Profile expression of STIM2.1, a newly discovered STIM2 splice variant in immune cells, in mouse brain structures at different times of development

• Autorzy: Majewski L. , Wasilewska I. , Niemeyer B.A. , Kuznicki J.
• Języki publikacji: EN

Abstrakty

EN

INTRODUCTION: STIM1 and STIM2 mediate the process of store-operated calcium entry (SOCE) by interacting with the ion channels in the cell membrane – ORAIs. SOCE is a process by which the depletion of Ca2+ from the ER causes an influx of Ca2+ from the extracellular space to replenish the intracellular stores. In T cells there are two splice variants of STIM2 – STIM2.1 and STIM2.2, which play opposite roles in regulation of SOCE. According to a paper by Niemeyer group, STIM2.1, in contrast to STIM2.2, has an inhibitory effect on Store‑Operated Calcium Entry (SOCE). AIM(S): One of our objectives was to check the distribution of STIM2.1 and STIM2.2 in mouse brain structures at different times of development. We also investigated the influence of neuronal‑specific STIM1 and ORAI1 overexpression on STIM2 mRNA level in the brain. METHOD(S): Using quantitative RealTime-PCR we compared the expression of STIM2 isoforms in wildtype and our novel transgenic mouse lines overexpressing STIM1 or ORAI1 specifically in brain neurons. RESULTS: We show that STIM2.1 splice variant is expressed in mouse brain at a low level with the highest STIM2.1/STIM2.2 ratio in the olfactory bulbs. These are the only structures in which expression of both STIM2 splice variants increases with aging. We also observed that overexpression of STIM1 in neurons tends to modify the expression of STIM2 isoforms in a region specific manner, eg. it decreases its level in the hippocampus, while increases in substantia nigra. Neither expression of STIM2.2 nor STIM2.1 isoform was affected by ORAI1 overexpression in brain neurons. CONCLUSIONS: Our data show for the first time the expression of STIM2 isoforms in mouse brain structures at different time points. The observation that STIM1 shapes the expression of STIM2 isoforms in a region specific manner could contribute to a better understanding of the interplay between these two key elements of SOCE in neurons. FINANCIAL SUPPORT: This work was supported by funds from Maestro grant to JK from a National Science Centre (2011/02/A/NZ3/00144). The transgenesis was performed in the Laboratory of Animal Models – Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland. We thank Prof. Dr. Barbara Niemeyer for hosting MSc. Iga Wasilewska in her laboratory in the framework of Short Term Mission funded by COST BM1406 action and providing us with the primers sequence of STIM2.1 and STIM2.2.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2017
• Tom: 77
• Numer: Suppl.1
• Opis fizyczny: p.86

Twórcy

autor

Majewski L.

• Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology in Warsaw, Warsaw, Poland

autor

Wasilewska I.

• Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology in Warsaw, Warsaw, Poland

autor

Niemeyer B.A.

• Center for Integrative Physiology and Molecular Medicine, Saarland University, Homburg, Germany

autor

Kuznicki J.

• Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology in Warsaw, Warsaw, Poland