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Peer-reviewedCC BY 4.0Physiological Genomics

Differential gene transcription following intravenous injection of air bubbles in rats with varying resistance to decompression sickness

  • Jérémy Orsat
  • Emmanuel Gouin
  • Anthony Guernec
  • Costantino Balestra
  • Michaël Théron
  • Géraldine Leman
  • François Guerrero
Open at sourcePDFDOICite

Abstract

This study suggests for the first time that DCS resistance may be associated with a better tolerance to VGE. This greater DCS resistance could be achieved through improved control of the procoagulant effects of bubbles via TFPI-dependent inhibitory mechanisms and an enhanced cellular stress response to VGE by HSP70, HSP27, and EGR-1. It also suggests that it may be possible to stratify the individual DCS risk based on the thromboinflammatory response to bubbles.

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Cite

BibTeXRIS
BibTeX
@article{orsat2026differential,
  title = {{Differential gene transcription following intravenous injection of air bubbles in rats with varying resistance to decompression sickness}},
  author = {Jérémy Orsat and Emmanuel Gouin and Anthony Guernec and Costantino Balestra and Michaël Théron and Géraldine Leman and François Guerrero},
  journal = {Physiological Genomics},
  year = {2026},
  month = jul,
  doi = {10.1152/physiolgenomics.00082.2026},
  url = {https://hal.science/hal-05828394v1},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Differential gene transcription following intravenous injection of air bubbles in rats with varying resistance to decompression sickness
AU  - Jérémy Orsat
AU  - Emmanuel Gouin
AU  - Anthony Guernec
AU  - Costantino Balestra
AU  - Michaël Théron
AU  - Géraldine Leman
AU  - François Guerrero
PY  - 2026
DA  - 2026/07/01
JO  - Physiological Genomics
DO  - 10.1152/physiolgenomics.00082.2026
UR  - https://hal.science/hal-05828394v1
AB  - This study suggests for the first time that DCS resistance may be associated with a better tolerance to VGE. This greater DCS resistance could be achieved through improved control of the procoagulant effects of bubbles via TFPI-dependent inhibitory mechanisms and an enhanced cellular stress response to VGE by HSP70, HSP27, and EGR-1. It also suggests that it may be possible to stratify the individual DCS risk based on the thromboinflammatory response to bubbles.
SN  - 1094-8341
SN  - 1531-2267
ER  -