NFκB signaling regulates embryonic and adult neurogenesis

Abstract

Both embryonic and adult neurogenesis involves the self-renewal/proliferation, survival, migration and lineage differentiation of neural stem/progenitor cells. Such dynamic process is tightly regulated by intrinsic and extrinsic factors and complex signaling pathways. Misregulated neurogenesis contributes much to a large range of neurodevelopmental defects and neurodegenerative diseases. The signaling of NFκB regulates many genes important in inflammation, immunity, cell survival and neural plasticity. During neurogenesis, NFκB signaling mediates the effect of numerous niche factors such as cytokines, chemokines, growth factors, extracellular matrix molecules, but also crosstalks with other signaling pathways such as Notch, Shh, Wnt/β-catenin. This review summarizes current progress on the NFκB signaling in all aspects of neurogenesis, focusing on the novel role of NFκB signaling in initiating early neural differentiation of neural stem cells and embryonic stem cells.

Propofol inhibits proliferation and induces neuroapoptosis of hippocampal neurons in vitro via downregulation of NF‐κB p65 and Bcl‐2 and upregulation of caspase‐3

“…NF‐κB, a ubiquitous nuclear transcription factor, is widely known for its pivotal roles in cell death, cell division and survival pathways . Similar to other organ systems, functional NF‐κB complexes existed in essentially all kinds of cells in the central nervous system (CNS), covering neurons, astrocytes, microglias, and oligodendrocytes . In vertebrates, the NF‐κB family is comprised of five members, namely, RelA (also known as p65), RelB, c‐Rel, p50 and p52.…”

The role of the Wnt canonical signaling in neurodegenerative diseases

“…Interestingly, it was found that the Wnt canonical pathway can modulate inflammatory responses also through the interaction with other signaling pathways. A cross-regulation between the Wnt and NF-κB signaling cascades [63,64,65,66,67,68] has been demonstrated, showing that β-catenin exerts an anti-inflammatory effect by physically inhibiting the NF-κB-mediated transcription of pro-inflammatory genes. This interaction in turn is regulated by GSK-3β which has a dual role: in part acts as a negative regulator of the β-catenin levels by promoting β-catenin degradation [39] [69], and in part acts as a positive modulator of the NF-κB signaling [70,71].…”

Structural and Functional Plasticity in the Maternal Brain Circuitry

“…Changes in the expression of key plasticity‐related genes occur in the CNS via activation of neuronal transcription factors, such as the cyclic AMP response‐element binding‐protein (CREB), the ternary complex factor Elk‐1, and the nuclear factor‐κ enhancer binding‐protein (NF‐κB) (Flavell & Greenberg, ; Silva, Kogan, Frankland, & Kida, ). Activation of nuclear CREB, Elk‐1 and NF‐κB, has been involved in stable learning‐associated neuronal plasticity, including long‐term potentiation (LTP), neurogenesis, neuritogenesis, and synaptogenesis (Meffert, Chang, Wiltgen, Fanselow, & Baltimore, ; Zhang & Hu, ). In this sense, mice lacking the two major CREB isoforms á and Ä (Creb‐α Δ −/−), exhibited impaired maternal behavior (Jin et al., ).…”