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Original Research: AIRWAY SMOOTH MUSCLE |

Characterization of Primary Cilia in Human Airway Smooth Muscle Cells

Jun Wu, MD; Hui Du, PhD; Xiangling Wang, PhD; Changlin Mei, MD; Gary C. Sieck, PhD; Qi Qian, MD
Author and Funding Information

From the Kidney Institute of the China People's Liberation Army (Drs. Wu and Mei), Changzheng Hospital, Second Military Medical University, Shanghai, People's Republic of China; and the Division of Nephrology and Hypertension (Drs. Du, Wang, and Qian), Department of Medicine, and the Department of Physiology and Biomedical Engineering (Drs. Sieck and Qian), Mayo Clinic College of Medicine, Rochester, MN.

Qi Qian, MD, Assistant Professor of Medicine and Physiology, Division of Nephrology and Hypertension, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905; e-mail: qian.qi@mayo.edu


This study was supported by National Institutes of Health grants DK63064 and DK073567, and Mayo Clinic Faculty Transition Research Award (Dr. Qian).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;136(2):561-570. doi:10.1378/chest.08-1549
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Background:  Considerable evidence indicates a key role for primary cilia of mammalian cells in mechanochemical sensing. Dysfunctions of primary cilia have been linked to the pathogenesis of several human diseases. However, cilia-related research has been limited to a few cell and tissue types; to our knowledge, no literature exists on primary cilia in airway smooth muscle (ASM). The aim of this study was to characterize primary cilia in human ASM.

Methods:  Primary cilia of human bronchial smooth muscle cells (HBSMCs) were examined using immunofluorescence confocal microscopy, and scanning and transmission electron microscopy. HBSMC migration and injury repair were examined by scratch-wound and epidermal growth factor (EGF)-induced migration assays.

Results:  Cross-sectional images of normal human bronchi revealed that primary cilia of HBSMCs within each ASM bundle aggregated at the same horizontal level, forming a “cilium layer.” Individual cilia of HBSMCs projected into extracellular matrix and exhibited varying degrees of deflection. Mechanochemical sensing molecules, polycystins, and α2-, α5-, and β1-integrins were enriched in cilia, as was EGF receptor, known to activate jointly with integrins during cell migration. Migration assays demonstrated a ciliary contribution to HBSMC migration and wound repair.

Conclusions:  The primary cilia of ASM cells exert a role in sensing and transducing extracellular mechanochemical signals and in ASM injury repair. Defects in ASM ciliary function could potentially affect airway wall maintenance and/or remodeling, possibly relating to the genesis of bronchiectasis in autosomal dominant polycystic kidney disease, a disease of ciliopathy.

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