83 research outputs found

    Supplemental Material, sj-tif-2-ptd-10.1177_08968608231165865 - Blockade of sodium–glucose co-transporters improves peritoneal ultrafiltration in uraemic rodent models

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    Supplemental Material, sj-tif-2-ptd-10.1177_08968608231165865 for Blockade of sodium–glucose co-transporters improves peritoneal ultrafiltration in uraemic rodent models by Marina Vorobiov, Boris Rogachev, Reut Riff, Cidio Chaimowitz, Endre Z Neulander, Anna Basok, Alla Shnaider, Amos Douvdevani and Yosef-Shmuel Haviv in Peritoneal Dialysis International</p

    Supplemental Material, sj-tif-1-ptd-10.1177_08968608231165865 - Blockade of sodium–glucose co-transporters improves peritoneal ultrafiltration in uraemic rodent models

    No full text
    Supplemental Material, sj-tif-1-ptd-10.1177_08968608231165865 for Blockade of sodium–glucose co-transporters improves peritoneal ultrafiltration in uraemic rodent models by Marina Vorobiov, Boris Rogachev, Reut Riff, Cidio Chaimowitz, Endre Z Neulander, Anna Basok, Alla Shnaider, Amos Douvdevani and Yosef-Shmuel Haviv in Peritoneal Dialysis International</p

    TNF-receptors on human peritoneal mesothelial cells: Regulation of receptor levels and shedding by IL-1α and TNFα

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    TNF-receptors on human peritoneal mesothelial cells: Regulation of receptor levels and shedding by IL-1α and TNFα. Human peritoneal mesothelial cells (HPMC) respond to tumor necrosis factor α (TNFα) by releasing various cytokines that may activate the endothelium and induce recruitment of leukocytes during peritonitis. We characterized the receptors for TNF on HPMC to elucidate their functions in peritonitis. Scatchard analysis determined the presence of 70 × 103 TNF receptors/cell with a kDa of 0.44nm. TNF receptor 1 (TNF-R1, p55) and TNF-R2 (p75) mRNA were demonstrated by reverse-transcriptase-PCR (RT-PCR). TNF-R1 protein was solely detected by flow cytometry (FCM). Interleukin-1α (IL-1α) induced down-regulation of TNF-R1. This was concomitant with accumulation of soluble TNF-R1 (sTNF-R1) detected by specific ELISA. LPS had a lower TNF-R1-shedding activity while TNFα did not induce shedding. The IL-1-induced-sTNF-R1-shedding was suppressed by the protein-kinase-A (PKA) inhibitor, H-8, or by H-7, the inhibitor of both PKC and PKA, but not by the specific PKC inhibitor GF. These experiments suggest a role for PKA in the IL-1-shedding signal. No change in TNF-R1 mRNA levels was observed after IL-1α or TNFα stimulation while TNF-R2 (p75) mRNA basal levels transiently increased three to fivefold, reaching a peak after four hours followed by an accumulation of sTNF-R2 in the supernatant. Our data suggest that the main receptor expressed on HPMC is TNF-R1. Down-regulation and shedding of TNF-R1 induced by IL-1, and the transient expression of TNF-R2 induced by IL-1 and TNF, may regulate the responses to TNF by HPMC. These results may be important in understanding the inflammatory process of peritonitis were TNF plays a major role
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