PMID- 36503009
OWN - NLM
STAT- MEDLINE
DCOM- 20230102
LR  - 20230217
IS  - 1879-2596 (Electronic)
IS  - 0167-4889 (Linking)
VI  - 1870
IP  - 2
DP  - 2023 Feb
TI  - Functions and cellular signaling by ribosomal extracellular RNA (rexRNA): Facts 
      and hypotheses on a non-typical DAMP.
PG  - 119408
LID - S0167-4889(22)00200-2 [pii]
LID - 10.1016/j.bbamcr.2022.119408 [doi]
AB  - Upon microbial infections with the subsequent host response of innate immunity, a 
      variety of fragmented RNA- and DNA-based "Pathogen-associated molecular patterns" 
      (PAMPs) are recognized mainly by endosomal or cytoplasmic host cell "Pattern 
      recognition receptors" (PRRs), particularly "Toll-like receptors" (TLRs). 
      Concomitantly, various self-extracellular RNA species (exRNAs) are present in 
      extracellular body fluids where they contribute to diverse physiological and 
      homeostatic processes. In principle, such exRNAs, including the most abundant 
      one, ribosomal exRNA (rexRNA), are designated as "Danger-associated molecular 
      patterns" (DAMPs) and are prevented by e.g. natural modifications from 
      uncontrolled signaling via TLRs to avoid hyper-inflammatory responses or 
      autoimmunity. Upon cellular stress or tissue damage/necrosis, the levels and 
      composition of released self-exRNA species, either in free form, in complex with 
      proteins or in association with extracellular vesicles (EVs), can change 
      considerably. Among the self-exRNAs, rexRNA is considered as a non-typical DAMP, 
      since it may induce inflammatory responses by cell membrane receptors, both in 
      the absence or presence of PAMPs. Yet, its mode of receptor activation to mount 
      inflammatory responses remains obscure. RexRNA also serves as a universal 
      damaging factor in cardiovascular and other diseases independent of PRRs. In 
      general, RNase1 provides a profound antagonist in these pathologies and in 
      rexRNA-mediated inflammatory cell responses. Based on the extrapolation of the 
      here described aspects of rexRNA-biology, further activities of this molecular 
      entity are hypothesized that may stimulate additional research in this area.
CI  - Copyright (c) 2022 Elsevier B.V. All rights reserved.
FAU - Preissner, Klaus T
AU  - Preissner KT
AD  - Kerckhoff-Heart Research Institute, Justus-Liebig-University, Giessen, Germany.
FAU - Fischer, Silvia
AU  - Fischer S
AD  - Department of Biochemistry, Medical Faculty, Justus-Liebig-University, Giessen, 
      Germany. Electronic address: Silvia.Fischer@biochemie.med.uni-giessen.de.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20221209
PL  - Netherlands
TA  - Biochim Biophys Acta Mol Cell Res
JT  - Biochimica et biophysica acta. Molecular cell research
JID - 101731731
RN  - 0 (RNA, Ribosomal)
RN  - 0 (Pathogen-Associated Molecular Pattern Molecules)
RN  - 0 (Receptors, Pattern Recognition)
RN  - 63231-63-0 (RNA)
RN  - 0 (Alarmins)
SB  - IM
MH  - *RNA, Ribosomal/genetics
MH  - *Pathogen-Associated Molecular Pattern Molecules
MH  - Immunity, Innate
MH  - Receptors, Pattern Recognition/metabolism
MH  - RNA/genetics
MH  - Alarmins/genetics
OTO - NOTNLM
OT  - Danger-associated molecular patterns
OT  - Extracellular nucleic acids
OT  - Inflammation
OT  - Pattern recognition receptors
OT  - RNase1
OT  - Ribosomal RNA
OT  - Toll-like receptors
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2022/12/13 06:00
MHDA- 2023/01/03 06:00
CRDT- 2022/12/12 08:58
PHST- 2022/07/12 00:00 [received]
PHST- 2022/11/07 00:00 [revised]
PHST- 2022/11/30 00:00 [accepted]
PHST- 2022/12/13 06:00 [pubmed]
PHST- 2023/01/03 06:00 [medline]
PHST- 2022/12/12 08:58 [entrez]
AID - S0167-4889(22)00200-2 [pii]
AID - 10.1016/j.bbamcr.2022.119408 [doi]
PST - ppublish
SO  - Biochim Biophys Acta Mol Cell Res. 2023 Feb;1870(2):119408. doi: 
      10.1016/j.bbamcr.2022.119408. Epub 2022 Dec 9.