S1P/S1P Receptor Signaling in Neuromuscolar Disorders

Meacci, Elisabetta; Garcia‐Gil, Mercedes

doi:10.3390/ijms20246364

Cited by 18 publications

(26 citation statements)

References 194 publications

(268 reference statements)

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“…Sphingosine-1-phosphate (S1P), a plateletderived lysophospholipid mediator, reduces plateletderived growth factor (PDGF)-promoted chemotaxis and cellular Rac activation [14]. The S1P/S1P receptor axis regulates several biologic functions such as tumor invasion and progression, angiogenesis and vasculogenesis as well as skeletal muscle and nervous system degeneration [15][16][17]. Interestingly, deleting the S1P2 receptor promotes murine embryonic fibroblast migration towards S1P and also PDGF, which stimulates S1P production; S1P 2 deletion also increases the enzymatic expression and activity of sphingosine kinase 1 (SphK1), which is responsible for producing S1P [18].…”

Section: Ivyspring International Publishermentioning

confidence: 99%

S1P promotes IL-6 expression in osteoblasts through the PI3K, MEK/ERK and NF-κB signaling pathways

Hu¹,

Huang²,

Tzeng³

et al. 2020

Int. J. Med. Sci.

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Rheumatoid arthritis (RA) is a systemic autoimmune inflammatory disease, in which the immune system attacks joint tissue. Interleukin (IL)-6 is a key proinflammatory cytokine in RA progression. Sphingosine-1-phosphate (S1P), a platelet-derived lysophospholipid mediator, reportedly regulates osteoimmunology. Here, we examined the effects of S1P on IL-6 expression in osteoblasts. Our results and records from the Gene Expression Omnibus (GEO) database demonstrate higher levels of IL-6 in patients with RA compared with those with osteoarthritis. Stimulation of osteoblasts with S1P increased mRNA and protein expression of IL-6. PI3K, MEK, ERK and NF-B inhibitors and their small interfering RNAs (siRNAs) reduced S1P-promoted IL-6 expression. S1P also facilitated PI3K, MEK/ERK and NF-B signaling cascades. Our results indicate that S1P promotes the expression of IL-6 in osteoblasts via the PI3K, MEK/ERK and NF-B signaling pathways.

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Section: Ivyspring International Publishermentioning

confidence: 99%

S1P promotes IL-6 expression in osteoblasts through the PI3K, MEK/ERK and NF-κB signaling pathways

Hu¹,

Huang²,

Tzeng³

et al. 2020

Int. J. Med. Sci.

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show abstract

“…Notably, the neurological symptoms reported in COVID-19 patients should be seriously considered, but the mechanism remains obscure since no cell type expressing both ACE2 and TMPRSS2 has been found in the CNS. We hypothesize that SARS-CoV-2 infection might impair the known pro-survival, trophic and neurogenic functions of S1P-S1PR axis [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

“…SLs are both structural and signaling molecules that regulate cell fate and inflammation in physiological and pathological conditions [ 16 , 17 , 18 ]. SLs are formed by sphingosine (Sph) backbone linked to one hydrophobic acyl chain and a phosphate head group ester.…”

Section: Sl Metabolism and The Role Of S1p On Inflammationmentioning

confidence: 99%

“…The metabolism of SLs is described in Figure 1 . Some sphingosine or S1P analogues, have been approved for the treatment of MS, and some have entered clinical trials for different diseases, including MS and amyotrophic lateral sclerosis [ 18 , 31 ]. In particular, the structure of Fingolimod (FTY720) is analogous to that of Sph, and it is phosphorylated to Fingolimod (FTY720)-phosphate, a structural analogue of S1P in vivo by SphK2.…”

Section: Sl Metabolism and The Role Of S1p On Inflammationmentioning

confidence: 99%

“…Sphingolipids (SLs) are a large group of bioactive signaling molecules that are critical in many physiological and pathological conditions, including viral infection [ 16 , 17 , 18 , 19 ]. The interplay and the ratio between the most studied bioactive SLs, sphingosine 1-phosphate (S1P) and its metabolic precursors, in particular, ceramide and sphingosine (Sph), are crucial in determining the cellular fate ( Figure 1 ) [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

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SARS-CoV-2 Infection: A Role for S1P/S1P Receptor Signaling in the Nervous System?

Meacci

Garcia‐Gil

Pierucci

2020

IJMS

Self Cite

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The recent coronavirus disease (COVID-19) is still spreading worldwide. The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the virus responsible for COVID-19, binds to its receptor angiotensin-converting enzyme 2 (ACE2), and replicates within the cells of the nasal cavity, then spreads along the airway tracts, causing mild clinical manifestations, and, in a majority of patients, a persisting loss of smell. In some individuals, SARS-CoV-2 reaches and infects several organs, including the lung, leading to severe pulmonary disease. SARS-CoV-2 induces neurological symptoms, likely contributing to morbidity and mortality through unknown mechanisms. Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid with pleiotropic properties and functions in many tissues, including the nervous system. S1P regulates neurogenesis and inflammation and it is implicated in multiple sclerosis (MS). Notably, Fingolimod (FTY720), a modulator of S1P receptors, has been approved for the treatment of MS and is being tested for COVID-19. Here, we discuss the putative role of S1P on viral infection and in the modulation of inflammation and survival in the stem cell niche of the olfactory epithelium. This could help to design therapeutic strategies based on S1P-mediated signaling to limit or overcome the host–virus interaction, virus propagation and the pathogenesis and complications involving the nervous system.

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S1P facilitates IL‐1β production in osteoblasts via the JAK and STAT3 signaling pathways

Huang

Tseng

et al. 2020

Environmental Toxicology

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Rheumatoid arthritis (RA) is a systemic autoimmune inflammatory disease, in which the immune system attacks synovial joint tissues. Interleukin (IL)‐1β is a critical proinflammatory cytokine in RA progression. Sphingosine‐1‐phosphate (S1P), a platelet‐derived lysophospholipid mediator, reportedly regulates osteoimmunology. Here, we investigated how S1P mediates IL‐1β expression in osteoblasts. Our analysis of records from the Gene Expression Omnibus (GEO) database demonstrate higher levels of IL‐1β in patients with RA compared with those with osteoarthritis. Stimulation of osteoblasts with S1P concentration dependently increased mRNA and protein expression of IL‐1β. Elevations in IL‐1β mRNA expression induced by S1P were reduced by the small interfering RNA (siRNA) against the S1P1 receptor. S1P also augmented JAK and STAT3 molecular cascades. We also found that JAK and STAT3 inhibitors and their siRNAs antagonized S1P‐promoted IL‐1β expression. Our results indicate that S1P promotes the expression of IL‐1β in osteoblasts via the S1P1 receptor and the JAK and STAT3 signaling pathways.

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S1P/S1P Receptor Signaling in Neuromuscolar Disorders

Cited by 18 publications

References 194 publications

S1P promotes IL-6 expression in osteoblasts through the PI3K, MEK/ERK and NF-κB signaling pathways

S1P promotes IL-6 expression in osteoblasts through the PI3K, MEK/ERK and NF-κB signaling pathways

SARS-CoV-2 Infection: A Role for S1P/S1P Receptor Signaling in the Nervous System?

S1P facilitates IL‐1β production in osteoblasts via the JAK and STAT3 signaling pathways

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