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© Christine Schmitt, Meriem El Ghachi, Jean-Marc Panaud
Bactérie Helicobacter pylori en microscopie électronique à balayage. Agent causal de pathologies de l'estomac : elle est responsable des gastrites chroniques, d'ulcères gastriques et duodénaux et elle joue un rôle important dans la genèse des cancers gastriques (adénocarcinomes et lymphomes).
Publication : Molecular and cellular biology

LIM-only protein FHL2 activates NF-κB signaling in the control of liver regeneration and hepatocarcinogenesis.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Molecular and cellular biology - 01 Aug 2013

Dahan J, Nouët Y, Jouvion G, Levillayer F, Adib-Conquy M, Cassard-Doulcier AM, Tebbi A, Blanc F, Remy L, Chen J, Cairo S, Werts C, Si-Tahar M, Tordjmann T, Buendia MA, Wei Y,

Link to Pubmed [PMID] – 23775124

Link to DOI – 10.1128/MCB.00105-13

Mol Cell Biol 2013 Aug; 33(16): 3299-308

Four-and-a-half LIM-only protein 2 (FHL2) is an important mediator in many signaling pathways. In this study, we analyzed the functions of FHL2 in nuclear factor κB (NF-κB) signaling in the liver. We show that FHL2 enhanced tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) activity in transcriptional activation of NF-κB targets by stabilizing the protein. TRAF6 is a binding partner of FHL2 and an important component of the Toll-like receptor-NF-κB pathway. Knockdown of FHL2 in 293-hTLR4/MD2-CD14 cells impaired lipopolysaccharide (LPS)-induced NF-κB activity, which regulates expression of inflammatory cytokines. Indeed, FHL2(-/-) macrophages showed significantly reduced production of TNF and interleukin 6 (IL-6) following LPS stimulation. TNF and IL-6 are the key cytokines that prime liver regeneration after hepatic injury. Following partial hepatectomy, FHL2(-/-) mice exhibited diminished induction of TNF and IL-6 and delayed hepatocyte regeneration. In the liver, NF-κB signaling orchestrates inflammatory cross talk between hepatocytes and hepatic immune cells that promote chemical hepatocarcinogenesis. We found that deficiency of FHL2 reduced susceptibility to diethylnitrosamine-induced hepatocarcinogenesis, correlating with the activator function of FHL2 in NF-κB signaling. Our findings demonstrate FHL2 as a positive regulator of NF-κB activity in liver regeneration and carcinogenesis and highlight the importance of FHL2 in both hepatocytes and hepatic immune cells.

https://pubmed.ncbi.nlm.nih.gov/23775124