Wiley Interdiscip Rev Syst Biol Med - Decoding the functions of post-transcriptional regulators in the determination of inflammatory states: focus on macrophage activation.

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Resumo

Inflammation involves a continuum of intercellular interactions and cellular responses targeting infectious or tissue damage while maintaining homeostasis. At its core, this continuum encompasses the alternating phenotypes of innate immune cells; each phenotype is typified by the expression of molecules which either support host defence or aid tissue restoration and the resolution of inflammation. The aberrant persistence of any such phenotype can drive chronic inflammatory pathology. For macrophages, these phenotypes arise as changes in cellular plasticity because of adaptation. As such their underlying gene expression programs may not be determined by robust transcriptomic and epigenetic programs but by more flexible means like post-transcriptional mechanisms affecting mRNA use. These mechanisms require the assemblies of RNA-binding proteins (RBPs) and non-coding RNAs onto specific elements on their RNA targets in Ribonucleoprotein particles (RNPs) which control mRNA maturation, turnover and translation. The collection of RNPs within a cell defines the ribonome, that is, a high order system of coordinative post-transcriptional determination. mRNAs involved in the definition of different macrophage activation phenotypes share elements of RBP recognition rendering them amenable to ribonomic regulation. The molecular features of their cognitive RBPs and the pathologies developing in the corresponding mouse mutants support their involvement in inflammatory reactions. We view this information in the context of macrophage activation states to propose that these states can be determined via differential--synergistic or antagonistic--RNP associations. In doing so, we substantiate the need for the use of systems platforms to model RNP hierarchies controlling the continuum of inflammation.

Resumo Limpo

inflamm involv continuum intercellular interact cellular respons target infecti tissu damag maintain homeostasi core continuum encompass altern phenotyp innat immun cell phenotyp typifi express molecul either support host defenc aid tissu restor resolut inflamm aberr persist phenotyp can drive chronic inflammatori patholog macrophag phenotyp aris chang cellular plastic adapt under gene express program may determin robust transcriptom epigenet program flexibl mean like posttranscript mechan affect mrna use mechan requir assembl rnabind protein rbps noncod rnas onto specif element rna target ribonucleoprotein particl rnps control mrna matur turnov translat collect rnps within cell defin ribonom high order system coordin posttranscript determin mrnas involv definit differ macrophag activ phenotyp share element rbp recognit render amen ribonom regul molecular featur cognit rbps patholog develop correspond mous mutant support involv inflammatori reaction view inform context macrophag activ state propos state can determin via differentialsynergist antagonisticrnp associ substanti need use system platform model rnp hierarchi control continuum inflamm

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