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Intercellular coupling between peripheral circadian oscillators by TGF-β signaling.

Anna-Marie Finger1,2, Sebastian Jäschke3,2, Marta Del Olmo4

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Peripheral circadian clocks synchronize through paracrine signaling, with transforming growth factor-beta (TGF-β) identified as a key factor. This discovery sheds light on maintaining rhythmic organ functions and circadian health.

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Area of Science:

  • Chronobiology
  • Molecular Biology
  • Cellular Physiology

Background:

  • Cell-autonomous circadian oscillators require coupling to prevent desynchronization and maintain tissue function.
  • Intercellular coupling is established in the central nervous system's suprachiasmatic nucleus, but mechanisms in peripheral tissues remain unclear.

Purpose of the Study:

  • To investigate the mechanisms of coupling between peripheral circadian oscillators.
  • To identify molecular factors mediating this peripheral coupling.

Main Methods:

  • Utilized in vitro (mammalian cell cultures, U-2 OS cells) and ex vivo models.
  • Investigated paracrine signaling pathways.
  • Analyzed the role of transforming growth factor-beta (TGF-β) in regulating core-clock genes.

Main Results:

  • Peripheral oscillators are coupled via paracrine pathways.
  • Transforming growth factor-beta (TGF-β) acts as a peripheral coupling factor, adjusting molecular clock phases.
  • TGF-β mediates clock synchrony through transcriptional regulation of core-clock genes.
  • Disruption of TGF-β signaling leads to oscillator desynchronization, reduced amplitude, and increased sensitivity to external cues.

Conclusions:

  • Peripheral circadian clocks synchronize through TGF-β-mediated paracrine signaling.
  • This mechanism is essential for maintaining rhythmic organ function and overall circadian health.