Silencing stromal interaction molecule 1 by RNA interference inhibits the proliferation and migration of endothelial progenitor cells

Kuang, Chunyan; Yu, Yang; Guo, R. S.; Qian, Dehui; Wang, Kui; den, M. Boer; Shi, Yankun; Huang, Lan

doi:10.1016/j.bbrc.2010.06.088

Cited by 44 publications

(40 citation statements)

References 26 publications

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“…Based on the importance of TRPC1 for vascular function, we focused on the role of TRPC1 in EPCs, which are important for repairing endothelial damage after vascular injury. Interestingly, our earlier work found that TRPC1-SOCs were involved in STIM1-induced Ca 2 + influx in EPCs [12]. Moreover, in the present study, we demonstrated that downregulation of TRPC1 by 2 different RNA silencing methods suppressed EPC proliferation and migration and decreased SOCE in vitro.…”

Section: Kuang Et Alsupporting

confidence: 64%

“…EPCs (2 · 10 5 ) at 48 h after transfection in 100 mL serum-free DMEM-L) were placed in the upper chamber. DMEM-L with 20% FCS was added to the lower chamber [12]. After 6 h, cells on top of the 8 mm filters were removed, and the filters were rinsed with PBS.…”

Section: Cell Migration Assaymentioning

confidence: 99%

“…Because EPCs can reduce neointimal formation after vascular injury, we hypothesize that TRPC1 can regulate the function of EPCs. Previously, we reported that TRPC1 is expressed in EPCs and cooperates with STIM1 to mediate the SOCE of EPCs [12]. However, the exact role of TRPC1 in EPCs is unclear.…”

mentioning

confidence: 99%

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Knockdown of Transient Receptor Potential Canonical-1 Reduces the Proliferation and Migration of Endothelial Progenitor Cells

Kuang

Wang

et al. 2012

Stem Cells and Development

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Endothelial progenitor cells (EPCs) play an important role in accelerating endothelial repair after vascular injury. The proliferation and migration of EPCs is a critical first step in restoring endothelial. However, mechanisms for modulating EPC proliferation and migration are still being elucidated. Our previous study found that transient receptor potential canonical-1 (TRPC1) is involved in regulating store-operated Ca 2 + entry in EPCs through stromal interaction molecule 1. Therefore, in the present study, we sought to further investigate the regulation of proliferation and migration of EPCs by TRPC1. We found that the silencing of TRPC1 by 2 different RNA interference methods suppressed the proliferation and migration of EPCs. In addition, knockdown of TRPC1 significantly reduced of the amplitude of store-operated Ca 2 + entry and caused arrest of the EPC cell cycle in G1 phase. Analysis of the expression of 84 cell cycle genes by microarray showed that 9 genes were upregulated and 4 were downregulated by > 2-fold in EPCs following TRPC1 silencing. The genes with expression changes were Ak1, Brca2, Camk2b, p21, Ddit3, Inha, Slfn1, Mdm2, Prm1, Bcl2, Mki67, Pmp22, and Ppp2r3a. Finally, we found that a Schlafen 1-blocking peptide partially reversed the abnormal cell cycle distribution and proliferation induced by TRPC1 knockdown, suggesting that Schlafen 1 is downstream of TRPC1 silencing in regulating EPC proliferation. In summary, these findings provide a new mechanism for modulating the biological properties of EPCs and suggest that TRPC1 may be a new target for inducing vascular repair by EPCs.

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Section: Kuang Et Alsupporting

confidence: 64%

Section: Cell Migration Assaymentioning

confidence: 99%

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Knockdown of Transient Receptor Potential Canonical-1 Reduces the Proliferation and Migration of Endothelial Progenitor Cells

Kuang

Wang

et al. 2012

Stem Cells and Development

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“…Disruption of Orai1 expression resulted in reduced SOCE and attenuated cell proliferation in human VSMCs, demonstrating that Orai1 is critical to this process (34). Additionally, the STIM1/Orai1 pathway seems to play a role in the SOCE-induced proliferatory activity of endothelial cells (35) and STIM1 siRNA abrogated both proliferation and migration of endothelial progenitor cells (36).…”

Section: Cardiovascular Diseasementioning

confidence: 98%

STIM1/Orai1-mediated store-operated Ca2+ entry: the tip of the iceberg

Giachini¹,

Lima²,

Hannan³

et al. 2011

Braz J Med Biol Res

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“…Our prior studies have shown that store-operated calcium entry (SOCE) plays a critical role in the functions of EPCs and smooth muscle cells [4][5][6]. SOCE is mediated by store-operated calcium channels (SOCCs), which are activated in response to the depletion of intracellular Ca 2 + stores.…”

Section: E Ndothelial Dysfunction Is the Process That Initiates Athermentioning

confidence: 99%

Reduction of Store-Operated Ca²⁺ Entry Correlates with Endothelial Progenitor Cell Dysfunction in Atherosclerotic Mice

Wang

Zhang

et al. 2015

Stem Cells and Development

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The dysfunction of endothelial progenitor cells (EPCs) has been shown to prevent endothelial repair during the development of atherosclerosis (AS). Previous studies have revealed that store-operated calcium entry (SOCE) is an important factor in regulating EPC functions. However, whether this is also the mechanism in AS has not been elucidated. Therefore, we evaluated the role of SOCE in EPCs isolated from an atherosclerotic mouse model. Atheromatous plaques were more frequent in the aortas of ApoE -/ -mice fed a high-fat diet for 16 weeks compared with controls, and the proliferative and migratory activities of atherosclerotic EPCs were significantly decreased. Accordingly, SOCE amplitude, as well as spontaneous or VEGF-induced Ca 2 + oscillations, decreased in atherosclerotic EPCs. These results may be associated with the downregulated expression of Stim1, Orai1, and TRPC1, which are major mediators of SOCE. In addition, eNOS expression and phosphorylation at Ser 1177 , which are critical regulators of EPC function, were markedly reduced in the atherosclerotic EPCs. The impairment of eNOS activity could also be induced by using an SOCE inhibitor or by Stim1 gene silencing, indicating a link between the activities of eNOS and SOCE in AS. Furthermore, decreased SOCE function inhibited EPC proliferation and migration in vitro. In conclusion, our results showed that the reduction of SOCE induced EPC dysfunction during AS, potentially through downregulation of store-operated calcium channel (SOCC) components and impaired eNOS activity. Approaches aimed at reestablishing SOCE activity may thus improve the function of EPCs during AS.

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Silencing stromal interaction molecule 1 by RNA interference inhibits the proliferation and migration of endothelial progenitor cells

Cited by 44 publications

References 26 publications

Knockdown of Transient Receptor Potential Canonical-1 Reduces the Proliferation and Migration of Endothelial Progenitor Cells

Knockdown of Transient Receptor Potential Canonical-1 Reduces the Proliferation and Migration of Endothelial Progenitor Cells

STIM1/Orai1-mediated store-operated Ca2+ entry: the tip of the iceberg

Reduction of Store-Operated Ca²⁺ Entry Correlates with Endothelial Progenitor Cell Dysfunction in Atherosclerotic Mice

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Silencing stromal interaction molecule 1 by RNA interference inhibits the proliferation and migration of endothelial progenitor cells

Cited by 44 publications

References 26 publications

Knockdown of Transient Receptor Potential Canonical-1 Reduces the Proliferation and Migration of Endothelial Progenitor Cells

Knockdown of Transient Receptor Potential Canonical-1 Reduces the Proliferation and Migration of Endothelial Progenitor Cells

STIM1/Orai1-mediated store-operated Ca2+ entry: the tip of the iceberg

Reduction of Store-Operated Ca2+ Entry Correlates with Endothelial Progenitor Cell Dysfunction in Atherosclerotic Mice

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Reduction of Store-Operated Ca²⁺ Entry Correlates with Endothelial Progenitor Cell Dysfunction in Atherosclerotic Mice