Murine cardiac growth, TRPC channels, and cGMP kinase I
Domes K, Patrucco E, Loga F, Dietrich A, Birnbaumer L, Wegener J, Hofmann F (2015)
Pflügers Archiv - European Journal of Physiology 467(10): 2229-2234.
Zeitschriftenaufsatz
| Veröffentlicht | Englisch
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Autor*in
Domes, Katrin;
Patrucco, Enrico;
Loga, Florian;
Dietrich, Alexander;
Birnbaumer, Lutz;
Wegener, JörgUniBi
;
Hofmann, Franz
![](https://pub.uni-bielefeld.de/images/icon_orcid.png)
Abstract / Bemerkung
Signaling via cGMP-dependent protein kinase I (cGKI) and canonical transient receptor potential (TRPC) channels appears to be involved in the regulation of cardiac hypertrophy. Recent evidence suggests that TRPC channels are targets for cGKI, and phosphorylation of these channels may mediate the antihypertrophic effects of cGMP signaling. We tested this concept by investigating the role of cGMP/cGKI signaling on angiotensin II (A II)-induced cardiac hypertrophy using a control group (Ctr), trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM mice, and trpc3−/−/6−/− × βRM mice. βRM mice express cGKIβ only in the smooth muscle on a cGKI−/− background. The control group was composed of littermate mice that contained at least one wild type gene of the respective genotype. A II was infused by minipumps (7 days; 2 mg/kg/day) in Ctr, trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM, and trpc3−/−/6−/− × βRM mice. Hypertrophy was assessed by measuring heart weight per tibia length (HW/TL) and fibrosis by staining of heart slices. A II-induced increase in HW/TL and fibrosis was absent in trpc3−/− mice, whereas an increase in HW/TL and fibrosis was evident in Ctr and trpc6−/−, minimal or absent in trpc3−/−, moderate in βRM, and dramatic in trpc3−/−/6−/− βRM mice. These results suggest that TRPC3 may be necessary for A II-induced cardiac hypertrophy. On the other hand, hypertrophy and fibrosis were massively increased in βRM mice on a TRPC3/6 × cGKI−/−KO background, indicating an “additive” coupling between both signaling pathways.
Erscheinungsjahr
2015
Zeitschriftentitel
Pflügers Archiv - European Journal of Physiology
Band
467
Ausgabe
10
Seite(n)
2229-2234
ISSN
0031-6768
eISSN
1432-2013
Page URI
https://pub.uni-bielefeld.de/record/2984476
Zitieren
Domes K, Patrucco E, Loga F, et al. Murine cardiac growth, TRPC channels, and cGMP kinase I. Pflügers Archiv - European Journal of Physiology. 2015;467(10):2229-2234.
Domes, K., Patrucco, E., Loga, F., Dietrich, A., Birnbaumer, L., Wegener, J., & Hofmann, F. (2015). Murine cardiac growth, TRPC channels, and cGMP kinase I. Pflügers Archiv - European Journal of Physiology, 467(10), 2229-2234. https://doi.org/10.1007/s00424-014-1682-0
Domes, Katrin, Patrucco, Enrico, Loga, Florian, Dietrich, Alexander, Birnbaumer, Lutz, Wegener, Jörg, and Hofmann, Franz. 2015. “Murine cardiac growth, TRPC channels, and cGMP kinase I”. Pflügers Archiv - European Journal of Physiology 467 (10): 2229-2234.
Domes, K., Patrucco, E., Loga, F., Dietrich, A., Birnbaumer, L., Wegener, J., and Hofmann, F. (2015). Murine cardiac growth, TRPC channels, and cGMP kinase I. Pflügers Archiv - European Journal of Physiology 467, 2229-2234.
Domes, K., et al., 2015. Murine cardiac growth, TRPC channels, and cGMP kinase I. Pflügers Archiv - European Journal of Physiology, 467(10), p 2229-2234.
K. Domes, et al., “Murine cardiac growth, TRPC channels, and cGMP kinase I”, Pflügers Archiv - European Journal of Physiology, vol. 467, 2015, pp. 2229-2234.
Domes, K., Patrucco, E., Loga, F., Dietrich, A., Birnbaumer, L., Wegener, J., Hofmann, F.: Murine cardiac growth, TRPC channels, and cGMP kinase I. Pflügers Archiv - European Journal of Physiology. 467, 2229-2234 (2015).
Domes, Katrin, Patrucco, Enrico, Loga, Florian, Dietrich, Alexander, Birnbaumer, Lutz, Wegener, Jörg, and Hofmann, Franz. “Murine cardiac growth, TRPC channels, and cGMP kinase I”. Pflügers Archiv - European Journal of Physiology 467.10 (2015): 2229-2234.