Noisy transcription factor NF-¿B oscillations stabilize and sensitize cytokine signaling in space
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Noisy transcription factor NF-¿B oscillations stabilize and sensitize cytokine signaling in space. / Gangstad, S.W.; Feldager, C.W.; Juul, Jeppe Søgaard; Trusina, A.
I: Physical Review E (Statistical, Nonlinear, and Soft Matter Physics), Bind 87, Nr. 2, 05.02.2013, s. 022702.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - Noisy transcription factor NF-¿B oscillations stabilize and sensitize cytokine signaling in space
AU - Gangstad, S.W.
AU - Feldager, C.W.
AU - Juul, Jeppe Søgaard
AU - Trusina, A.
PY - 2013/2/5
Y1 - 2013/2/5
N2 - NF-¿B is a major transcription factor mediating inflammatory response. In response to a pro-inflammatory stimulus, it exhibits a characteristic response - a pulse followed by noisy oscillations in concentrations of considerably smaller amplitude. NF-¿B is an important mediator of cellular communication, as it is both activated by and upregulates production of cytokines, signals used by white blood cells to find the source of inflammation. While the oscillatory dynamics of NF-¿B has been extensively investigated both experimentally and theoretically, the role of the noise and the lower secondary amplitude has not been addressed. We use a cellular automaton model to address these issues in the context of spatially distributed communicating cells. We find that noisy secondary oscillations stabilize concentric wave patterns, thus improving signal quality. Furthermore, both lower secondary amplitude as well as noise in the oscillation period might be working against chronic inflammation, the state of self-sustained and stimulus-independent excitations. Our findings suggest that the characteristic irregular secondary oscillations of lower amplitude are not accidental. On the contrary, they might have evolved to increase robustness of the inflammatory response and the system's ability to return to a pre-stimulated state.
AB - NF-¿B is a major transcription factor mediating inflammatory response. In response to a pro-inflammatory stimulus, it exhibits a characteristic response - a pulse followed by noisy oscillations in concentrations of considerably smaller amplitude. NF-¿B is an important mediator of cellular communication, as it is both activated by and upregulates production of cytokines, signals used by white blood cells to find the source of inflammation. While the oscillatory dynamics of NF-¿B has been extensively investigated both experimentally and theoretically, the role of the noise and the lower secondary amplitude has not been addressed. We use a cellular automaton model to address these issues in the context of spatially distributed communicating cells. We find that noisy secondary oscillations stabilize concentric wave patterns, thus improving signal quality. Furthermore, both lower secondary amplitude as well as noise in the oscillation period might be working against chronic inflammation, the state of self-sustained and stimulus-independent excitations. Our findings suggest that the characteristic irregular secondary oscillations of lower amplitude are not accidental. On the contrary, they might have evolved to increase robustness of the inflammatory response and the system's ability to return to a pre-stimulated state.
UR - http://www.scopus.com/inward/record.url?scp=84873658947&partnerID=8YFLogxK
U2 - 10.1103/PhysRevE.87.022702
DO - 10.1103/PhysRevE.87.022702
M3 - Journal article
AN - SCOPUS:84873658947
VL - 87
SP - 022702
JO - Physical Review E
JF - Physical Review E
SN - 2470-0045
IS - 2
ER -
ID: 45773220