Pathophysiological Significance of Store-Operated Calcium Entry in Cardiovascular and Skeletal Muscle Disorders and Angiogenesis

Ávila-Médina, Javier; Mayoral-González, Isabel; Galeano-Otero, Isabel; Redondo, Pedro C.; Rosado, Juan A.; Smani, Tarik

doi:10.1007/978-3-030-12457-1_19

Cited by 13 publications

(9 citation statements)

References 115 publications

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“…VEGF-induced increase in the intracellular Ca 2+ concentration ([Ca 2+ ] i ) was related to the activation of the store-operated calcium entry (SOCE) pathway (Li et al, 2011), which is required to the angiogenic activity in EC (Chen et al, 2016). Within the key elements of SOCE, Orai1, the pore-forming subunit of the store-operated calcium channel (SOCC), and stromal interacting molecule 1 (STIM1), are the most studied proteins (Avila-Medina et al, 2020). Both assemble to allow the activation of Ca 2+ release-activated Ca Ca 2+ (CRAC) channels, responsible for SOCE currents.…”

Section: Introductionmentioning

confidence: 99%

SARAF and Orai1 Contribute to Endothelial Cell Activation and Angiogenesis

Galeano-Otero

Khatib

Rosado

et al. 2021

Front. Cell Dev. Biol.

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Angiogenesis is a multistep process that controls endothelial cells (ECs) functioning to form new blood vessels from preexisting vascular beds. This process is tightly regulated by pro-angiogenic factors, such as vascular endothelial growth factor (VEGF), which promote signaling pathways involving the increase in the intracellular Ca2+ concentration ([Ca2+]i). Recent evidence suggests that store-operated calcium entry (SOCE) might play a role in angiogenesis. However, little is known regarding the role of SARAF, SOCE-associated regulatory factor, and Orai1, the pore-forming subunit of the store-operated calcium channel (SOCC), in angiogenesis. Here, we show that SOCE inhibition with GSK-7975A blocks aorta sprouting, as well as human umbilical vein endothelial cell (HUVEC) tube formation and migration. The intraperitoneal injection of GSK-7975A also delays the development of retinal vasculature assessed at postnatal day 6 in mice, since it reduces vessel length and the number of junctions, while it increases lacunarity. Moreover, we find that SARAF and Orai1 are involved in VEGF-mediated [Ca2+]i increase, and their knockdown using siRNA impairs HUVEC tube formation, proliferation, and migration. Finally, immunostaining and in situ proximity ligation assays indicate that SARAF likely interacts with Orai1 in HUVECs. Therefore, these findings show for the first time a functional interaction between SARAF and Orai1 in ECs and highlight their essential role in different steps of the angiogenesis process.

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Section: Introductionmentioning

confidence: 99%

SARAF and Orai1 Contribute to Endothelial Cell Activation and Angiogenesis

Galeano-Otero

Khatib

Rosado

et al. 2021

Front. Cell Dev. Biol.

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“…Post-ischemic angiogenesis is considered a protective mechanism motivated by the lack of oxygen and blood supply necessary for physiological heart repair after a MI [84,85]. Angiogenesis involves sprouting, proliferation, migration, and tube formation thanks to the stimulation of endothelial cells (ECs) by growth factors such as vascular endothelial growth factor (VEGF), considered as the most potent pro-angiogenic factor specific for ECs (reviewed elsewhere [86,87]). Compelling evidence demonstrated that chronic and transient ischemia significantly increase the expression of VEGF [88][89][90].…”

Section: Trpc Channels In Post-ischemia Angiogenesismentioning

confidence: 99%

TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease

Falcón

Galeano-Otero

Martín-Bórnez

et al. 2020

Cells

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Transient receptor potential canonical (TRPC) channels are ubiquitously expressed in excitable and non-excitable cardiac cells where they sense and respond to a wide variety of physical and chemical stimuli. As other TRP channels, TRPC channels may form homo or heterotetrameric ion channels, and they can associate with other membrane receptors and ion channels to regulate intracellular calcium concentration. Dysfunctions of TRPC channels are involved in many types of cardiovascular diseases. Significant increase in the expression of different TRPC isoforms was observed in different animal models of heart infarcts and in vitro experimental models of ischemia and reperfusion. TRPC channel-mediated increase of the intracellular Ca2+ concentration seems to be required for the activation of the signaling pathway that plays minor roles in the healthy heart, but they are more relevant for cardiac responses to ischemia, such as the activation of different factors of transcription and cardiac hypertrophy, fibrosis, and angiogenesis. In this review, we highlight the current knowledge regarding TRPC implication in different cellular processes related to ischemia and reperfusion and to heart infarction.

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“…Ca 2+ influx also affects muscle tissue development since it influences neuromuscular junction formation and their functionality through muscle nicotinic acetylcholine receptors (nAChRs) [ 61 ]. The role Ca 2+ ions play for skeletal muscle tissue integrity has been deemed so important that several studies investigated the correlation between Ca 2+ signaling, muscle growth or hypertrophy (even in the heart) and muscle stem cells proliferation in both health and disease [ 34 , 62 , 63 ].…”

Section: The Role Of Mitochondria In Muscles and Physical Activitymentioning

confidence: 99%

Sport Performance and Manual Therapies: A Review on the Effects on Mitochondrial, Sarcoplasmatic and Ca2+ Flux Response

Regno¹,

Parisi

Chiera³

et al. 2021

Healthcare

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The present narrative review aims to highlight the possible effects manual therapies could have on cells and mitochondria, as these effects could improve athletic performance management. To this aim, this review summarizes the relationship between mechanical stimulation, with a special focus on physical activity, and cell response based on the most recent mechanobiology findings. Mechanobiology analyzes how cells respond to mechanical stressors coming from the environment. Indeed, endogenous (e.g., blood pressure, heartbeat and gastrointestinal motility) and exogenous (e.g., physical activity and manual therapies) stimuli can induce biochemical and epigenetic modifications that alter protein synthesis with heavy consequences on cell behavior. Mechanical stress can also influence mitochondrial behavior (i.e., biogenesis, autophagy, fusion, fission and energy production), sarcoplasmic response and calcium ion (Ca2+) flux. Since manual therapies have been shown to affect the extracellular matrix, which represents a primary source of mechanical stress that may alter both the cytoskeleton and mitochondrial metabolism, it is conceivable manual therapies could also affect cellular and mitochondrial behavior. Lastly, by suggesting possible directions for future laboratory and clinical studies, the authors expect this review to inspire further research on how manual therapies could affect bioenergetic metabolism and, thus, athletic performance.

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Pathophysiological Significance of Store-Operated Calcium Entry in Cardiovascular and Skeletal Muscle Disorders and Angiogenesis

Cited by 13 publications

References 115 publications

SARAF and Orai1 Contribute to Endothelial Cell Activation and Angiogenesis

SARAF and Orai1 Contribute to Endothelial Cell Activation and Angiogenesis

TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease

Sport Performance and Manual Therapies: A Review on the Effects on Mitochondrial, Sarcoplasmatic and Ca2+ Flux Response

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