TRPC1 is required for survival and proliferation of cochlear spiral ganglion stem/progenitor cells. Issue 12 (December 2015)

• Record Type: Journal Article
• Authors: Chen, Hsin-Chien; Wang, Chih-Hung; Shih, Cheng-Ping; Chueh, Sheau-Huei; Liu, Shu-Fan; Chen, Hang-Kang; Lin, Yi-Chun
• Is Part Of: International journal of pediatric otorhinolaryngology. Volume 79:Issue 12(2015:Dec.)
• Page Start: 2290
• Page End: 2294
• Publication Date: 2015-12
• Subjects: Canonical transient receptor potential channel -- Cochlea -- Spiral ganglion neuron -- Proliferation -- Stem/progenitor cell; Otolaryngology -- Periodicals; Pediatrics -- Periodicals; Otolaryngology -- Periodicals; Pediatrics -- Periodicals; Oto-rhino-laryngologie -- Périodiques; Pédiatrie -- Périodiques; 618.9209751
• DOI: 10.1016/j.ijporl.2015.10.027
• Languages: English
• ISSNs: 0165-5876

Abstract

Abstract: Objective: The present studies were designed to test the hypothesis that canonical transient receptor potential channel 1 (TRPC1) is required for the proliferation of cochlear spiral ganglion stem/progenitor cells (SPCs). Methods and materials: TRPC1 were detected and evaluated in postnatal day 1 CBA/CaJ mice pups derived-cochlear spiral ganglion SPCs by reverse transcription-polymerase chain reaction, Western blot, immunocytochemistry, and calcium imaging. The cell viability and proliferation of the spiral ganglion SPCs following si-RNA mediated knockdown of TRPC1 or addition of TRPC channel blocker SKF9635 were compared to controls. Results: In spiral ganglion SPCs, TRPC1 was found to be the most abundantly expressed TRPC subunit and shown to contribute to store-operated calcium entry. Silencing of TRPC1 or addition of TRPC channel blockers significantly decreased the rate of cell proliferation. Conclusion: The results suggest that TRPC1 might serve as an essential molecule in regulating the proliferation of spiral ganglion SPCs.