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Farkas L Farkas D Warburton D Gauldie J Shi W Stampfli MR Voelkel NF Kolb M 《American journal of physiology. Lung cellular and molecular physiology》2011,301(4):L391-L401
The concept of genetic susceptibility factors predisposing cigarette smokers to develop emphysema stems from the clinical observation that only a fraction of smokers develop clinically significant chronic obstructive pulmonary disease. We investigated whether Smad3 knockout mice, which develop spontaneous air space enlargement after birth because of a defect in transforming growth factor-β (TGF-β) signaling, develop enhanced alveolar cell apoptosis and air space enlargement following cigarette smoke exposure. We investigated Smad3(-/-) and Smad3(+/+) mice at different adult ages and determined air space enlargement, alveolar cell proliferation, and apoptosis. Furthermore, laser-capture microdissection and real-time PCR were used to measure compartment-specific gene expression. We then compared the effects of cigarette smoke exposure on Smad3(-/-) and littermate controls. Smad3 knockout resulted in the development of air space enlargement in the adult mouse and was associated with decreased alveolar VEGF levels and activity and increased alveolar cell apoptosis. Cigarette smoke exposure aggravated air space enlargement and alveolar cell apoptosis. We also found increased Smad2 protein expression and phosphorylation, which was enhanced following cigarette smoke exposure, in Smad3-knockout animals. Double immunofluorescence analysis revealed that endothelial apoptosis started before epithelial apoptosis. Our data indicate that balanced TGF-β signaling is not only important for regulation of extracellular matrix turnover, but also for alveolar cell homeostasis. Impaired signaling via the Smad3 pathway results in alveolar cell apoptosis and alveolar destruction, likely via increased Smad2 and reduced VEGF expression and might represent a predisposition for accelerated development of emphysema due to cigarette smoke exposure. 相似文献
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Severino A Lucena Leile S Lima Luís SA Cordeiro Jr Celso Sant’Anna Reginaldo Constantino Patricia Azambuja Wanderley de Souza Eloi S Garcia Fernando A Genta 《Biotechnology for biofuels》2011,4(1):1-9
Background
Short rotation coppice willow is a potential lignocellulosic feedstock in the United Kingdom and elsewhere; however, research on optimising willow specifically for bioethanol production has started developing only recently. We have used the feedstock Salix viminalis × Salix schwerinii cultivar 'Olof' in a three-month pot experiment with the aim of modifying cell wall composition and structure within the stem to the benefit of bioethanol production. Trees were treated for 26 or 43 days with tension wood induction and/or with an application of the cellulose synthesis inhibitor 2,6-dichlorobenzonitrile that is specific to secondary cell walls. Reaction wood (tension and opposite wood) was isolated from material that had received the 43-day tension wood induction treatment.Results
Glucan content, lignin content and enzymatically released glucose were assayed. All measured parameters were altered without loss of total stem biomass yield, indicating that enzymatic saccharification yield can be enhanced by both alterations to cell wall structure and alterations to absolute contents of either glucan or lignin.Conclusions
Final glucose yields can be improved by the induction of tension wood without a detrimental impact on biomass yield. The increase in glucan accessibility to cell wall degrading enzymes could help contribute to reducing the energy and environmental impacts of the lignocellulosic bioethanol production process. 相似文献14.
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目的研究长爪沙鼠发情周期,揭示发情规律,优化判定方法。方法连续18 d采集50只长爪沙鼠阴道上皮脱落细胞涂片,采用角化细胞计数法研究长爪沙鼠发情周期规律。比较瑞氏染色、HE染色和直接镜检判定发情周期4个时相的优缺点。结果长爪沙鼠的发情周期有稳定型、不稳定型、假孕三种类型。其中稳定型占68.6%,发情周期为(106.3±35.0)h,可分为4个时相。4个时相角化细胞的比例分别为发情前期(13.5±7.8)%、发情期(86.7±9.9)%、发情后期(27.9±12.8)%和发情间期(3.3±2.8)%。结论角化细胞计数能准确地判定长爪沙鼠的发情周期及各个时相。直接镜检法能快速反映阴道脱落细胞的形态。 相似文献
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In this study we examined the action of arachidonic acid in the isolated rat lung perfused with a cell- and protein-free physiological salt solution. When pulmonary vascular tone was elevated by hypoxia, bolus injection of a large dose of arachidonic acid (75 micrograms) caused transient vasoconstriction followed by vasodilation. When arachidonic acid (100 micrograms) was injected during normoxia and at base-line perfusion pressure (low vascular tone) or when vascular tone was elevated by KCl, arachidonic acid (50 micrograms) caused only vasoconstriction. Doses less than 7.5 micrograms caused vasodilation only when injected during hypoxic vasoconstriction and subsequent blunting of either angiotensin II- or hypoxia-induced pulmonary vasoconstriction. The higher doses of arachidonic acid (7.5 and 75 micrograms), but not the lower doses (7.5-750 ng), caused increases in effluent 6-ketoprostaglandin F1 alpha, thromboxane B2, and prostaglandin E2 and F2 alpha. 6-Ketoprostaglandin F1 alpha was the major cyclooxygenase product. Meclofenamate (10(-5) M) blocked the increased metabolite synthesis over the entire dose range of arachidonic acid tested (7.5 ng-75 micrograms). Because vasodilation immediately after arachidonic acid was cyclooxygenase-independent, we investigated whether this effect was due to the unsaturated fatty acid properties of arachidonic acid and compared its action with that of oleic acid and docosahexaenoic acid. Because neither compound mimicked the vasodilation observed with arachidonic acid, we concluded that the cyclooxygenase-independent action of arachidonic acid could not be explained by unsaturated fatty acid properties per se. Because 1-aminobenzotriazole, a cytochrome P-450 inhibitor, partially inhibited the immediate arachidonic acid-induced pulmonary vasodilation, we concluded that cytochrome P-450-dependent metabolites can account for some of the cyclooxygenase-independent vasodilation of arachidonic acid. 相似文献
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Endothelial progenitor cells (EPC) participate in revascularization and angiogenesis. EPC can be cultured in vitro from mononuclear cells of peripheral blood, umbilical cord blood or bone marrow; they also can be transdifferentiated from mesenchymal stem cells (MSC). We isolated EPCs from Wharton's jelly (WJ) using two methods. The first method was by obtaining MSC from WJ and characterizing them by flow cytometry and their adipogenic and osteogenic differentiation, then applying endothelial growth differentiating media. The second method was by direct culture of cells derived from WJ into endothelial differentiating media. EPCs were characterized by morphology, Dil-LDL uptake/UEA-1 immunostaining and testing the expression of endothelial markers by flow cytometry and RT-PCR. We found that MSC derived from WJ differentiated into endothelial-like cells using simple culture conditions with endothelium induction agents in the medium. 相似文献
20.
Haynes J.; Chang S. W.; Morris K. G.; Voelkel N. F. 《Journal of applied physiology》1988,65(5):1921-1928
Platelet-activating factor (PAF) administered to the pulmonary circulation in low dose (nanogram) has vasodilatory properties. Therefore, we investigated whether endogenous PAF plays a role in the control of tone in the pulmonary circulation. The PAF receptor antagonists, SRI 63-441 (2.6 X 10(-4) M) and L659,989 (1 X 10(-5) M), were the major investigative tools. In isolated perfused rat lungs, both agents caused a persistent increase in base-line perfusion pressure (Ppa), potentiated angiotensin II (ANG II) vasoconstriction, and potentiated hypoxic vasoconstriction (HPV). This potentiation of ANG II and HPV was found to be independent of circulating blood elements. Vasodilation in the presence of PAF blockade was also impaired. The combination of cyclooxygenase inhibition and PAF receptor blockade had an additive effect on ANG II vasoconstriction but did not cause more potentiation of HPV than achieved with PAF antagonism alone. In vivo, SRI 63-441 (10 mg/kg) caused only a transient increase in base-line Ppa without altering ANG II and hypoxic vasoconstriction. These findings support a vasodilatory role for endogenous PAF in the pulmonary circulation. 相似文献