NOX4-stimulated ROS generation led to JNK-mediated phosphorylation of cytosolic HuR at Ser221, thereby increasing TNF-α protein expression by stabilizing TNF-α mRNA. Consequently, DTX induced TNF-α-dependent death in U937 cells.

In this study, we tested the hypothesis that NOX4 is a proximal mediator of IL-1β-dependent activation of PKCδ and increases IL-1β-stimulated c-Jun kinase (JNK) signaling in primary rat aortic VSM cells.

Jan 1, 2013 · IL-1β stimulates reactive oxygen species production in rat aortic vascular smooth muscle cells via NOX4. PKCδ is required for IL-1β-mediated activation of JNK. NOX4 is upstream of PKCδ and regulates inducible NO synthase expression. Our results support a role for NOX4 during vascular injury.

May 8, 2008 · Nox4 overexpression induced basal activation of ERK1/2 and JNK whereas Nox2-transfected cells showed a modest increase in p38MAPK activation. After angiotensin II or TNFα treatment, JNK activation was augmented in Nox2 but not Nox4-transfected cells, whereas insulin augmented phosphorylation of p38MAPK, Akt, and GSK3β specifically in Nox4 ...

In unstimulated HEK cells, Nox4 can activate Erk1/2 and JNK signaling pathways and Akt and p38 MAPK in response to challenge with insulin (Anilkumar et al., 2008). These data suggest that Nox4-dervived ROS can influence distinct signaling pathways that depend on the presence or absence of agonists.

Jan 12, 2018 · To elucidate the signaling mechanisms of iohexol- and Nox4-mediated apoptosis, we analyzed the activation of redox-sensitive MAPK pathways (p38, c-Jun N-terminal kinase [JNK], and extracellular signal-regulated kinase [ERK] pathways).

Ethanol‑induced apoptosis and cell death of L‑02 cells was accompanied by the generation of ROS, elevated expression of NOX, as well as phosphorylation of JNK and P‑38. In addition, increased expression of Bcl‑2 was induced by 400 mM ethanol.

In this study, the JNK and p38 pathways were critical in mediating hypoxia-induced HK-2 cell apoptosis. Although phosphorylation of JNK, ERK and p38 increased after hypoxia exposure, only phosphorylation of JNK and p38 decreased after knockdown of Nox4.

Jan 1, 2022 · NOX4-stimulated ROS generation led to JNK-mediated phosphorylation of cytosolic HuR at Ser221, thereby increasing TNF-α protein expression by stabilizing TNF-α mRNA. Consequently, DTX induced TNF-α-dependent death in U937 cells.

Feb 6, 2019 · In the present study, we found that tumoral NOX4-educated macrophages exhibited elevated activity of JNK, and inhibition of JNK in M2 macrophages suppressed HB-EGF production. Therefore, our data support that M2 macrophages educated by tumoral NOX4 promotes NSCLC cell growth via JNK/HB-EGF axis.