Role of STIM1 in survival and neural differentiation of mouse embryonic stem cells independent of Orai1-mediated Ca2+ entry

Baixia Hao, Yingying Lu, Qian Wang, Wenjing Guo, King-Ho Cheung, Jianbo Yue*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

24 Citations (Scopus)

Abstract

Store-operated Ca2 + entry (SOCE) is an important Ca2 + influx pathway in non-excitable cells. STIM1, an ER Ca2 + sensor, and Orai1, a plasma membrane Ca2 + selective channel, are the two essential components of the Ca2 + release activated channel (CRAC) responsible for SOCE activity. Here we explored the role of STIM1 and Orai1 in neural differentiation of mouse embryonic stem (ES) cells. We found that STIM1 and Orai1 were expressed and functionally active in ES cells, and expressions of STIM1 and Orai1 were dynamically regulated during neural differentiation of mouse ES cells. STIM1 knockdown inhibited the differentiation of mouse ES cells into neural progenitors, neurons, and astrocytes. In addition, STIM1 knockdown caused severe cell death and markedly suppressed the proliferation of neural progenitors. Surprisingly, Orai1 knockdown had little effect on neural differentiation of mouse ES cells, but the neurons derived from Orai1 knockdown ES cells, like those from STIM1 knockdown cells, had defective SOCE. Taken together, our data indicate that STIM1 is involved in both early neural differentiation of ES cells and survival of early differentiated ES cells independent of Orai1-mediated SOCE.
Original languageEnglish
Pages (from-to)452-466
Number of pages15
JournalStem Cell Research
Volume12
Issue number2
DOIs
Publication statusPublished - Mar 2014

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