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排序方式: 共有157条查询结果,搜索用时 15 毫秒
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Seung Ho Jung Arpit Saxena Kamaljeet Kaur Emma Fletcher Venkatesh Ponemone James M. Nottingham Joseph A. Sheppe Maria Petroni Jennifer Greene Kelly Graves Manjeshwar Shrinath Baliga Raja Fayad 《Cytokine》2013,61(2):459-468
Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders of the gastrointestinal tract that affect more than 3 million people worldwide, but the pathological etiology is still unknown. The overall purpose of our investigations was to elucidate the possibility of pathological causes of IBD, and therefore, we determined the difference of inflammatory cytokine profiles in adipose tissue macrophages (ATMs) and T lymphocytes (ATTs) obtained near active lesions of IBD; investigated whether the alteration in ATM activation induces genes involved in collagen formation; and evaluated the effects of fatty acid oxidation inhibitors on factors involved in inflammation and collagen production by ATMs in IBD. Adipose tissues (ATs) were collected near active lesions and also at the margin of resected segments of the bowel from IBD patients with ulcerative colitis (UC) and CD (n = 14/group). Normal appearing ATs from control subjects (n = 14) who had colon resection for adenocarcinoma were collected as far away from the cancer lesion as possible to rule out possible changes. Compared with inactive disease lesions, ATMs and ATTs from active lesions released more IL-6, IL-4 and IL-13. Treatments of cytokine IL-4 and/or IL-13 to ATMs reduced iNOS expression but increased Arg-I expression which were exacerbated when treated with T cell- and adipocyte-conditioned medium. However, fatty acid oxidation inhibitors prevented the effects of cytokines IL-4 and/or IL-13 on iNOS and Arg-I expressions. This study was the first to show the effect of IL-4 and IL-13 on collagen formation, through iNOS and Arg-I expressions, that was exacerbated in a condition that mimics in vivo condition of active lesions. Moreover, our study was the first to provide potential benefits of fatty acid oxidation inhibitors to ATMs on preventing collagen formation; thus, providing therapeutic implications for individuals with intestinal fibrosis and stricture lesions, although future study should be guaranteed to elucidate the underlying mechanisms. 相似文献
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Manoj Bhosale Anujith Kumar Mrinmoy Das Chetana Bhaskarla Vikas Agarwal Dipankar Nandi 《Microbiological research》2013,168(1):56-64
Peptidase N (PepN), the sole M1 family member in Escherichia coli, displays broad substrate specificity and modulates stress responses: it lowers resistance to sodium salicylate (NaSal)-induced stress but is required during nutritional downshift and high temperature (NDHT) stress. The expression of PepN does not significantly change during different growth phases in LB or NaSal-induced stress; however, PepN amounts are lower during NDHT stress. To gain mechanistic insights on the roles of catalytic activity of PepN in modulating these two stress responses, alanine mutants of PepN replacing E264 (GAMEN motif) and E298 (HEXXH motif) were generated. There are no major structural changes between purified wild type (WT) and mutant proteins, which are catalytically inactive. Importantly, growth profiles of ΔpepN upon expression of WT or mutant proteins demonstrated the importance of catalytic activity during NDHT but not NaSal-induced stress. Further fluorescamine reactivity studies demonstrated that the catalytic activity of PepN is required to generate higher intracellular amounts of free N-terminal amino acids; consequently, the lower growth of ΔpepN during NDHT stress increases with high amounts of casamino acids. Together, this study sheds insights on the expression and functional roles of the catalytic activity of PepN during adaptation to NDHT stress. 相似文献
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Shearwin-Whyatt L Baliga B Doumanis J Kumar S 《Biochemical and biophysical research communications》2001,282(5):1114-1119
Cellular defects which prevent apoptotic cell death can result in the generation of hyperproliferative disorders and can prevent the effective treatment of such diseases. The majority of cellular defects which result in apoptosis resistance lie upstream of caspase activation. We have described chimeric caspase molecules consisting of the prodomain of caspase-2 fused to the amino terminus of caspase-3, and which are tagged at the carboxyl terminus with green fluorescent protein (GFP) to allow direct visualisation of transfected cells. Here we show that these chimeric caspase molecules possess potent, rapid cell-killing activity in cell lines which display a range of defects resulting in apoptosis resistance. 相似文献
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BACKGROUND: Symptomatic striated muscle involvement in sarcoidosis is rare. Muscle biopsy is usually required for the diagnosis. Fine needle aspiration biopsy (FNAB) has been successfully used in diagnosing soft tissue lesions. To the best of our knowledge, FNAB of sarcoid myositis has not been reported. CASE: A 31-year-old, black female with a history of sarcoidosis presented with an enlarging, painful, left calf mass. Infected thrombi were suspected. FNAB showed numerous loosely arranged epithelioid histiocytes, multinucleated giant cells and skeletal muscle cells. The overall cytologic picture was that of granulomatous myositis. The cytologic features coupled with the patient's history and magnetic resonance imaging findings suggested sarcoid myositis. Subsequent muscle biopsy showing noncaseating granulomata and negative stains for organisms confirmed the diagnosis of nodular sarcoid myositis. CONCLUSION: Nodular sarcoid myositis can be suggested by FNAB cytology in a patient with a past history of sarcoidosis. 相似文献
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Vines CM Revankar CM Maestas DC LaRusch LL Cimino DF Kohout TA Lefkowitz RJ Prossnitz ER 《The Journal of biological chemistry》2003,278(43):41581-41584
Arrestins mediate phosphorylation-dependent desensitization, internalization, and initiation of signaling cascades for the majority of G protein-coupled receptors (GPCRs). Many GPCRs undergo agonist-mediated internalization through arrestin-dependent mechanisms, wherein arrestin serves as an adapter between the receptor and endocytic proteins. To understand the role of arrestins in N-formyl peptide receptor (FPR) trafficking, we stably expressed the FPR in a mouse embryonic fibroblast cell line (MEF) that lacked endogenous arrestin 2 and arrestin 3 (arrestin-deficient). We compared FPR internalization and recycling kinetics in these cells to congenic wild type MEF cell lines. Internalization of the FPR was not altered in the absence of arrestins. Since the FPR remains associated with arrestins following internalization, we investigated whether the rate of FPR recycling was altered in arrestin-deficient cells. While the FPR was able to recycle in the wild type cells, receptor recycling was largely absent in the arrestin double knockout cells. Reconstitution of the arrestin-deficient line with either arrestin 2 or arrestin 3 restored receptor recycling. Confocal fluorescence microscopy studies demonstrated that in arrestin-deficient cells the FPR may become trapped in the perinuclear recycling compartment. These observations indicate that, although the FPR can internalize in the absence of arrestins, recycling of internalized receptors to the cell surface is prevented. Our results suggest a novel role for arrestins in the post-endocytic trafficking of GPCRs. 相似文献
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Jagetia GC Baliga MS 《Birth defects research. Part B, Developmental and reproductive toxicology》2003,68(6):472-478
BACKGROUND: The teratogenic effect of hydroalcoholic extract of Alstonia scholaris (ASE) was studied in the pregnant Swiss albino mice administered with 0, 60, 120, 240, 360, and 480 mg/kg ASE on Day 11 of gestation. METHODS: Females were allowed to complete the term and parturiate. The litters were monitored regularly for mortality, growth retardation, congenital malformations, and appearance of physiological markers up to 7 weeks post‐parturition (p.p.). RESULTS: The administration of 60, 120, 180, and 240 mg/kg ASE to the pregnant mice on Day 11 did not induce mortality, congenital malformations, or alter the normal growth patterns. A further increase in the herbal extract dose up to 360 or 480 mg/kg resulted in a dose dependent increase in the mortality, growth retardation, and congenital malformations, characterized mainly by bent tails and syndactyly. The administration of higher doses (360 or 480 mg) of ASE also caused a significant delay in the morphological parameters such as fur development, eye opening, pinna detachment, and vaginal opening. The incisor eruption and testes decent were found to be delayed in litters born to the mothers treated with 240–480 mg/kg ASE. CONCLUSIONS: Our study indicates clearly that ASE treatment caused teratogenic effect only at doses above 240 mg/kg (>20% of LD50). Lower doses had no developmental toxicity. Birth Defects Res B 68:472–478, 2003. © 2003 Wiley‐Liss, Inc. 相似文献