Essential role of STIM1 in the development of cardiomyocyte hypertrophy

Ohba, Takayoshi; Watanabe, Hiroyuki; Murakami, Manabu; Sato, Takako; Ono, Koichi; Itoh, Hiroshi

doi:10.1016/j.bbrc.2009.08.117

Cited by 77 publications

(75 citation statements)

References 21 publications

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“…Ohba and colleagues were among the first to demonstrate a potential role for STIM1 in mediating cardiac hypertrophy (77). Similar to our earlier studies with PE and ANG II (38), they demonstrated that in neonatal cardiomyocytes endothelin-1 (ET-1) induced activation of SOCE, NFAT nuclear translocation, and cardiomyocyte hypertrophy; importantly, however, all were attenuated following knockdown of STIM1.…”

Section: Orai1/trpcsupporting

confidence: 68%

“…Ohba et al (77) identified STIM1 protein expression in both the neonatal and adult rat heart and, consistent with the earlier findings of Voelkers et al (130), we have recently shown the expression of both STIM1 and Orai1 protein in neonatal rat ventricular myocytes as well as in the intact adult rat heart (153). The existence of SOCE and expression of both STIM1 and Orai1 have also recently been shown to occur in HL-1 cardiomyocytes, an immortalized mouse atrial cell line (120).…”

Section: Orai1/trpcmentioning

confidence: 99%

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STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

Collins

Zhu-Mauldin

Marchase

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

108

101

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Collins HE, Zhu-Mauldin X, Marchase RB, Chatham JC. STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology. Am J Physiol Heart Circ Physiol 305: H446 -H458, 2013. First published June 21, 2013 doi:10.1152/ajpheart.00104.2013.-Store-operated Ca 2ϩ entry (SOCE) is critical for Ca 2ϩ signaling in nonexcitable cells; however, its role in the regulation of cardiomyocyte Ca 2ϩ homeostasis has only recently been investigated. The increased understanding of the role of stromal interaction molecule 1 (STIM1) in regulating SOCE combined with recent studies demonstrating the presence of STIM1 in cardiomyocytes provides support that this pathway co-exists in the heart with the more widely recognized Ca 2ϩ handling pathways associated with excitation-contraction coupling. There is now substantial evidence that STIM1-mediated SOCE plays a key role in mediating cardiomyocyte hypertrophy, both in vitro and in vivo, and there is growing support for the contribution of SOCE to Ca 2ϩ overload associated with ischemia/reperfusion injury. Here, we provide an overview of our current understanding of the molecular regulation of SOCE and discuss the evidence supporting the role of STIM1/Orai1-mediated SOCE in regulating cardiomyocyte function.store-operated Ca 2ϩ entry; stromal interaction molecule 1; orai1; cardiomyocytes STORE-OPERATED CA 2ϩ ENTRY (SOCE), also known as capacitative calcium entry (CCE), is the major mechanism of Ca 2ϩ entry in nearly all nonexcitable cells (97, 99). In addition, it is increasingly recognized to co-exist with voltage-gated Ca 2ϩ channels in excitable cells, including neurons, skeletal muscle cells, and cardiomyocytes (1,38,45,83,121). In response to inositol 1,4,5-triphosphate (IP 3 )-(43) or ryanodine receptor (RyR)-mediated (3) Ca 2ϩ release from ER/SR stores, SOCE facilitates the influx of Ca 2ϩ from the extracellular space, resulting in a sustained increase in cytosolic Ca 2ϩ levels. Thus, although one of the roles of SOCE is to rapidly refill the depleted ER/SR stores, the subsequent sustained increase in cytosolic Ca 2ϩ also regulates numerous gene transcription pathways (33,50,151). Indeed, aberrant SOCE has been observed in a growing number of diseases including severe combined immunodeficiency, acute pancreatitis, and Alzheimer's disease (86).The integration of SOCE into well-established models of Ca 2ϩ homeostasis was hampered for many years by the lack of specific molecular mediators; even as recently as 2004 there was considerable controversy as to the specific mechanisms regulating SOCE (90, 113). However, in 2005, stromal interaction molecule 1 (STIM1) was found to localize to the ER/SR membrane and shown to function as a primary mediator of SOCE (54, 102). The putative physiological and pathophysiological roles of SOCE and STIM1 that have been identified to date are summarized in Table 1. A number of studies have recently reported the presence of STIM1 in adult cardiomyocytes (37,59,153), and consistent with earlier evidence supporting a rol...

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Section: Orai1/trpcsupporting

confidence: 68%

Section: Orai1/trpcmentioning

confidence: 99%

STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

Collins

Zhu-Mauldin

Marchase

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

108

101

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“…Outside this consideration, SOCE may be an important mechanism for SR Ca 2ϩ loading in fetal and neonatal cardiomyocytes, 66 consistent with the observation that SOCE was decreased with STIM1 downregulation. 67,68 STIM1 downregulation also prevented endothelin- 69 Reactive oxygen species (ROS) generated during GPCRdependent pressure-overload hypertrophy could also contribute to TRPC channel activation in hypertrophy. TRPC3 and TRPC4 can be activated by ROS in endothelial cells, 13 and ROS activates TRPC1 in the mdx mouse, a model of muscular dystrophy.…”

Section: Regulation Of Trpc Channels In the Heartmentioning

confidence: 99%

TRPC Channels As Effectors of Cardiac Hypertrophy

Eder

Molkentin²

2011

Circulation Research

213

177

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Transient receptor potential (TRP) channels of multiple subclasses are expressed in the heart, although their functions are only now beginning to emerge, especially for the TRPC subclass that appears to regulate the cardiac hypertrophic response. Although TRP channels permeate many different cations, they are most often ascribed a specific biological function because of Ca 2؉ influx, either for microdomain signaling or to reload internal Ca 2؉ stores in the endoplasmic reticulum through a store-operated mechanism. However, adult cardiac myocytes arguably do not require store-operated Ca 2؉ entry to regulate sarcoplasmic reticulum Ca 2؉ levels and excitation-contraction coupling; hence, TRP channels expressed in the heart most likely coordinate signaling within local domains or through direct interaction with Ca 2؉ -dependent regulatory proteins. Here, we review the emerging evidence that TRP channels, especially TRPCs, are critical regulators of microdomain signaling in the heart to control pathological hypertrophy in coordination with signaling through effectors such as calcineurin and NFAT (nuclear factor of activated T cells). (Circ Res. 2011;108:265-272.)

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“…STIM1 is an endo/sarcoplasmic reticulum (ER/SR) Ca 2+ -sensitive protein that interacts with Orai1 to activate the channel function of Orai1, a Ca 2+ selective channel, and thus permit Ca 2+ entry. SOCE is clearly present in nonexcitable cells such as T lymphocytes and some excitable cells including skeletal muscle cells (4,(6)(7)(8)(9)(10)(11)(12)(13). STIM1 is a membrane-spanning ER/SR protein with a single transmembrane domain and a luminal Ca 2+ ( [Ca 2+ ] ER/SR )-sensing domain.…”

mentioning

confidence: 99%

STIM1 enhances SR Ca ²⁺ content through binding phospholamban in rat ventricular myocytes

Zhao

Brochet

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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In ventricular myocytes, the physiological function of stromal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum (ER/SR) Ca2+ sensor, is unclear with respect to its cellular localization, its Ca2+-dependent mobilization, and its action on Ca2+ signaling. Confocal microscopy was used to measure Ca2+ signaling and to track the cellular movement of STIM1 with mCherry and immunofluorescence in freshly isolated adult rat ventricular myocytes and those in short-term primary culture. We found that endogenous STIM1 was expressed at low but measureable levels along the Z-disk, in a pattern of puncta and linear segments consistent with the STIM1 localizing to the junctional SR (jSR). Depleting SR Ca2+ using thapsigargin (2–10 µM) changed neither the STIM1 distribution pattern nor its mobilization rate, evaluated by diffusion coefficient measurements using fluorescence recovery after photobleaching. Two-dimensional blue native polyacrylamide gel electrophoresis and coimmunoprecipitation showed that STIM1 in the heart exists mainly as a large protein complex, possibly a multimer, which is not altered by SR Ca2+ depletion. Additionally, we found no store-operated Ca2+ entry in control or STIM1 overexpressing ventricular myocytes. Nevertheless, STIM1 overexpressing cells show increased SR Ca2+ content and increased SR Ca2+ leak. These changes in Ca2+ signaling in the SR appear to be due to STIM1 binding to phospholamban and thereby indirectly activating SERCA2a (Sarco/endoplasmic reticulum Ca2+ ATPase). We conclude that STIM1 binding to phospholamban contributes to the regulation of SERCA2a activity in the steady state and rate of SR Ca2+ leak and that these actions are independent of store-operated Ca2+ entry, a process that is absent in normal heart cells.

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Essential role of STIM1 in the development of cardiomyocyte hypertrophy

Cited by 77 publications

References 21 publications

STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

TRPC Channels As Effectors of Cardiac Hypertrophy

STIM1 enhances SR Ca ²⁺ content through binding phospholamban in rat ventricular myocytes

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Essential role of STIM1 in the development of cardiomyocyte hypertrophy

Cited by 77 publications

References 21 publications

STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

TRPC Channels As Effectors of Cardiac Hypertrophy

STIM1 enhances SR Ca 2+ content through binding phospholamban in rat ventricular myocytes

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Product

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STIM1 enhances SR Ca ²⁺ content through binding phospholamban in rat ventricular myocytes