Arterial Myogenic Activation through Smooth Muscle Filamin A

Kevin Retailleau, Malika Arhatte, Sophie Demolombe, Rémi Peyronnet, Véronique Baudrie, Martine Jodar, Jennifer Bourreau, Daniel Henrion, Stefan Offermanns, Fumihiko Nakamura, Yuanyi Feng, Amanda Patel, Fabrice Duprat, Eric Honoré*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


Mutations in the filamin A (FlnA) gene are frequently associated with severe arterial abnormalities, although the physiological role for this cytoskeletal element remains poorly understood in vascular cells. We used a conditional mouse model to selectively delete FlnA in smooth muscle (sm) cells at the adult stage, thus avoiding the developmental effects of the knockout. Basal blood pressure was significantly reduced in conscious smFlnA knockout mice. Remarkably, pressure-dependent tone of the resistance caudal artery was lost, whereas reactivity to vasoconstrictors was preserved. Impairment of the myogenic behavior was correlated with a lack of calcium influx in arterial myocytes upon an increase in intraluminal pressure. Notably, the stretch activation of CaV1.2 was blunted in the absence of smFlnA. In conclusion, FlnA is a critical upstream element of the signaling cascade underlying the myogenic tone. These findings allow a better understanding of the molecular basis of arterial autoregulation and associated disease states.

Original languageEnglish (US)
Pages (from-to)2050-2058
Number of pages9
JournalCell reports
Issue number9
StatePublished - Mar 8 2016

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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