Suppressor of Cytokine Signaling 1 Is a Positive Regulator of TGF-β–Induced Prostaglandin Production in Human Follicular Dendritic Cell–like Cells

Cho, Whajung; Kim, Youngmi; Kim, Jini; Park, Seongji; Park, Deokbum; Kim, Byung-Chul; Jeoung, Dooil; Kim, Young‐Myeong; Choe, Jongseon

doi:10.4049/jimmunol.1401615

Cited by 9 publications

(8 citation statements)

References 55 publications

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“…For example, LPS-induced COX-2 expression was inhibited by ERK and p38 inhibitors, which was verified by the actual induction of phosphorylation of these MAPKs by LPS [18]. TGF-β-stimulated COX-2 induction also required ERK and p38 [19]. In the present study, we extended our previous reports and explored the intracellular pathway of PGE 2 -induced COX-2 expression in FDC-like cells.…”

Section: Introductionsupporting

confidence: 80%

“…In this study, we further investigated the underlying intracellular mechanism by examining the potential role of ERK and p38 MAPKs in this process. Our earlier results suggest that both ERK and p38 molecules are involved in the signaling pathway to COX-2 expression [19]. First, the effects of PGE 2 on the phosphorylation degrees of ERK and p38 proteins were analyzed by immunoblotting.…”

Section: Resultsmentioning

confidence: 99%

“…PGE 2 was purchased from Cayman Chemical, and IL-1β from R&D Systems. All the siRNA duplexes were obtained from Ambion Inc. as described previously [19]. PD098059 and SB203580 were purchased from A.G. Scientific, Inc.…”

Section: Antibodies and Other Reagentsmentioning

confidence: 99%

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Prostaglandin E2 stimulates COX-2 expression via mitogen-activated protein kinase p38 but not ERK in human follicular dendritic cell-like cells

Cho¹,

Choe²

2020

BMC Immunol

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Background: Prostaglandin E2 (PGE 2) is an endogenous lipid mediator of inflammation. Its production is regulated by the rate-limiting upstream enzyme cyclooxygenase-2 (COX-2). We have recently demonstrated that the major cell type expressing COX-2 in the germinal center is follicular dendritic cell (FDC). In this study, to elucidate the molecular mechanism of PGE 2 in COX-2 production, we asked whether mitogen-activated protein kinases ERK and p38 might regulate COX-2 expression. Results: FDC-like cells were used to analyze the phosphorylation kinetics of ERK and p38 and the impact of genetic knockdown. PGE 2 stimulation gave rise to a rapid increase of p38 but not ERK phosphorylation. In contrast, IL-1β induced phosphorylation of both MAPKs. Knockdown of p38 resulted in a marked suppression of COX-2 expression induced by either PGE 2 or IL-1β. ERK knockdown did not significantly affect the effect of PGE 2 and IL-1β on COX-2 induction. The differential results of p38 and ERK siRNA transfection were reproduced in the production of prostaglandins and in experiments performed with pharmacologic inhibitors. Conclusions: Our data indicate that p38 is essentially required for PGE 2 to induce COX-2 expression in FDC-like cells. The current study helps to expand our understanding of the biological function of FDC at the molecular level and provides a potential rationale for the pharmacologic or genetic approaches to regulate p38 MAPK in the treatment of various inflammatory disorders.

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Section: Introductionsupporting

confidence: 80%

Section: Resultsmentioning

confidence: 99%

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Prostaglandin E2 stimulates COX-2 expression via mitogen-activated protein kinase p38 but not ERK in human follicular dendritic cell-like cells

Cho¹,

Choe²

2020

BMC Immunol

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“…CsA treatment for up to 24 h increased Smad 3 phosphorylation in rat glomerular mesangial cells [ 54 ]. Induction of the Smad pathway by TGF-β1 increases Snail expression [ 55 ], a known regulator of EMT [ 56 , 57 ]. Studies by Cano and coworkers (2000) have shown that TGF-β1 can trigger EMT by decreasing expression of epithelial junction proteins through the activation of Snail [ 56 , 58 ].…”

Section: Discussionmentioning

confidence: 99%

Chrysin Ameliorates Cyclosporine-A-Induced Renal Fibrosis by Inhibiting TGF-β1-Induced Epithelial–Mesenchymal Transition

Nagavally

Sunilkumar

Akhtar

et al. 2021

IJMS

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Cyclosporine A (CsA) is a nephrotoxicant that causes fibrosis via induction of epithelial–mesenchymal transition (EMT). The flavonoid chrysin has been reported to have anti-fibrotic activity and inhibit signaling pathways that are activated during EMT. This study investigated the nephroprotective role of chrysin in the prevention of CsA-induced renal fibrosis and elucidated a mechanism of inhibition against CsA-induced EMT in proximal tubule cells. Treatment with chrysin prevented CsA-induced renal dysfunction in Sprague Dawley rats measured by blood urea nitrogen (BUN), serum creatinine and creatinine clearance. Chrysin inhibited CsA-induced tubulointerstitial fibrosis, characterized by reduced tubular damage and collagen deposition. In vitro, chrysin significantly inhibited EMT in LLC-PK1 cells, evidenced by inhibition of cell migration, decreased collagen expression, reduced presence of mesenchymal markers and elevated epithelial junction proteins. Furthermore, chrysin co-treatment diminished CsA-induced TGF-β1 signaling pathways, decreasing Smad 3 phosphorylation which lead to a subsequent reduction in Snail expression. Chrysin also inhibited activation of the Akt/ GSK-3β pathway. Inhibition of both pathways diminished the cytosolic accumulation of β-catenin, a known trigger for EMT. In conclusion, flavonoids such as chrysin offer protection against CsA-induced renal dysfunction and interstitial fibrosis. Chrysin was shown to inhibit CsA-induced TGF-β1-dependent EMT in proximal tubule cells by modulation of Smad-dependent and independent signaling pathways.

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“…SOCS1 also plays a regulatory role in anaphylactic shock viscera injury processes [ 13 ]. SOCS1 promotes TGF-β-induced COX-2 expression and prostaglandin (PG) production by facilitating Smad3 phosphorylation and Snail binding to the COX-2 promoter [ 14 ]. The role of COX-2 in allergic inflammation and cellular interaction during allergic inflammation has been reported [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

miR-122-SOCS1-JAK2 axis regulates allergic inflammation and allergic inflammation-promoted cellular interactions

Noh

Kim

et al. 2017

Oncotarget

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The regulatory role of suppressor of cytokine signaling 1 (SOCS1) in inflammation has been reported. However, its role in allergic inflammation has not been previously reported. SOCS1 mediated in vitro and in vivo allergic inflammation. Histone deacetylase-3 (HDAC3), a mediator of allergic inflammation, interacted with SOCS1, and miR-384 inhibitor, a positive regulator of HDAC3, induced features of allergic inflammation in an SOCS1-dependent manner. miRNA array analysis showed that the expression of miR-122 was decreased by antigen-stimulation. TargetScan analysis predicted the binding of miR-122 to the 3′-UTR of SOCS1. miR-122 inhibitor induced in vitro and in vivo allergic features in SOCS1-dependent manner. SOCS1 was necessary for allergic inflammation-promoted enhanced tumorigenic and metastatic potential of cancer cells. SOCS1 and miR-122 regulated cellular interactions involving cancer cells, mast cells and macrophages during allergic inflammation. SOCS1 mimetic peptide, D-T-H-F-R-T-F-R-S-H-S-D-Y-R-R-I, inhibited in vitro and in vivo allergic inflammation, allergic inflammation-promoted enhanced tumorigenic and metastatic potential of cancer cells, and cellular interactions during allergic inflammation. Janus kinase 2 (JAK2) exhibited binding to SOCS1 mimetic peptide and mediated allergic inflammation. Transforming growth factor- Δ1 (TGF-Δ1) was decreased during allergic inflammation and showed an anti-allergic effect. SOCS1 and JAK2 regulated the production of anti-allergic TGF-Δ1. Taken together, our results show that miR-122-SOCS1 feedback loop can be employed as a target for the development of anti-allergic and anti-cancer drugs.

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Suppressor of Cytokine Signaling 1 Is a Positive Regulator of TGF-β–Induced Prostaglandin Production in Human Follicular Dendritic Cell–like Cells

Cited by 9 publications

References 55 publications

Prostaglandin E2 stimulates COX-2 expression via mitogen-activated protein kinase p38 but not ERK in human follicular dendritic cell-like cells

Prostaglandin E2 stimulates COX-2 expression via mitogen-activated protein kinase p38 but not ERK in human follicular dendritic cell-like cells

Chrysin Ameliorates Cyclosporine-A-Induced Renal Fibrosis by Inhibiting TGF-β1-Induced Epithelial–Mesenchymal Transition

miR-122-SOCS1-JAK2 axis regulates allergic inflammation and allergic inflammation-promoted cellular interactions

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