Cot Kinase Induces Cyclooxygenase-2 Expression in T Cells through Activation of the Nuclear Factor of Activated T Cells

Gregorio, Rosa de; Íñiguez, Miguel A.; Fresno, Manuel; Alemany, Susana

doi:10.1074/jbc.m100885200

Cited by 74 publications

(73 citation statements)

References 52 publications

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“…However, a possible participation of NF-AT in this process cannot be ruled out. A similar inability of CsA to abolish the COX-2 induction mediated by Cot kinase-dependent NF-AT activation has been described [11]. The authors have suggested that the activity of this factor is regulated downstream of CaN activation or through the operation of parallel pathway(s).…”

Section: Discussionsupporting

confidence: 54%

“…Although the capacity of human T lymphocytes to induce COX-2 synthesis has been reported [10,11,21,22], no studies have analysed this protein in B and NK lymphocytes. For this reason, our results also demonstrate, for first time, that COX-2 can be up-regulated in these two lymphocyte subsets upon their promoted activation by allergens via CD23 cross-linking.…”

Section: Discussionmentioning

confidence: 99%

“…In our case, only p38 appeared necessary for NF-jB activation since the MEK inhibitor PD098059 did not abolish the stimulation of COX-2 expression by allergens. A relationship between COX-2 expression and NF-AT activation has been suggested in T lymphocytes [10,11] and endothelial cells [40]. In these cells, the inhibitor of CaN [27], CsA, potently abrogates the NF-AT-dependent COX-2 induction caused by Ca 2+ -mobilising agents.…”

Section: Discussionmentioning

confidence: 99%

“…MAPK activities have also been associated with allergic inflammation [8,9]. The transcriptional activation of COX-2 is mediated by the binding of transcription factors to regulatory elements in the COX-2 promoter, such as nuclear factor of activated T cells (NF-AT) [10,11] or NF-jB [12,13]. Available data also reveals an important role of NF-AT and NF-jB in allergic asthma [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Induction of cyclooxygenase-2 expression by allergens in lymphocytes from allergic patients

et al. 2005

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Cyclooxygenase (COX) is a key enzyme in prostaglandin (PG) synthesis. Up-regulation of COX-2 expression is responsible for increased PG release during inflammatory conditions and is thought to be also involved in allergic states. In this study, we demonstrate that in human T, B and natural killer lymphocytes from allergic patients, COX-2 expression became induced upon cell challenge with specific allergens and that this process is presumably IgE dependent and occurs after CD23 receptor ligation. This induction took place at both mRNA and protein levels and was accompanied by PGD 2 release. IgE-dependent lymphocyte treatment elicited, in parallel, an activation of the MAPK p38 and extracellular signal-regulated kinase 1/2, an enhancement of calcineurin (CaN) activity, and an increase of the DNA-binding activity of the nuclear factor of activated T cells and of NF-jB, with a concomitant decrease in the levels of the cytosolic inhibitor of jB, IjB. In addition, specific chemical inhibitors of MAPK, such as PD098059 and SB203580, as well as MG-132, an inhibitor of proteasomal activity, abolished allergen-induced COX-2 up-regulation, suggesting that this process is mediated by MAPK and NF-jB. However, induction of COX-2 expression was not hampered by the CaN inhibitor cyclosporin A. We also examined the effect of a selective COX-2 inhibitor, NS-398, on cytokine production by human lymphocytes. Treatment with NS-398 severely diminished the IgE-dependently induced production of IL-8 and TNF-a. These results underscore the relevant role of lymphocyte COX-2 in allergy and suggest that COX-2 inhibitors may contribute to the improvement of allergic inflammation through the reduction of inflammatory mediator production by human lymphocytes.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Induction of cyclooxygenase-2 expression by allergens in lymphocytes from allergic patients

et al. 2005

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“…Two NFAT binding sites are present in the mouse COX-2 promoter region. Both distal (-105/-97) and proximal (-76/-61) NFAT response elements in the COX-2 promoter are essential for COX-2 induction in T lymphocytes (43).…”

Section: Discussionmentioning

confidence: 99%

Ionizing radiation synergistic induction of cyclooxygenase-2 with benzo[a]pyrene diol-epoxide through nuclear factor of activated T cells in mouse epidermal Cl 41 cells

Zhang

Li²,

Burns³

et al. 2006

Oncol Rep

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DYRK1A activates NFATC1 to increase glioblastoma migration

et al. 2021

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Glioma is the most common brain cancer, and high-grade gliomas, including glioblastoma multiforme (GBM), are the most aggressive types of glioma. 1 The current standard treatment for GBM involves surgical resection followed by the administration of an alkylating agent, temozolomide, both concurrent with and after radiotherapy. Bevacizumab is administered as a second-line treatment after relapse. 2,3 However, GBM is resistant to chemotherapy and radiotherapy, with a median patient survival time of approximately one year. 1,4 The highly invasive nature of GBM cells is thought to contribute to the poor prognosis of this tumor, necessitating the exploration of alternative therapies. Many factors are involved in the migration and invasion of malignant tumors, including the nuclear factor of activated T cells (NFAT). [5][6][7] NFAT, originally found in activated T cells, is a transcription factor that induces gene transcription during the immune response. 8 The NFAT transcription factor family consists of five members: NFAT1 (NFATC2, NFATp),

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Cot Kinase Induces Cyclooxygenase-2 Expression in T Cells through Activation of the Nuclear Factor of Activated T Cells

Cited by 74 publications

References 52 publications

Induction of cyclooxygenase-2 expression by allergens in lymphocytes from allergic patients

Induction of cyclooxygenase-2 expression by allergens in lymphocytes from allergic patients

Ionizing radiation synergistic induction of cyclooxygenase-2 with benzo[a]pyrene diol-epoxide through nuclear factor of activated T cells in mouse epidermal Cl 41 cells

DYRK1A activates NFATC1 to increase glioblastoma migration

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