Interleukin-1  Regulates Phospholipase D-1 Expression in Rat Pancreatic  -Cells

Chen, M.-C.

doi:10.1210/en.141.8.2822

Cited by 12 publications

(12 citation statements)

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“…The choice of cytokine concentrations used is based on our previous dose-response experiments (10,15,22 and B. Kutlu and D.L.E., unpublished data). The inducible NO synthase (iNOS) blocker N G -methyl-L-arginine (LMA; Sigma, Steinheim, Germany) was used at 1.0 mmol/l, a concentration that prevents cytokine-induced NO production (23). The SERCA blockers thapsigargin and cyclopiazonic acid (CPA; Sigma, Steinheim, Germany) were used at different concentrations, as indicated in RESULTS.…”

Section: Methodsmentioning

confidence: 99%

Cytokines Downregulate the Sarcoendoplasmic Reticulum Pump Ca2+ ATPase 2b and Deplete Endoplasmic Reticulum Ca2+, Leading to Induction of Endoplasmic Reticulum Stress in Pancreatic β-Cells

Cardozo

Ortis²,

Størling³

et al. 2005

Diabetes

490

475

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Section: Methodsmentioning

confidence: 99%

Cytokines Downregulate the Sarcoendoplasmic Reticulum Pump Ca2+ ATPase 2b and Deplete Endoplasmic Reticulum Ca2+, Leading to Induction of Endoplasmic Reticulum Stress in Pancreatic β-Cells

Cardozo

Ortis²,

Størling³

et al. 2005

Diabetes

490

475

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“…TNF-α and IL-1 activate PLD-A few studies have shown activation of PLD by TNF-α (161-163) or IL-1 (164). In some studies (161)(162)(163), PLD activation was determined as increased activity measured by its transphosphatidylation reaction and thus did not differentiate whether PLD1, PLD2, or both were induced.…”

Section: 14mentioning

confidence: 99%

Integration of cytokine biology and lipid metabolism in stroke

Adibhatla

Dempsy²,

Hatcher³

2008

Front Biosci

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Cytokines regulate the innate and adaptive immune responses and are pleiotropic, redundant and multifunctional. Expression of most cytokines, including TNF-α and IL-1α/ß, is very low in normal brain. Metabolism of lipids is of particular interest due to their high concentration in the brain. Inflammatory response after stroke suggests that cytokines (TNF-α, IL-1 α/ß, IL-6), affect the phospholipid metabolism and subsequent production of eicosanoids, ceramide, and ROS that may potentiate brain injury. Phosphatidylcholine and sphingomyelin are source for lipid messengers. Sphingomyelin synthase serves as a bridge between metabolism of glycerolipids and sphingolipids. TNF-α and IL-1 α/ß can induce phospholipases (A 2 , C, and D) and sphingomyelinases, and concomitantly proteolyse phosphatidylcholine and sphingomyelin synthesizing enzymes. Together, these alterations contribute to loss of phosphatidylcholine and sphingomyelin after stroke that can be attenuated by inhibiting TNF-α or IL-1 α/ß signaling. Inflammatory responses are instrumental in the formation and destabilization of atherosclerotic plaques. Secretory PLA 2 IIA is found in human atherosclerotic lesions and is implicated in initiation, progression and maturation of atherosclerosis, a risk factor for stroke. Lipoprotein-PLA 2 , part of apolipoprotein B-100 of LDL, plays a role in vascular inflammation and coronary endothelial dysfunction. Cytokine antagonism attenuated secretory PLA 2 IIA actions, suggesting cytokine-lipid integration studies will lead to new concepts contributing to bench-to-bedside transition for stroke therapy.

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“…Their inhibition, together with the impaired mitochondrial ATP production, can explain the cytokine-induced ␤-cell dysfunction, which precedes cell death by several days (4). Changes in gene expression of Fas (see above), caspase 1 (35), iNOS (24), AS (24), MnSOD (47), PC-2 (36,45), interferon regulatory factor 1 (IRF-1) (48), SPI-3 (43), phospholipase D-1 (PLD-1) (40,49), and PDX-1 (45) are a direct result of cytokine exposure, whereas induction of other mRNAs, such as hsp 70 (33,50,51) and HO-1 (24,45), is probably secondary to cytokine-induced iNOS expression and NO production. …”

Section: Gene Expression Patterns and The Non-nitric Oxide Component mentioning

confidence: 99%

beta-cell apoptosis and defense mechanisms: lessons from type 1 diabetes.

Eizirik

Darville²

2001

Diabetes

160

109

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Increased evidence suggests that apoptosis is the main mode of ␤-cell death in early type 1 diabetes. Cytokines mediate ␤-cell apoptosis, and in this article, we discuss some of the cytokine-modified genes that may contribute to ␤-cell survival or death. The gene encoding for the inducible form of nitric oxide synthase is induced by interleukin (IL)-1␤ or IL-1␤ plus ␥-interferon in rodent and human islets, respectively. This leads to nitric oxide (NO) formation, which contributes to a major extent to ␤-cell necrosis and to a minor extent to the process of ␤-cell apoptosis. The main mode of cell death induced by cytokines in human ␤-cells is apoptosis, whereas cytokines lead to both necrosis and apoptosis in rat and mouse ␤-cells. It is suggested that the necrotic component in rodent islets is due to NO-induced mitochondrial impairment and consequent decreased ATP production. Human islets, possessing better antioxidant defenses, are able to preserve glucose oxidation and ATP production, and can thus complete the apoptotic program after the death signal delivered by cytokines. We propose that this death signal results from cytokine-induced parallel and/or sequential changes in the expression of multiple proapoptotic and prosurvival genes. The identity of these "gene modules" and of the transcription factors regulating them remains to be established. Diabetes 50 (Suppl. 1):S64-S69, 2001 H yperglycemia in type 1 diabetes probably results from a long-term negative balance between immune-mediated ␤-cell damage (1) and ␤-cell repair/regeneration (2). Once macrophages and T-cells have been attracted to the islets and activated, they secrete soluble mediators such as cytokines, oxygen free radicals, and nitric oxide (NO), which probably contribute to ␤-cell dysfunction and death (3-5). Under in vitro conditions, interleukin (IL)-1␤, in combination with interferon (IFN)-␥ and/or tumor necrosis factor (TNF)-␣, induces severe functional suppression and death by apoptosis in rodent pancreatic islet cells (3,6,7). Human islets are less sensitive to the deleterious effects of cytokines, but their exposure for several days to IL-1␤ plus TNF-␣ plus IFN-␥ induces ␤-cell functional impairment and death by apoptosis (4,8). Interestingly, neither IL-1␤ nor IFN-␥ alone induces apoptosis in human ␤-cells, whereas the combination of these cytokines directly induces ␤-cell death (8,9). A potential indirect effect of cytokines is upregulation of the ␤-cell Fas receptor, increasing the susceptibility of these cells to apoptosis mediated by Fas ligand (FasL), expressed on the surface of invading T-cells and macrophages (10)(11)(12). Recent data indicate that Fas expression and apoptosis are also present in human ␤-cells in the early stages of type 1 diabetes (11,13).Apoptosis is apparently the main mode of ␤-cell death in NOD mice (14). In this species, ␤-cell apoptosis precedes massive T-cell infiltration (15), reinforcing a putative role for inflammatory mediators produced by early infiltrating cells such as macrophages and dendritic cel...

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Interleukin-1 Regulates Phospholipase D-1 Expression in Rat Pancreatic -Cells

Cited by 12 publications

References 0 publications

Cytokines Downregulate the Sarcoendoplasmic Reticulum Pump Ca2+ ATPase 2b and Deplete Endoplasmic Reticulum Ca2+, Leading to Induction of Endoplasmic Reticulum Stress in Pancreatic β-Cells

Cytokines Downregulate the Sarcoendoplasmic Reticulum Pump Ca2+ ATPase 2b and Deplete Endoplasmic Reticulum Ca2+, Leading to Induction of Endoplasmic Reticulum Stress in Pancreatic β-Cells

Integration of cytokine biology and lipid metabolism in stroke

beta-cell apoptosis and defense mechanisms: lessons from type 1 diabetes.

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