Abstract
Cardiac, skeletal, and smooth muscle cells shared the common feature of contraction in response to different stimuli. Agonist-induced muscle's contraction is triggered by a cytosolic free Ca2+ concentration increase due to a rapid Ca2+ release from intracellular stores and a transmembrane Ca2+ influx, mainly through L-type Ca2+ channels. Compelling evidences have demonstrated that Ca2+ might also enter through other cationic channels such as Store-Operated Ca2+ Channels (SOCCs), involved in several physiological functions and pathological conditions. The opening of SOCCs is regulated by the filling state of the intracellular Ca2+ store, the sarcoplasmic reticulum, which communicates to the plasma membrane channels through the Stromal Interaction Molecule 1/2 (STIM1/2) protein. In muscle cells, SOCCs can be mainly non-selective cation channels formed by Orai1 and other members of the Transient Receptor Potential-Canonical (TRPC) channels family, as well as highly selective Ca2+ Release-Activated Ca2+ (CRAC) channels, formed exclusively by subunits of Orai proteins likely organized in macromolecular complexes. This review summarizes the current knowledge of the complex role of Store Operated Calcium Entry (SOCE) pathways and related proteins in the function of cardiac, skeletal, and vascular smooth muscle cells.
Highlights
This review summarizes the current knowledge of the complex role of Store Operated Calcium Entry (SOCE) pathways and related proteins in the function of cardiac, skeletal, and vascular smooth muscle cells
This study suggested that these Orai1 mutations produce constitutively active channels, permeable of Ca2+ even in the absence of store depletion
Sztretye et al showed that reduced expression of Orai1, together with Stromal Interaction Molecule-1 (STIM1) and STIM1L, correlates with a reduction in SOCE, SR calcium content and depolarization-evoked calcium release in mice with myostatin mutation (Sztretye et al, 2017)
Summary
The molecular mechanism of SOCE in VSMCs still remains intriguing (Figure 1). The first evidence of SOCE presence in VSMCs, as we mentioned previously, relies to Casteels and Droogmans studies (Casteels and Droogmans, 1981). They suggested two pathways for the transport of Ca2+ from the extracellular medium to the noradrenalin-sensitive intracellular store, one including a direct route into the store similar to Putney’s description (Putney, 1986). SOCE is essential in VSMCs because it preserves SR Ca2+ homeostasis adequately, it makes possible a proper Ca2+ signaling (Manjarrés et al, 2010). At the same time SOCE is involved in vascular disorders as essential and pulmonary hypertension or restenosis (Tanwar et al, 2017)
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