Transforming growth factors type‐β and dexamethasone attenuate group II phospholipase A<sub>2</sub> gene expression by interleukin‐1 and forskolin in rat mesangial cells

Mühl, Heiko; Geiger, Thomas; Pignat, Werner; Märki, F; Bosch, H. van den; Cerletti, Nico; Cox, David A.; McMaster, Gary; Vosbeck, K; Pfeilschifter, Josef

doi:10.1016/0014-5793(92)81245-h

Cited by 40 publications

(13 citation statements)

References 41 publications

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“…On the other hand, they did synergistically potentiate the TNF␣-induced increase in PGE 2 production. Synergism between cAMP elevating agents and TNF␣ or interleukin-1␤ have also been reported in up-regulation of group II PLA 2 mRNA in rat mesangial cells (52)(53)(54). Agents that increase cellular levels of cAMP used alone have additionally been shown to increase secretion of PLA 2 from vascular smooth muscle cells (55) and in mesangial cells (54).…”

Section: Discussionmentioning

confidence: 98%

Tumor Necrosis Factor-α Inversely Regulates Prostaglandin D2 and Prostaglandin E2 Production in Murine Macrophages

Fournier

Fadok

Henson

1997

Journal of Biological Chemistry

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Increased synthesis of insulin-like growth factor-1 is induced in murine macrophages by prostaglandin E 2 (PGE 2 ) and tumor necrosis factor-␣ (TNF␣). Accordingly, we have investigated mechanisms regulating synthesis of PGE 2 that might contribute to autocrine/paracrine effects on insulin-like growth factor-1 production. In response to zymosan, TNF␣ specifically induced a 5-fold increase in PGE 2 synthesis, at the same time decreasing PGD 2 production in a reciprocal fashion. Activators of cyclic AMP-dependent protein kinase (PKA), such as PGE 2 itself or dibutyryl cyclic AMP, did not modify PGE 2 production by themselves but potentiated the TNF␣-induced increase in PGE 2 ; this effect required both RNA and protein synthesis. No significant change in arachidonate release or production of other eicosanoids was observed. The inducible form of cyclooxygenase-2 (COX2) but not of the constitutive form COX1 was implicated in the generation of both PGE 2 and PGD 2 in these cells by use of specific inhibitors and effects of dexamethasone. Neither COX1 nor COX2 protein levels were affected by TNF␣ or PKA activators used alone, whereas in association, marked up-regulation of COX2 mRNA and protein was observed. Incubations of cells carried out with PGH 2 demonstrated that PGE 2 synthase activity was increased after a TNF␣ pretreatment. Taken together, our results suggest that TNF␣ induced a switch from the PGD 2 to PGE 2 synthesis pathway by regulating PGE 2 synthase expression and/or activity and that activators of PKA markedly potentiated the TNF␣-induced increase in PGE 2 through up-regulation of COX2 gene expression.

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Section: Discussionmentioning

confidence: 98%

Tumor Necrosis Factor-α Inversely Regulates Prostaglandin D2 and Prostaglandin E2 Production in Murine Macrophages

Fournier

Fadok

Henson

1997

Journal of Biological Chemistry

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“…Under chronic renal disease, it exerts profibrotic activities leading to glomerulosclerosis and interstitial fibrosis (50). In acute disorders, TGF-␤ acts as a potent anti-inflammatory agent to reduce pro-inflammatory parameters including NO and prostaglandins in resident tissue cells and macrophages (40,51,52). In addition, TGF-␤ suppresses the respiratory burst of macrophages and stimulates the synthesis of IL-1 receptor antagonist.…”

Section: Discussionmentioning

confidence: 99%

Sphingosine 1-Phosphate Cross-activates the Smad Signaling Cascade and Mimics Transforming Growth Factor-β-induced Cell Responses

Xin

Ren

Kleuser

et al. 2004

Journal of Biological Chemistry

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172

143

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Exposure of renal mesangial cells to sphingosine 1-phosphate (S1P) leads to a rapid and transient activation of the mitogen-and stress-activated protein kinases but also the protein kinase B. Here, we show that S1P also induces phosphorylation of Smad proteins, which are members of the transforming growth factor-␤ (TGF-␤) signaling device. However, Smad phosphorylation occurred more slowly with a maximal effect after 20 -30 min of S1P stimulation when compared with the rapid activation of the MAPKs. Interestingly, Smad phosphorylation is increased by pertussis toxin, which is in contrast to the complete inhibition of S1P-induced MAPK phosphorylation by pertussis toxin. TGF-␤ is a potent anti-inflammatory cytokine, which in mesangial cells attenuates the expression of (i) inducible nitricoxide synthase (iNOS) caused by interleukin (IL)-1␤, (ii) secreted phospholipase A 2 (sPLA 2 ), and (iii) matrix metalloproteinase-9 (MMP-9). These gene products are also down-regulated by S1P in a concentration-dependent manner. Furthermore, the expression of connective tissue growth factor is enhanced by both TGF-␤ 2 and S1P. These effects of S1P are not mediated by the MAPK cascade as neither pertussis toxin nor the MAPK cascade inhibitor U0126 are able to reverse this inhibition. Overexpression of the inhibitory Smad-7 or down-regulation of co-Smad-4 lead to a reversal of the blocking effect of S1P on IL-1␤-induced NO release. Moreover, down-regulating the TGF-␤ receptor type II by the siRNA technique or antagonizing the S1P 3 receptor subtype with suramin abrogates S1P-stimulated Smad phosphorylation. In summary, our data show that S1P trans-activates the TGF-␤ receptor and triggers activation of Smads followed by activation of connective tissue growth factor gene transcription and inhibition of IL-1␤-induced expression of iNOS, sPLA 2 , and MMP-9.

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“…IL-1 and TNF can both induce the messenger RNA (mRNA) encoding the low molecular weight PLA, in chondrocytes as well as in smooth muscle cells, astrocytes, and mesangial cells (50)(51)(52)(53)(54). Similar findings have been observed in organs from rats treated with endotoxin (55).…”

Section: Stimulation Of Pla By Cytokinesmentioning

confidence: 58%

Phospholipase A₂ and arthritis

Bomalaski¹,

Clark²

1993

Arthritis & Rheumatism

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Transforming growth factors type‐β and dexamethasone attenuate group II phospholipase A₂ gene expression by interleukin‐1 and forskolin in rat mesangial cells

Cited by 40 publications

References 41 publications

Tumor Necrosis Factor-α Inversely Regulates Prostaglandin D2 and Prostaglandin E2 Production in Murine Macrophages

Tumor Necrosis Factor-α Inversely Regulates Prostaglandin D2 and Prostaglandin E2 Production in Murine Macrophages

Sphingosine 1-Phosphate Cross-activates the Smad Signaling Cascade and Mimics Transforming Growth Factor-β-induced Cell Responses

Phospholipase A₂ and arthritis

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Transforming growth factors type‐β and dexamethasone attenuate group II phospholipase A2 gene expression by interleukin‐1 and forskolin in rat mesangial cells

Cited by 40 publications

References 41 publications

Tumor Necrosis Factor-α Inversely Regulates Prostaglandin D2 and Prostaglandin E2 Production in Murine Macrophages

Tumor Necrosis Factor-α Inversely Regulates Prostaglandin D2 and Prostaglandin E2 Production in Murine Macrophages

Sphingosine 1-Phosphate Cross-activates the Smad Signaling Cascade and Mimics Transforming Growth Factor-β-induced Cell Responses

Phospholipase A2 and arthritis

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Transforming growth factors type‐β and dexamethasone attenuate group II phospholipase A₂ gene expression by interleukin‐1 and forskolin in rat mesangial cells

Phospholipase A₂ and arthritis