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Role of the store-operated calcium entry proteins Stim1 and Orai1 in muscarinic cholinergic receptor-stimulated calcium oscillations in human embryonic kidney cells.
J Physiol. 2007 Mar 15; 579(Pt 3):679-89.JP

Abstract

We have investigated the nature of the Ca2+ entry supporting [Ca2+]i oscillations in human embryonic kidney (HEK293) cells by examining the roles of recently described store-operated Ca2+ entry proteins, Stim1 and Orai1. Knockdown of Stim1 by RNA interference (RNAi) reduced the frequency of [Ca2+]i oscillations in response to a low concentration of methacholine to the level seen in the absence of external Ca2+. However, knockdown of Stim1 did not block oscillations in canomical transient receptor potential 3 channel (TRPC3)-expressing cells and did not affect Ca2+ entry in response to arachidonic acid. The effects of knockdown of Stim1 could be reversed by inhibiting Ca2+ extrusion with a high concentration of Gd3+, or by rescuing the knockdown by overexpression of Stim1. Similarly, knockdown of Orai1 abrogated [Ca2+]i oscillations, and this was reversed by use of high concentrations of Gd3+; however, knockdown of Orai1 did not affect arachidonic acid-activated entry. RNAi targeting 34 members of the transient receptor potential (TRP) channel superfamily did not reveal a role for any of these channel proteins in store-operated Ca2+ entry in HEK293 cells. These findings indicate that the Ca2+ entry supporting [Ca2+]i oscillations in HEK293 cells depends upon the Ca2+ sensor, Stim1, and calcium release-activated Ca2+ channel protein, Orai1, and provide further support for our conclusion that it is the store-operated mechanism that plays the major role in this pathway.

Authors+Show Affiliations

Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Intramural

Language

eng

PubMed ID

17218358

Citation

Wedel, Barbara, et al. "Role of the Store-operated Calcium Entry Proteins Stim1 and Orai1 in Muscarinic Cholinergic Receptor-stimulated Calcium Oscillations in Human Embryonic Kidney Cells." The Journal of Physiology, vol. 579, no. Pt 3, 2007, pp. 679-89.
Wedel B, Boyles RR, Putney JW, et al. Role of the store-operated calcium entry proteins Stim1 and Orai1 in muscarinic cholinergic receptor-stimulated calcium oscillations in human embryonic kidney cells. J Physiol. 2007;579(Pt 3):679-89.
Wedel, B., Boyles, R. R., Putney, J. W., & Bird, G. S. (2007). Role of the store-operated calcium entry proteins Stim1 and Orai1 in muscarinic cholinergic receptor-stimulated calcium oscillations in human embryonic kidney cells. The Journal of Physiology, 579(Pt 3), 679-89.
Wedel B, et al. Role of the Store-operated Calcium Entry Proteins Stim1 and Orai1 in Muscarinic Cholinergic Receptor-stimulated Calcium Oscillations in Human Embryonic Kidney Cells. J Physiol. 2007 Mar 15;579(Pt 3):679-89. PubMed PMID: 17218358.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of the store-operated calcium entry proteins Stim1 and Orai1 in muscarinic cholinergic receptor-stimulated calcium oscillations in human embryonic kidney cells. AU - Wedel,Barbara, AU - Boyles,Rebecca R, AU - Putney,James W,Jr AU - Bird,Gary S, Y1 - 2007/01/11/ PY - 2007/1/16/pubmed PY - 2007/5/17/medline PY - 2007/1/16/entrez SP - 679 EP - 89 JF - The Journal of physiology JO - J Physiol VL - 579 IS - Pt 3 N2 - We have investigated the nature of the Ca2+ entry supporting [Ca2+]i oscillations in human embryonic kidney (HEK293) cells by examining the roles of recently described store-operated Ca2+ entry proteins, Stim1 and Orai1. Knockdown of Stim1 by RNA interference (RNAi) reduced the frequency of [Ca2+]i oscillations in response to a low concentration of methacholine to the level seen in the absence of external Ca2+. However, knockdown of Stim1 did not block oscillations in canomical transient receptor potential 3 channel (TRPC3)-expressing cells and did not affect Ca2+ entry in response to arachidonic acid. The effects of knockdown of Stim1 could be reversed by inhibiting Ca2+ extrusion with a high concentration of Gd3+, or by rescuing the knockdown by overexpression of Stim1. Similarly, knockdown of Orai1 abrogated [Ca2+]i oscillations, and this was reversed by use of high concentrations of Gd3+; however, knockdown of Orai1 did not affect arachidonic acid-activated entry. RNAi targeting 34 members of the transient receptor potential (TRP) channel superfamily did not reveal a role for any of these channel proteins in store-operated Ca2+ entry in HEK293 cells. These findings indicate that the Ca2+ entry supporting [Ca2+]i oscillations in HEK293 cells depends upon the Ca2+ sensor, Stim1, and calcium release-activated Ca2+ channel protein, Orai1, and provide further support for our conclusion that it is the store-operated mechanism that plays the major role in this pathway. SN - 0022-3751 UR - https://www.unboundmedicine.com/medline/citation/17218358/Role_of_the_store_operated_calcium_entry_proteins_Stim1_and_Orai1_in_muscarinic_cholinergic_receptor_stimulated_calcium_oscillations_in_human_embryonic_kidney_cells_ L2 - https://doi.org/10.1113/jphysiol.2006.125641 DB - PRIME DP - Unbound Medicine ER -