What is a biological oscillator?

1984 ◽  
Vol 246 (6) ◽  
pp. R847-R853 ◽  
Author(s):  
W. O. Friesen ◽  
G. D. Block

Biological oscillators are amenable to qualitative analysis even before they have been described exhaustively in quantitative terms. Qualitative analysis can identify the elements essential for generating the oscillations and can enhance our understanding of underlying oscillator mechanisms. Two essential elements of a biological oscillator are 1) an inhibitory feedback loop, which includes one or more oscillating variables, and 2) a source of delay in this feedback loop, which allows an oscillating variable to overshoot a steady-state value before the feedback inhibition is fully effective. The analysis of the patterns of interactions and delays observed in biological oscillators is simplified by the translation of variables, interactions, and delays into schematic representations. To illustrate how such translations can be implemented, three biological oscillators are described schematically: 1) the glycolytic oscillator, 2) the bursting of the molluscan neuron, R15, and 3) the oscillations underlying smooth muscle contractions.

2006 ◽  
Vol 175 (4S) ◽  
pp. 63-63 ◽  
Author(s):  
Stephanie Oger ◽  
Delphine Behr-Roussel ◽  
Jacques Bernabe ◽  
Pierre Denys ◽  
Eva Camperat ◽  
...  

2014 ◽  
Vol 1 ◽  
pp. 636-639
Author(s):  
Fernanda S. Matias ◽  
Pedro V. Carelli ◽  
Claudio R. Mirasso ◽  
Mauro Copelli

1992 ◽  
Vol 23 (2) ◽  
pp. 211-215 ◽  
Author(s):  
Shigeru Hishinuma ◽  
Ikuko Hongo ◽  
Masaatsu K. Uchida ◽  
Masanori Kurokawa

CHEST Journal ◽  
1992 ◽  
Vol 102 (4) ◽  
pp. 1251-1257 ◽  
Author(s):  
Kunihiko Iizuka ◽  
Kunio Dobashi ◽  
Shinobu Houjou ◽  
Hiromi Sakai ◽  
Kouichi Itoh ◽  
...  

2022 ◽  
Vol 23 (2) ◽  
pp. 867
Author(s):  
Sebastian F. Mause ◽  
Elisabeth Ritzel ◽  
Annika Deck ◽  
Felix Vogt ◽  
Elisa A. Liehn

Endothelial progenitor cells (EPCs) are involved in vascular repair and modulate properties of smooth muscle cells (SMCs) relevant for their contribution to neointima formation following injury. Considering the relevant role of the CXCL12–CXCR4 axis in vascular homeostasis and the potential of EPCs and SMCs to release CXCL12 and express CXCR4, we analyzed the engagement of the CXCL12–CXCR4 axis in various modes of EPC–SMC interaction relevant for injury- and lipid-induced atherosclerosis. We now demonstrate that the expression and release of CXCL12 is synergistically increased in a CXCR4-dependent mechanism following EPC–SMC interaction during co-cultivation or in response to recombinant CXCL12, thus establishing an amplifying feedback loop Additionally, mechanical injury of SMCs induces increased release of CXCL12, resulting in enhanced CXCR4-dependent recruitment of EPCs to SMCs. The CXCL12–CXCR4 axis is crucially engaged in the EPC-triggered augmentation of SMC migration and the attenuation of SMC apoptosis but not in the EPC-mediated increase in SMC proliferation. Compared to EPCs alone, the alliance of EPC–SMC is superior in promoting the CXCR4-dependent proliferation and migration of endothelial cells. When direct cell–cell contact is established, EPCs protect the contractile phenotype of SMCs via CXCL12–CXCR4 and reverse cholesterol-induced transdifferentiation toward a synthetic, macrophage-like phenotype. In conclusion we show that the interaction of EPCs and SMCs unleashes a CXCL12–CXCR4-based autoregulatory feedback loop promoting regenerative processes and mediating SMC phenotype control to potentially guard vascular homeostasis.


2012 ◽  
Vol 38 (7) ◽  
pp. 1004-1010 ◽  
Author(s):  
Shoko Tsuji ◽  
Katsuhiko Yasuda ◽  
Genichiro Sumi ◽  
Hisayuu Cho ◽  
Tomoko Tsuzuki ◽  
...  

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