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1 Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, USA; Baltimore Veterans Affairs Medical Center, Baltimore, MD, USA
2 MedicineDepartment of, University of California, San Diego, La Jolla, CA, USA
3 Department of Physiology, University of Maryland School of Medicine, Baltimore, MD, USA
4 Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, USA; Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA; Baltimore Veterans Affairs Medical Center, Baltimore, MD, USA
5 Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, USA; Department of Physiology, University of Maryland School of Medicine, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: jwang{at}smail.umaryland.edu.
An increase in cytosolic free Ca2+ concentration ([Ca2+]cyt) results from Ca2+ release from intracellular stores and extracellular Ca2+ influx through Ca2+ permeable ion channels and is crucial for initiating intestinal epithelial restitution to reseal superficial wounds after mucosal injury. Capacitative Ca2+ entry (CCE) induced by Ca2+ store depletion represents a major Ca2+ influx mechanism, but the exact molecular components constituting this process remain elusive. This study determined whether TRPC1 (canonical transient receptor potential-1) served as a candidate protein for Ca2+-permeable channels mediating CCE in intestinal epithelial cells and played an important role in early epithelial restitution. Normal intestinal epithelial cells (IEC-6 line) expressed TRPC1 and TPRC5 and displayed typical records of whole cell store-operated Ca2+ currents (Isoc) and CCE generated by Ca2+ influx after depletion of intracellular stores. Induced TRPC1 expression by stable transfection with the TRPC1 gene increased CCE and enhanced cell migration during restitution. Differentiated IEC-Cdx2L1 cells induced by forced expression of the Cdx2 gene highly expressed endogenous TRPC1 and TRPC5 and exhibited increased CCE and cell migration. Inhibition of TRPC1 expression by small interfering RNA specially targeting TRPC1 not only reduced CCE but also inhibited cell migration after wounding. These findings strongly suggest that TRPC1 functions as the store-operated Ca2+ channels and plays a critical role in intestinal epithelial restitution by regulating CCE and intracellular [Ca2+]cyt.
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