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Increased Turnover (increased + turnover)
Selected AbstractsIncreased turnover of Na-K ATPase molecules in rat brain after rapid eye movement sleep deprivationJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2003Sudipta Majumdar Abstract It has been shown that rapid eye movement (REM) sleep deprivation increases Na-K ATPase activity. Based on kinetic study, it was proposed that increased activity was due to enhanced turnover of enzyme molecules. To test this, anti-,1 Na-K ATPase monoclonal antibody (mAb 9A7) was used to label Na-K ATPase molecules. These labeled enzymes were quantified on neuronal membrane by two methods: histochemically on neurons in tissue sections from different brain areas, and by Western blot analysis in control and REM sleep-deprived rat brains. The specific enzyme activity was also estimated and found to be increased, as in previous studies. The results confirmed our hypothesis that after REM sleep deprivation, increased Na-K ATPase activity was at least partly due to increased turnover of Na-K ATPase molecules in the rat brain. © 2003 Wiley-Liss, Inc. [source] Calpain-dependent proteolysis of NF2 protein: Involvement in schwannomas and meningiomasNEUROPATHOLOGY, Issue 3 2000Yoriyoshi Kimura The neurofibromatosis type 2 (NF2) protein, known as merlin or schwannomin, is a tumor suppressor, and the NF2 gene has been found to be mutated in the majority of schwannomas and meningiomas, including both sporadically occurring and familial NF2 cases. Although the development of these tumors depends on the loss of merlin, the presence of tumors lacking detectable NF2 mutations suggests different mechanisms for inactivating merlin. Recent studies have demonstrated cleavage of merlin by calpain, a calcium-dependent neutral cysteine protease, and marked activation of the calpain system resulting in the degradation of merlin in these tumors. Increased turnover of merlin by calpain in some schwannomas and meningiomas exemplifies tumorigenesis linked to the calpain-mediated proteolytic pathway. [source] Interactive effects of elevated CO2, N deposition and climate change on extracellular enzyme activity and soil density fractionation in a California annual grasslandGLOBAL CHANGE BIOLOGY, Issue 10 2005Hugh A. L. Henry Abstract Elevated CO2, N deposition and climate change can alter ecosystem-level nutrient cycling both directly and indirectly. We explored the interactive effects of these environmental changes on extracellular enzyme activity and organic matter fractionation in soils of a California annual grassland. The activities of hydrolases (polysaccharide-degrading enzymes and phosphatase) increased significantly in response to nitrate addition, which coincided with an increase in soluble C concentrations under ambient CO2. Water addition and elevated CO2 had negative but nonadditive effects on the activities of these enzymes. In contrast, water addition resulted in an increase in the activities of lignin-degrading enzymes (phenol oxidase and peroxidase), and a decrease in the free light fraction (FLF) of soil organic matter. Independent of treatment effects, lignin content in the FLF was negatively correlated with the quantity of FLF across all samples. Lignin concentrations were lower in the aggregate-occluded light fraction (OLF) than the FLF, and there was no correlation between percent lignin and OLF quantity, which was consistent with the protection of soil organic matter in aggregates. Elevated CO2 decreased the quantity of OLF and increased the OLF lignin concentration, however, which is consistent with increased degradation resulting from increased turnover of soil aggregates. Overall, these results suggest that the effects of N addition on hydrolase activity are offset by the interactive effects of water addition and elevated CO2, whereas water and elevated CO2 may cause an increase in the breakdown of soil organic matter as a result of their effects on lignin-degrading enzymes and soil aggregation, respectively. [source] Remodeling and Vascular Spaces in BoneJOURNAL OF BONE AND MINERAL RESEARCH, Issue 1 2007Erik Fink Eriksen Abstract In recent years, we have come to appreciate that the close association between bone and vasculature plays a pivotal role in the regulation of bone remodeling and fracture repair. In 2001, Hauge et al. characterized a specialized vascular structure, the bone remodeling compartment (BRC), and showed that the outer lining of this compartment was made up of flattened cells, displaying all the characteristics of lining cells in bone. A decrease in bone turnover leads to a decrease in surfaces covered with remodeling compartments, whereas increased turnover causes an increase. Immunoreactivity for all major osteotropic growth factors and cytokines including osteoprotegerin (OPG) and RANKL has been shown in the cells lining the BRC, which makes the BRC the structure of choice for coupling between resorption and formation. The secretion of these factors inside a confined space separated from the bone marrow would facilitate local regulation of the remodeling process without interference from growth factors secreted by blood cells in the marrow space. The BRC creates an environment where cells inside the structure are exposed to denuded bone, which may enable direct cellular interactions with integrins and other matrix factors known to regulate osteoclast/osteoblast activity. However, the denuded bone surface inside the BRC also constitutes an ideal environment for the seeding of bone metastases, known to have high affinity for bone matrix. Reduction in BRC space brought about by antiresorptive therapies such as bisphosphonates reduce the number of skeletal events in advanced cancer, whereas an increase in BRC space induced by remodeling activators like PTH may increase the bone metastatic burden. The BRC has only been characterized in detail in trabecular bone; there is, however, evidence that a similar structure may exist in cortical bone, but further characterization is needed. [source] Growth Hormone Increases Bone Mineral Content in Postmenopausal Osteoporosis: A Randomized Placebo-Controlled TrialJOURNAL OF BONE AND MINERAL RESEARCH, Issue 3 2003Kerstin Landin-Wilhelmsen Abstract Eighty osteoporotic, postmenopausal women, 50,70 years of age, with ongoing estrogen therapy (HRT), were randomized to recombinant human growth hormone (GH), 1.0 U or 2.5 U/day, subcutaneous, versus placebo. This study was double-blinded and lasted for 18 months. The placebo group then stopped the injections, but both GH groups continued for a total of 3 years with GH and followed for 5 years. Calcium (750 mg) and vitamin D (400 U) were given to all patients. Bone mineral density and bone mineral content were measured with DXA. At 18 months, when the double-blind phase was terminated, total body bone mineral content was highest in the GH 2.5 U group (p = 0.04 vs. placebo). At 3 years, when GH was discontinued, total body and femoral neck bone mineral content had increased in both GH-treated groups (NS between groups). At 4-year follow-up, total body and lumbar spine bone mineral content increased 5% and 14%, respectively, for GH 2.5 U (p = 0.01 and p = 0.0006 vs. placebo). Femoral neck bone mineral density increased 5% and bone mineral content 13% for GH 2.5 U (p = 0.01 vs. GH 1.0 U). At 5-year follow-up, no differences in bone mineral density or bone mineral content were seen between groups. Bone markers showed increased turnover. Three fractures occurred in the GH 1.0 U group. No subjects dropped out. Side effects were rare. In conclusion, bone mineral content increased to 14% with GH treatment on top of HRT and calcium/vitamin D in postmenopausal women with osteoporosis. There seems to be a delayed, extended, and dose-dependent effect of GH on bone. Thus, GH could be used as an anabolic agent in osteoporosis. [source] Flk prevents premature secretion of the anti-, factor FlgM into the periplasmMOLECULAR MICROBIOLOGY, Issue 3 2006Phillip Aldridge Summary The flk locus of Salmonella typhimurium was identified as a regulator of flagellar gene expression in strains defective in P- and l -ring formation. Flk acts as a regulator of flagellar gene expression by modulating the protein levels of the anti-,28 factor FlgM. Evidence is presented which suggests that Flk is a cytoplasmic-facing protein anchored to the inner membrane by a single, C-terminal transmembrane-spanning domain (TMS). The specific amino acid sequence of the TMS is not essential for Flk activity, but membrane anchoring is essential. Membrane fractionation and visualization of protein fusions of green fluorescent protein derivatives to Flk suggested that the Flk protein is present in the membrane as punctate spots in number that are much greater than the number of flagellar basal structures. The turnover of the anti-,28 factor FlgM was increased in flk mutant strains. Using FlgM,,-lactamase fusions we show the increased turnover of FlgM in flk null mutations is due to FlgM secretion into the periplasm where it is degraded. Our data suggest that Flk inhibits FlgM secretion by acting as a braking system for the flagellar-associated type III secretion system. A model is presented to explain a role for Flk in flagellar assembly and gene regulatory processes. [source] | |||||||||||||