Sphingosine 1-phosphate stimulates proliferation and migration of satellite cells

Calise, S. John; Blescia, Sabrina; Cencetti, Francesca; Bernacchioni, Caterina; Donati, Chiara; Bruni, Paola

doi:10.1016/j.bbamcr.2011.11.016

Cited by 79 publications

(107 citation statements)

References 40 publications

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“…S1PR2 is also involved in the reduction of platelet‐derived growth factor mediated‐cell motility and proliferation 44. A knockdown in the expression of S1PR2 by shRNA in satellite cells resulted in a twofold increase in cell migration 45. As mentioned above, we observed that S1P can enhance BCA cancer cell growth when it binds to S1PR1 and in the KM plotter analysis, S1PR2 expression was found to have a better survival benefit than S1PR1 expression.…”

Section: Discussionsupporting

confidence: 64%

Survival benefit of sphingosin‐1‐phosphate and receptors expressions in breast cancer patients

Cheng

Liao

et al. 2018

Cancer Medicine

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Sphingosine‐1‐phosphate (S1P) is a bioactive lipid that exerts various pathophysiological functions through binding to its receptor family (S1PRs). Since first report of the breast cancer (BCA) promoting function by S1P production (through the function of sphingosine kinases) and S1P/S1PR signaling, their antagonists have never been successfully progress to clinics after three decades. Taking advantage of bioinformatics linking to gene expression to disease prognosis, we examined the impact of associated genes in BCA patients. We found high gene expressions involved in S1P anabolism suppressed disease progression of patients who are basal cell type BCA or receiving adjuvant therapy. In addition, S1PRs expression also suppressed disease progress of multiple categories of BCA patient progression. This result is contradictory to tumor promoter role of S1P/S1PRs which revealed in the literature. Further examination by directly adding S1P in BCA cells found a cell growth suppression function, which act via the expression of S1PR1. In conclusion, our study is the first evidence claiming a survival benefit function of S1P/S1PR signaling in BCA patients, which might explain the obstacle of relative antagonist apply in clinics.

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Section: Discussionsupporting

confidence: 64%

Survival benefit of sphingosin‐1‐phosphate and receptors expressions in breast cancer patients

Cheng

Liao

et al. 2018

Cancer Medicine

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“…27 Because S1P has proproliferative effects on numerous cell types, [28][29][30] including human PASMCs, 10 we investigated whether S1P induces proliferation of rat PAECs and PASMCs. Cultured PAECs and PASMCs were serum-deprived for 24 hour and then treated with 5 μM S1P or vehicle (0.1% ethanol) for 24 and 48 hours.…”

Section: Exogenous S1p Induces Proliferation Of Rat Paecs and Pasmcsmentioning

confidence: 99%

Sphingosine‐1‐Phosphate is Involved in the Occlusive Arteriopathy of Pulmonary Arterial Hypertension

et al. 2016

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Despite several advances in the pathobiology of pulmonary arterial hypertension (PAH), its pathogenesis is not completely understood. Current therapy improves symptoms but has disappointing effects on survival. Sphingosine-1-phosphate (S1P) is a lysophospholipid synthesized by sphingosine kinase 1 (SphK1) and SphK2. Considering the regulatory roles of S1P in several tissues leading to vasoconstriction, inflammation, proliferation, and fibrosis, we investigated whether S1P plays a role in the pathogenesis of PAH. To test this hypothesis, we used plasma samples and lung tissue from patients with idiopathic PAH (IPAH) and the Sugen5416/hypoxia/normoxia rat model of occlusive PAH. Our study revealed an increase in the plasma concentration of S1P in patients with IPAH and in early and late stages of PAH in rats. We observed increased expression of both SphK1 and SphK2 in the remodeled pulmonary arteries of patients with IPAH and PAH rats. Exogenous S1P stimulated the proliferation of cultured rat pulmonary arterial endothelial and smooth-muscle cells. We also found that 3 weeks of treatment of late-stage PAH rats with an SphK1 inhibitor reduced the increased plasma levels of S1P and the occlusive pulmonary arteriopathy. Although inhibition of SphK1 improved cardiac index and the total pulmonary artery resistance index, it did not reduce right ventricular systolic pressure or right ventricular hypertrophy. Our study supports that S1P is involved in the pathogenesis of occlusive arteriopathy in PAH and provides further evidence that S1P signaling may be a novel therapeutic target.Keywords: occlusive lesions, S1P, pulmonary, cardiac. Pulmonary arterial hypertension (PAH) remains debilitating and deadly despite advanced and expensive medical treatment. 1 Its pathogenic mechanisms have not been fully identified and therapeutically targeted. A limitation in the current treatment of patients with PAH is the inability of prostanoids, endothelin receptor blockers, phosphodiesterase inhibitors, or their various combinations to reverse the pulmonary arteriopathy. 2,3 An effective strategy in the development of more efficacious therapy would be to identify the molecular determinants of the arterial wall remodeling.Sphingosine-1-phosphate (S1P) is a biologically active lipid synthesized intracellularly by sphingosine kinase 1 (SphK1) and SphK2 and degraded by S1P lyase and various phosphatases. It is released by endothelial cells, red blood cells, activated platelets, and monocytes and has regulatory roles in several physiological and pathological processes. 4,5 Physiological levels of circulating S1P are vasculoprotective, whereas abnormal activation of SphK/S1P signaling is associated with diseases such as cancer, fibrosis, diabetes, and hypertension. [6][7][8][9][10] At high cellular or tissue levels, S1P is a proproliferative, antiapoptotic, promigratory, profibrotic, and proinflammatory signaling molecule. 11 SphK activity and S1P production are stimulated by numerous signals, including growth factors, cytokines, m...

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Section: Introductionmentioning

confidence: 99%

“…Moreover, this lysosphingolipid has been reported to be capable of stimulating the motility of activated satellite cells, which is critical for their correct recruitment at the site of tissue lesions [6]. Interestingly, these biological effects induced by S1P appear to be transmitted by ligation to S1P receptors: S1P 2 and S1P 3 are involved in transmission of the mitogenic effect of the sphingolysolipid [6,7], whereas S1P 1 and S1P 4 appear to be implicated in the migratory response elicited by S1P [6]. Interestingly, recent studies performed in mice in which S1P 2 was genetically ablated or pharmacologically blocked have provided experimental evidence that this receptor subtype promotes skeletal muscle regeneration [8], while altered cell-cycle progression has been observed in satellite cells of S1P 3 knockout mice [9].…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, S1P has been shown to act as powerful mitogenic cue in quiescent and activated mouse satellite cells [5,6]. Moreover, this lysosphingolipid has been reported to be capable of stimulating the motility of activated satellite cells, which is critical for their correct recruitment at the site of tissue lesions [6]. Interestingly, these biological effects induced by S1P appear to be transmitted by ligation to S1P receptors: S1P 2 and S1P 3 are involved in transmission of the mitogenic effect of the sphingolysolipid [6,7], whereas S1P 1 and S1P 4 appear to be implicated in the migratory response elicited by S1P [6].…”

Section: Introductionmentioning

confidence: 99%

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Lysophosphatidic acid stimulates cell migration of satellite cells. A role for the sphingosine kinase/sphingosine 1‐phosphate axis

et al. 2014

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Regulation of the motility of skeletal muscle precursor cells, such as satellite cells, is critically important for their proper recruitment at the site of tissue damage, and ultimately for its correct repair. Here we show that lysophosphatidic acid (LPA), which is well-recognized as a powerful bioactive agent, strongly stimulates cell migration of activated murine satellite cells. The biological effect exerted by LPA was found to be induced via activation of LPA 1 and LPA 3 , being abolished by cell treatment with the antagonist Ki16425, and severely impaired by siRNA-mediated down-regulation of the two receptor isoforms. In contrast, silencing of LPA 2 potentiated the stimulation of cell motility by LPA, suggesting that it is negatively coupled to cell migration. Pharmacological inhibition of both sphingosine kinase (SK) isoforms using VPC96047, or the selective blocking of SK1 using VPC96091, abolished cell responsiveness to LPA; in agreement, gene silencing of SK1 or SK2 significantly reduced the biological effect of LPA. Moreover, the LPA-dependent stimulation of cell chemotaxis was found to be impaired by down-regulation of the sphingosine 1-phosphate (S1P) receptors S1P 1 or S1P 4 by specific siRNAs. In summary, the results obtained support the notion that the sphingosine kinase/sphingosine 1-phosphate (SK/S1P) axis is critically involved in the mechanism by which LPA elicits its pro-migratory action. This study provides compelling new information on the regulatory mechanisms of satellite cell motility, and reinforces the view that the SK/S1P signaling pathway plays a crucial role in the control of skeletal muscle precursor cell biology.

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Sphingosine 1-phosphate stimulates proliferation and migration of satellite cells

Cited by 79 publications

References 40 publications

Survival benefit of sphingosin‐1‐phosphate and receptors expressions in breast cancer patients

Survival benefit of sphingosin‐1‐phosphate and receptors expressions in breast cancer patients

Sphingosine‐1‐Phosphate is Involved in the Occlusive Arteriopathy of Pulmonary Arterial Hypertension

Lysophosphatidic acid stimulates cell migration of satellite cells. A role for the sphingosine kinase/sphingosine 1‐phosphate axis

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