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ODC Activity (odc + activity)
Selected AbstractsPolyamines and hair: a couple in search of perfectionEXPERIMENTAL DERMATOLOGY, Issue 9 2010Yuval Ramot Please cite this paper as: Polyamines and hair: a couple in search of perfection. Experimental Dermatology 2010; 19: 784,790. Abstract:, Polyamines (spermidine, putrescine and spermine) are multifunctional cationic amines that are indispensable for cellular proliferation; of key significance in the growth of rapidly regenerating tissues and tumors. Given that the hair follicle (HF) is one of the most highly proliferative organs in mammalian biology, it is not surprising that polyamines are crucial to HF growth. Indeed, growing (anagen) HFs show the highest activity of ornithine decarboxylase (ODC), the rate-limiting enzyme of polyamine biosynthesis, while inhibition of ODC, using eflornithine, results in a decreased rate of excessive facial hair growth in vivo and inhibits human scalp hair growth in organ culture. In sheep, manipulation of dietary intake of polyamines also results in altered wool growth. Polyamine-containing nutraceuticals have therefore been proposed as promoters of human hair growth. Recent progress in polyamine research, coupled with renewed interest in the role of polyamines in skin biology, encourages one to revisit their potential roles in HF biology and highlights the need for a systematic evaluation of their mechanisms of action and clinical applications in the treatment of hair disorders. The present viewpoint essay outlines the key frontiers in polyamine-related hair research and defines the major open questions. Moreover, it argues that a renaissance in polyamine research in hair biology, well beyond the inhibition of ODC activity in hirsutism therapy, is important for the development of novel therapeutic strategies for the manipulation of human hair growth. Such targets could include the manipulation of polyamine biosynthesis and the topical administration of selected polyamines, such as spermidine. [source] Astroglia growth retardation and increased microglia proliferation by lithium and ornithine decarboxylase inhibitor in rat cerebellar cultures: Cytotoxicity by combined lithium and polyamine inhibition,JOURNAL OF NEUROSCIENCE RESEARCH, Issue 3 2007Gad M. Gilad Abstract Lithium, the most prevalent treatment for manic-depressive illness, might have a neuroprotective effect after brain injury. In culture, lithium can exert neurotoxic effects associated with reduction in polyamine synthesis but neuroprotective effects as cultured neurons mature. Cumulative evidence suggests that lithium may exert some of its effects on neurons indirectly, by initially acting on glial cells. We used rat cerebellar cultures to ascertain the effects of lithium on ornithine decarboxylase (ODC) activity, the enzyme catalyzing the first step in polyamine synthesis, and to compare effects of lithium with those of the ODC inhibitor ,-difluoromethylornithine (DFMO) on neuron survival and glial growth. Switching cultures from high (25 mM) to low (5 mM) KCl concentrations served as the traumatic neuronal insult. The results indicate the following. 1) Whereas high depolarizing KCl concentration enhances neuron survival, it inhibits astroglial growth. 2) Lithium (LiCl; 1,5 mM) enhances neuronal survival but inhibits astroglial growth. 3) Lithium treatment leads to reduced ODC activity. 4) DFMO enhances neuron survival but inhibits astroglial growth. 5) Lithium and DFMO lead to transformation of astroglia from epithelioid (flat) to process-bearing morphology and to increased numbers of microglia. 6) Combined lithium plus DFMO treatment is cytolethal to both neurons and glia in culture. In conclusion, lithium treatment results in growth retardation and altered cell morphology of cultured astroglia and increased microglia proliferation, and these effects may be associated with inhibition of polyamine synthesis. This implies that direct effects on astrocytes and microglia may contribute to the effects of lithium on neurons. © 2006 Wiley-Liss, Inc. [source] APC-dependent regulation of ornithine decarboxylase in human colon tumor cellsMOLECULAR CARCINOGENESIS, Issue 1 2002Kimberly E. Fultz Abstract Mutation/deletion of the adenomatous polyposis coli (APC) tumor suppressor gene in germline cells of rodents and humans is associated with increased intestinal activity of ornithine decarboxylase (ODC), the first enzyme in polyamine synthesis, and intestinal neoplasia. To study the role of APC in signaling ODC expression, we used the human colon tumor cell line HT29 (wtAPC,/,), which has been stably transfected with a zinc-inducible wild-type APC gene. The addition of ZnCl2 to HT29-APC cells increased wild-type APC protein and Mad1 RNA and protein and decreased levels of c- myc and ODC RNA and protein, relative to these parameters in HT29 cells transfected with the same plasmid containing the ,-galactosidase gene in place of APC. Upon induction of APC expression, ODC promoter activity and RNA levels were suppressed. When the e-box domain in the 5, flanking region of the ODC gene was mutated, ODC promoter activity was unaffected by wild-type APC expression. Antisense, but not missense, c- myc oligonucleotides decreased ODC activity in HT29 cells expressing mutant APC. These results demonstrated that wild-type APC suppressed c-myc and activated Mad1 expression in HT29 colon-derived cells. These proteins, in turn, regulated the transcription of target genes, including ODC. The data presented indicate that ODC is a modifier of APC-dependent signaling in intestinal cells and tissues. © 2002 Wiley-Liss, Inc. [source] Ornithine decarboxylase activity of L929 cells after exposure to continuous wave or 50 Hz modulated radiofrequency radiation,a replication studyBIOELECTROMAGNETICS, Issue 7 2007A. Höytö Abstract A replication study with some extensions was made to confirm enhancement of ornithine decarboxylase (ODC) activity in murine L929 fibroblasts after radiofrequency (RF) field exposure reported in earlier studies. L929 cells purchased from two cell banks were exposed for 2, 8, or 24 h to continuous wave or DAMPS (burst modulated at 50 Hz, with 33% duty cycle) signals at specific absorption rate (SAR) levels of 2.5 or 6.0 W/kg. Exposures were carried out in Crawford and waveguide chambers, at frequencies 835 and 872 MHz, respectively. The results did not confirm findings of previous studies reporting increased ODC activity in RF-exposed cells. When Crawford cell exposure system was used, ODC activity was either not affected (in the case of 8 or 24 h exposures) or decreased after 2 h exposure at the highest SAR level (6 W/kg). The decrease was most pronounced when cooling with air flow was not used, and is most likely related to increased temperature. The minor methodological differences (use of antibiotics, increased sensitivity of ODC assay) are not likely to explain the inconsistency of the findings of the present and previous studies. Different results were obtained in experiments with the waveguide system that involves more efficient temperature control. In this exposure system, ODC activity was increased after 8 h exposure at 6 W/kg. Further studies are warranted to explore whether this finding reflects a true non-thermal effect. The present study did not provide evidence for modulation-specific effects reported in earlier studies. Bioelectromagnetics 28:501,508, 2007. © 2007 Wiley-Liss, Inc. [source] Brain Neurons Express Ornithine Decarboxylase-Activating Antizyme Inhibitor 2 with Accumulation in Alzheimer's DiseaseBRAIN PATHOLOGY, Issue 3 2010Laura T. Mäkitie Abstract Polyamines are small cationic molecules that in adult brain are connected to neuronal signaling by regulating inward-rectifier K+ -channels and different glutamate receptors. Antizyme inhibitors (AZINs) regulate the cellular uptake of polyamines and activate ornithine decarboxylase (ODC), the rate-limiting enzyme of polyamine synthesis. Elevated levels of ODC activity and polyamines are detected in various brain disorders including stroke and Alzheimer's disease (AD). We originally reported a novel brain- and testis-specific AZIN, called AZIN2, the distribution of which we have now studied in normal and diseased human brain by in situ hybridization and immunohistochemistry. We found the highest accumulation of AZIN2 in a pearl-on-the-string-like distribution along the axons in both the white and gray matter. AZIN2 was also detected in a vesicle-like distribution in the somas of selected cortical pyramidal neurons. Double-immunofluorescence staining revealed co-localization of AZIN2 and N-methyl D-aspartate-type glutamate receptors (NMDARs) in pyramidal neurons of the cortex. Moreover, we found accumulation of AZIN2 in brains affected by AD, but not by other neurodegenerative disorders (CADASIL or Lewy body disease). ODC activity is mostly linked to cell proliferation, whereas its regulation by AZIN2 in post-mitotically differentiated neurons of the brain apparently serves different purposes. The subcellular distribution of AZIN2 suggests a role in vesicular trafficking. [source] | |||||||||||||