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Moruzzi, N. ; Valladolid-Acebes, I.* ; Kannabiran, S.A. ; Bulgaro, S.* ; Burtscher, I. ; Leibiger, B.* ; Leibiger, I.B.* ; Berggren, P.O.* ; Brismar, K.*

Mitochondrial impairment and intracellular reactive oxygen species alter primary cilia morphology.

Life Sci. All. 5:e202201505 (2022)
Verlagsversion DOI
Open Access Gold
Creative Commons Lizenzvertrag
Primary cilia have recently emerged as cellular signaling organelles. Their homeostasis and function require a high amount of energy. However, how energy depletion and mitochondria impairment affect cilia have barely been addressed. We first studied the spatial relationship between a mitochondria subset in proximity to the cilium in vitro, finding similar mitochondrial activity measured as mitochondrial membrane potential compared with the cellular network. Next, using common primary cilia cell models and inhibitors of mitochondrial energy production, we found alterations in cilia number and/or length due to energy depletion and mitochondrial reactive oxygen species (ROS) overproduction. Finally, by using a mouse model of type 2 diabetes mellitus, we provided in vivo evidence that cilia morphology is impaired in diabetic nephropathy, which is characterized by ROS overproduction and impaired mitochondrial metabolism. In conclusion, we showed that energy imbalance and mitochondrial ROS affect cilia morphology and number, indicating that conditions characterized by mitochondria and radicals imbalances might lead to ciliary impairment.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 2575-1077
e-ISSN 2575-1077
Zeitschrift Life Science Alliance
Quellenangaben Band: 5, Heft: 12, Seiten: , Artikelnummer: e202201505 Supplement: ,
Verlag EMBO Press
Verlagsort Heidelberg
Begutachtungsstatus Peer reviewed