显著(P<0.05);血府逐瘀汤能显著提高缺氧条件下PASMC培养液中NO的量(P<0.05)。结论血府逐瘀汤能抑制缺氧条件下PASMC增殖;提高NO水平可能是血府逐瘀汤抑制缺氧条件下PASMC增殖作用的途径之一。  相似文献   
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运用流式细胞仪及细胞原位杂交方法测定低氧对培养的新生牛肺动脉平滑肌细胞(PASMC)生长的影响,并探讨血小板源生长因子(PDGF)在其中的作用,结果表明:培养的PASMC的低氧12h时,由G0/G1期进入S斯的细胞数明显增多,为对照组的157.7%(P〈0.05);PDGF可进一步促进低氧状态下PASMC的增殖,S期细胞为对照组的242.3%(P〈0.01),原位杂交结果显示:低氧(12h)条件下  相似文献   
10.
Green tea polyphenolic catechins have been shown to prevent various types of diseases such as pulmonary hypertension (PAH), cancer and cardiac and neurological disorders. Matrix metalloproteinases (MMPs) play an important role in the development of PAH. The present study demonstrated that among the four green tea catechins (EGCG, ECG, EC and EGC), EGCG and ECG inhibit pro-/active MMP-9 activities in pulmonary artery smooth muscle cell culture supernatant. Based on the above, we investigated the interactions of pro-/active MMP-9 with the green tea catechins by computational methods. In silico molecular docking analysis revealed a strong interaction between pro-/active MMP-9 and EGCG/ECG, and galloyl group appears to be responsible for this enhanced interaction. The molecular docking studies corroborate our experimental observation that EGCG and ECG are mainly active in preventing both the proMMP-9 and MMP-9 activities.  相似文献   
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