Disease relevance of Dexi

• Cloning of dexamethasone-induced transcript: a novel glucocorticoid-induced gene that is upregulated in emphysema [1].
• EXPERIMENTAL DESIGN: PCDGF functions and signaling pathways in dexamethasone-induced apoptosis were studied using a representative dexamethasone-sensitive multiple myeloma cell line ARP-1 [2].
• Three different functions were examined: growth stimulation in factor-dependent pro-B Ba/F3 cells, protection against dexamethasone-induced apoptosis, and Ly-6A2 induction in BW5147 lymphoma cells [3].
• In line with these data, analysis of sorted 5T2MM cells demonstrated a significant decrease in invasive capacity and a significant increase in (dexamethasone-induced) apoptosis sensitivity and in proliferation during the disease progression [4].
• Cytoplasmic micro heavy chain confers sensitivity to dexamethasone-induced apoptosis in early B-lineage acute lymphoblastic leukemia [5].

Psychiatry related information on Dexi

• Dexamethasone induced an enhanced phagocytic activity when administered at any time after culture initiation provided that it was in culture during this critical period [6].

High impact information on Dexi

• Expression of IP3R3 antisense constructs in S49 T cells blocked dexamethasone-induced apoptosis, whereas IP3R3 sense, IP3R1 sense, or IP3R1 antisense control constructs did not block cell death [7].
• Dexamethasone induced the following order of appearance of caspase activities as judged by flow cytometry: LEHDase, WEHDase, VEIDase, IETDase, and DEVDase [8].
• This was observed both in anti-CD3- and dexamethasone-induced apoptosis [9].
• In vitro, leptin protected thymocytes from dexamethasone-induced apoptosis [10].
• Dexamethasone-induced expression of activated Gs alpha markedly delayed differentiation in comparison with uninduced stably transfected cells, which differentiated normally in mitogen-depleted media [11].

Chemical compound and disease context of Dexi

• Antioxidants, including bovine liver catalase, bovine erythrocyte CuZn-SOD, sodium selenite and Trolox, a water soluble vitamin E analogue, as well as hypoxia, inhibited dexamethasone-induced apoptosis [12].
• Dexamethasone-induced hyperglycemia in obese Avy/a (viable yellow) female mice entails preferential induction of a hepatic estrogen sulfotransferase [13].
• The adrenal medullary catecholamine epinephrine was found to induce neutrophilia in both intact and adrenalectomized rats, and the glucocorticosteroid analog dexamethasone induced a profound lymphopenia in rats as reported by previous investigators [14].
• These results suggest that glycyrrhetinic acid inhibited dexamethasone-induced changes in the histamine synthesis of mastocytoma P-815 cells, and in the histamine release from rat mast cells [15].
• The effects of glycyrrhizin and its aglycone, glycyrrhetinic acid, on dexamethasone-induced changes in the histamine synthesis of mastocytoma P-815 cells and in the histamine release from antigen-stimulated rat peritoneal mast cells were investigated [15].

Biological context of Dexi

• Nonetheless, these T cells are efficiently protected from dexamethasone-induced apoptosis [16].
• Dexamethasone-induced antagonism of growth hormone (GH) action by down-regulation of GH binding in 3T3-F442A fibroblasts [17].
• The effects of insulin-induced down-regulation and dexamethasone-induced up-regulation on the rates of insulin receptor synthesis and decay were assessed by the heavy-isotope density-shift technique [18].
• Cyclosporin A potentiates the dexamethasone-induced mouse mammary tumor virus-chloramphenicol acetyltransferase activity in LMCAT cells: a possible role for different heat shock protein-binding immunophilins in glucocorticosteroid receptor-mediated gene expression [19].
• 125I-BSA, 51Cr-EDTA dilution techniques were used to evaluate dexamethasone induced changes in tumor plasma water, capillary permeability, and extracellular water volumes, while 59Fe and 51Cr labeled erythrocyte techniques were used to assess changes in tumor exchangeable erythrocyte volumes [20].

Anatomical context of Dexi

• This study has investigated molecular pathways implicated in Dexamethasone-induced apoptosis of osteocytes, using a cell line and primary chicken cells [21].
• Furthermore, expression of a bcl-2 transgene rescued pre-B and immature B cells from dexamethasone-induced cell death, indicating that Bcl-2 can inhibit the apoptotic cell death of progenitors and early B cells [22].
• Control of insulin receptor level in 3T3 cells: effect of insulin-induced down-regulation and dexamethasone-induced up-regulation on rate of receptor inactivation [18].
• Dexamethasone-induced insulin resistance in 3T3-L1 adipocytes is due to inhibition of glucose transport rather than insulin signal transduction [23].
• Ectopic overexpression of Id-1 in the SCp2 nontumorigenic mammary epithelial cells, which does not undergo complete dexamethasone-dependent tight junction reorganization, enhanced the dexamethasone-induced ZO-1 tight junction localization and stimulated the monolayer TER [24].

Associations of Dexi with chemical compounds

• Furthermore, they suggest that dexamethasone-induced reduction of IRS-1 expression may be important for the impaired activation of MAP kinase by insulin-like peptides in steroid-treated cells [25].
• Dexamethasone-induced thymocyte apoptosis: apoptotic signal involves the sequential activation of phosphoinositide-specific phospholipase C, acidic sphingomyelinase, and caspases [26].
• An increase to 1.4-fold parental cell catalase activity delayed cell loss after dexamethasone treatment, whereas a 2.0-fold parental catalase activity prevented dexamethasone-induced cell loss for 48 h after treatment [27].
• The nonsteroidal antiinflammatory agent indomethacin inhibited dexamethasone-induced differentiation only when added before the time of commitment of the cells to differentiation [28].
• To test whether resistance to oxidative stress causes resistance to dexamethasone-induced apoptosis, WEHI7.2 cell variants selected for resistance to 50, 100 and 200 microM H(2)O(2) were developed [29].

Physical interactions of Dexi

• Since the effect of troglitazone was greater in dexamethasone-treated adipocytes, troglitazone is likely to act by preventing dexamethasone-induced alterations which may include (i) binding to glucocorticoid receptor and (ii) effect on glucose uptake [30].

Regulatory relationships of Dexi

• 4. The dexamethasone-induced decline in preosteoblast proliferation correlated with a 30-40% reduction in protein kinase C/TPA-stimulated mitogen-activated protein kinase (MAPK) activity [31].
• During the isolation of apoptosis-related genes involved in glucocorticoid (GC)-induced cell death in murine thymic lymphomas, we found that the antisense gene of the transcription factor activator protein-4 (AP-4) inhibited dexamethasone-induced apoptosis [32].
• The fact that spermine inhibited caspase activation only in the thymocytes implies that spermine inhibited dexamethasone-induced apoptosis upstream of caspase-9 activation [33].
• IFN-gamma also inhibited dexamethasone-induced differentiation of T22-3 cells [34].

Other interactions of Dexi

• Conversely, NF-kappaB induction diminished dexamethasone-induced death [35].
• In preconfluent C3H10T1/2 and MC3T3-E1 cells, PTH and PTHrP protected against dexamethasone-induced reduction in cell viability, which was dependent on cAMP activation [36].
• IL-7 inhibits dexamethasone-induced apoptosis via Akt/PKB in mature, peripheral T cells [37].
• IL-7 blocked dexamethasone-induced apoptosis and the processing of caspase-3 and caspase-7 [37].
• The glucocorticoid receptor is essential for maintaining basal and dexamethasone-induced repression of the murine corticosteroid-binding globulin gene [38].

Analytical, diagnostic and therapeutic context of Dexi

• Moreover, dexamethasone-induced GR translocation from the cytoplasm to the nucleus was comparable in all xenografts [39].
• Therefore, we used oligonucleotide microarrays to identify the pattern of dexamethasone-induced changes in gene expression in two well characterized models of glucocorticoid-induced apoptosis, the murine lymphoma cell lines S49.A2 and WEHI7 [40].
• Addition of dexamethasone to these cocultures did not lead to a further increase in the percentage of apoptotic thymocytes, underlining the protective effect of NO on dexamethasone-induced apoptosis [41].
• By contrast, dexamethasone induced a 69% increase in the level of PI 3-kinase as determined by immunoblotting [42].
• Several Kampo medicines, e.g. Oren-gedoku-to and San'o-shashin-to, were found to inhibit dexamethasone-induced apoptosis in murine thymocytes [43].

References