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1.
Pi-Kwang Tsung S.W. Kegeles E.L. Becker 《Biochimica et Biophysica Acta (BBA)/General Subjects》1977,499(2):212-227
The intracellular localization and properties of the chymotrypsin-like esterase activity ( esterase acitivity) of the rabbit peritoneal neutrophil has been studied and shown to differ from that of the human neutrophil.The major portion of the esterase activity in the rabbit neutrophil is in the 100 000 × g supernatant fraction with distinctly less activity in the lysosomal fraction. The 100 000 × g supernatant contained the highest relative specific activity of any of the subcellular fractions. Rabbit peripheral blood neutrophils gave the same distribution.The 100 000 × g supernatant esterase is 95% esterase 1 and 5% esterase 3, whereas, the lysosomal esterase is 78% esterase 1, 10–16% esterase 2 and 9% esterase 3 as defined by their ability to be inhibited by p-nitrophenyllethyl-5-chloropentylphosphonate. The 100 000 × g supernatant The 100 000 × g supernatant and lysosomal esterase activities further differ in their susceptibility to other inhibitors, their pH optima, ease of elution from DEAE and isoelectric points. Two molecular weight species of 174 000 and 70 000 were found in the 100 000 × g supernatant fraction and extracts of the lysosomal fraction but usually in differing proportions.In confirmation of others, essentially all of the chymotrypsin-like esterase activity ( esterase activity) of the human neutrophil is in the lysosomal fraction, unlike the rabbit cell. The human neutrophil esterase was less susceptible to inhibition by p-nitrophenylethyl-5-chloropentylphosphonate and diisopropylphosphofluoridate but more susceptible to soybean trypsin inhibitor than rabbit esterase activity. The pH optimum of the human neutrophil esterase differed from either the rabbit lysosomal or 100 000 × g supernatant esterase, as did the isoelectric point and molecular weights. 相似文献
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Tai‐An Chiang Yu‐Lin Yang Ya‐Ying Yang Min‐Hsiu Hu Pei‐Fen Wu Shu‐Fen Liu Ruay‐Ming Huang Tung‐Nan Liao Chien‐Ya Hung Tsung‐Jen Hung Tao‐Chen Lee 《Journal of cellular biochemistry》2010,109(4):663-671
Hyperosmolarity plays an essential role in the pathogenesis of diabetic tubular fibrosis. However, the mechanism of the involvement of hyperosmolarity remains unclear. In this study, mannitol was used to evaluate the effects of hyperosmolarity on a renal distal tubule cell line (MDCK). We investigated transforming growth factor‐β receptors and their downstream fibrogenic signal proteins. We show that hyperosmolarity significantly enhances the susceptibility to exogenous transforming growth factor (TGF)‐β1, as mannitol (27.5 mM) significantly enhanced the TGF‐β1‐induced increase in fibronectin levels compared with control experiments (5.5 mM). Specifically, hyperosmolarity induced tyrosine phosphorylation on TGF‐β RII at 336 residues in a time (0–24 h) and dose (5.5–38.5 mM) dependent manner. In addition, hyperosmolarity increased the level of TGF‐β RI in a dose‐ and time‐course dependent manner. These observations may be closely related to decreased catabolism of TGF‐β RI. Hyperosmolarity significantly downregulated the expression of an inhibitory Smad (Smad7), decreased the level of Smurf 1, and reduced ubiquitination of TGF‐β RI. In addition, through the use of cycloheximide and the proteasome inhibitor MG132, we showed that hyperosmolarity significantly increased the half‐life and inhibited the protein level of TGF‐β RI by polyubiquitination and proteasomal degradation. Taken together, our data suggest that hyperosmolarity enhances cellular susceptibility to renal tubular fibrosis by activating the Smad7 pathway and increasing the stability of type I TGF‐β receptors by retarding proteasomal degradation of TGF‐β RI. This study clarifies the mechanism underlying hyperosmotic‐induced renal fibrosis in renal distal tubule cells. J. Cell. Biochem. 109: 663–671, 2010. © 2010 Wiley‐Liss, Inc. 相似文献
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Intellectual disability-associated dBRWD3 regulates gene expression through inhibition of HIRA/YEM-mediated chromatin deposition of histone H3.3 下载免费PDF全文
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Sitagliptin attenuates sympathetic innervation via modulating reactive oxygen species and interstitial adenosine in infarcted rat hearts 下载免费PDF全文
Tsung‐Ming Lee Wei‐Ting Chen Chen‐Chia Yang Shinn‐Zong Lin Nen‐Chung Chang 《Journal of cellular and molecular medicine》2015,19(2):418-429
We investigated whether sitagliptin, a dipeptidyl peptidase‐4 (DPP‐4) inhibitor, attenuates arrhythmias through inhibiting nerve growth factor (NGF) expression in post‐infarcted normoglycemic rats, focusing on adenosine and reactive oxygen species production. DPP‐4 bound adenosine deaminase has been shown to catalyse extracellular adenosine to inosine. DPP‐4 inhibitors increased adenosine levels by inhibiting the complex formation. Normoglycemic male Wistar rats were subjected to coronary ligation and then randomized to either saline or sitagliptin in in vivo and ex vivo studies. Post‐infarction was associated with increased oxidative stress, as measured by myocardial superoxide, nitrotyrosine and dihydroethidium fluorescent staining. Measurement of myocardial norepinephrine levels revealed a significant elevation in vehicle‐treated infarcted rats compared with sham. Compared with vehicle, infarcted rats treated with sitagliptin significantly increased interstitial adenosine levels and attenuated oxidative stress. Sympathetic hyperinnervation was blunted after administering sitagliptin, as assessed by immunofluorescent analysis and western blotting and real‐time quantitative RT‐PCR of NGF. Arrhythmic scores in the sitagliptin‐treated infarcted rats were significantly lower than those in vehicle. Ex vivo studies showed a similar effect of erythro‐9‐(2‐hydroxy‐3‐nonyl) adenine (an adenosine deaminase inhibitor) to sitagliptin on attenuated levels of superoxide and NGF. Furthermore, the beneficial effects of sitagliptin on superoxide anion production and NGF levels can be reversed by 8‐cyclopentyl‐1,3‐dipropulxanthine (adenosine A1 receptor antagonist) and exogenous hypoxanthine. Sitagliptin protects ventricular arrhythmias by attenuating sympathetic innervation via adenosine A1 receptor and xanthine oxidase‐dependent pathways, which converge through the attenuated formation of superoxide in the non‐diabetic infarcted rats. 相似文献
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NFIL3 Suppresses Hypoxia‐induced Apoptotic Cell Death by Targeting the Insulin‐like Growth Factor 2 Receptor 下载免费PDF全文
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ZAKβ antagonizes and ameliorates the cardiac hypertrophic and apoptotic effects induced by ZAKα 下载免费PDF全文
Chien‐Yao Fu Wei‐Wen Kuo Tsung‐Jung Ho Su‐Ying Wen Ling‐Chun Lin Yan‐Shen Tseng Hui‐Chuan Hung Vijaya Padma Viswanadha Chih‐Yang Huang 《Cell biochemistry and function》2016,34(8):606-612
ZAK (sterile alpha motif and leucine zipper containing kinase AZK), a serine/threonine kinase with multiple biochemical functions, has been associated with various cell processes, including cell proliferation, cell differentiation, and cardiac hypertrophy. In our previous reports, we found that the activation of ZAKα signaling was critical for cardiac hypertrophy. In this study, we show that the expression of ZAKα activated apoptosis through both a FAS‐dependent pathway and a mitochondria‐dependent pathway by subsequently inducing caspase‐3. ZAKβ, an isoform of ZAKα, is dramatically expressed during cardiac hypertrophy and apoptosis. The interaction between ZAKα and ZAKβ was demonstrated here using immunoprecipitation. The results show that ZAKβ has the ability to diminish the expression level of ZAKα. These findings reveal an inherent regulatory role of ZAKβ to antagonize ZAKα and to subsequently downregulate the cardiac hypertrophy and apoptosis induced by ZAKα. 相似文献
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In this paper, near‐infrared spectroscopy (NIRS) and jumping optical tweezers were used to measure the tissue oxygenation and the elasticity of erythrocytes, respectively. The correlation between tissue oxygenation induced by arterial occlusion test (AOT) and the mechanical properties of individual erythrocytes from a blood sample obtained after AOT was studied. The experimental results show a linear correlation between the oxygenation signal caused by AOT and the elasticity of erythrocytes. (© 2011 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim) 相似文献
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Hui‐Min Wang Yan‐Ping Shih Su‐Ming Hu Wen‐Tsung Lo Hui‐Min Lin Shih‐Shiu Ding Hsin‐Chi Liao Po‐Huang Liang 《Biotechnology progress》2009,25(6):1582-1586
To quickly find an optimal expression system for recombinant protein production, a set of vectors with the same restriction sites were constructed for parallel cloning of a target gene and recombinant protein production in prokaryotic and eukaryotic expression systems, simultaneously. These vectors include nucleotide sequences encoding protein tags and protease recognition sites for tag removal, followed by the cloning sites 5′‐EcoRI/3′‐XhoI identical in these vectors for ligating with the sticky‐end PCR product of a target gene. Our vectors allow parallel gene cloning and protein production in multiple expression systems with minimal cloning effort. © 2009 American Institute of Chemical Engineers Biotechnol. Prog., 2009 相似文献