sphingosine/hypoxia

Intermittent hypoxia (IH) induced by obstructive sleep apnea (OSA) is the key factor in oxidative stress and the concomitant inflammation of endothelial cells (ECs). In recent years, the lipid sphingosine-1-phosphate (S1P) has been reported to probably play a central role in inflammatory diseases.

Our group has recently reported that in the immortal human HepG2 liver cell line, sphingosine 1‑phosphate (S1P) increases transcription of plasminogen activator inhibitor type‑1 (PAI‑1), the major physiological inhibitor of fibrinolysis, within 4 h. The present study aimed to elucidate the molecular

The lysophospholipids sphingosine-1-phosphate (S1P) and lysophosphatidic acid (LPA) stimulate cellular proliferation and affect numerous cellular functions by signaling through G protein-coupled endothelial differentiation gene-encoded (Edg) receptors. S1P and LPA also act as survival factors in

BACKGROUND The physiological challenges posed by hypobaric hypoxia warrant exploration of pharmacological entities to improve acclimatization to hypoxia. The present study investigates the preclinical efficacy of sphingosine-1-phosphate (S1P) to improve acclimatization to simulated hypobaric

OBJECTIVE Sphingosine-1-phosphate (S1P) is a potent bioactive phospholipid responsible for a variety of vascular cell responses. Hypoxia-inducible factor-1 (HIF-1) is a transcriptional activator of genes essential for adaptation to low oxygen. S1P and HIF-1 are both important mediators of vascular

Among many signals to regulate hypoxia inducible factor 1α (HIF-1α), sphingosine kinase 1 (SPHK1) is also involved in various biological activities such as cell growth, survival, invasion, angiogenesis, and carcinogenesis. Thus, in the present study, molecular mechanisms of coumestrol were

The lipid mediator sphingosine 1-phosphate (S1P) confers survival benefits in cardiomyocytes and isolated hearts subjected to oxidative stress. High-density lipoprotein (HDL) is a major carrier of S1P in the serum, but whether HDL-associated S1P directly mediates survival in a preparation composed

Sphingosine-1-phosphate (S1P) has a role in transpiration in patho-physiological signaling in skeletal muscles. The present study evaluated the pre-conditioning efficacy of S1P in facilitating differentiation of C2C12 myoblasts under a normoxic/hypoxic cell culture environment. Under normoxia,

Sphingosine-1-phosphate (S1P) is emerging as a hypoxia responsive bio-lipid; systemically raised levels of S1P are proposed to have potential hypoxia pre-conditioning effects. The study aims to evaluate the hypoxia pre-conditioning efficacy of exogenously administered S1P in rats exposed to acute

OBJECTIVE To investigate the role of sphingosine kinase 1 (SphK1) in regulating the proliferation of hypoxia-exposed glioma cells in vitro and explore the possible molecular mechanisms. METHODS Human glioblastoma U87MG cells was transfected with specific small interfering RNA (siRNA) constructs

OBJECTIVE Experimental and clinical studies have shown that administration of insulin during reperfusion is cardioprotective, but the mechanisms underlying this effect are still unknown. In this study, the ability of insulin to protect apoptotic cardiomyocytes from hypoxia/reoxygenation injury using

Hypoxia, defined as reduced tissue oxygen concentration, is a characteristic of solid tumors and is an indicator of unfavorable diagnosis in patients. At the cellular level, the adaptation to hypoxia is under the control of two related transcription factors, HIF-1α and HIF-2α (Hypoxia-Inducible

Both acute and chronic hypoxia had no effect on S1P(1), S1P(3) or LPA(1) receptor transcript expression in human pulmonary smooth muscle cells. However, acute hypoxia increased sphingosine kinase SK1/2 and LPP1 mRNA transcript levels, while chronic hypoxia increased SK1 mRNA transcript alone. Acute

Sphingosine kinase 1 (SphK1) upregulation is associated with pathologic pulmonary vascular remodeling in pulmonary arterial hypertension (PAH), but the mechanisms controlling its expression are undefined. In this study, we sought to characterize the regulation of SphK1 expression by micro-RNAs

Therapeutic angiogenesis provides a promising approach to treat ischemic cardiovascular diseases through the delivery of proangiogenic cells and/or molecules. Outgrowth endothelial cells (OECs) are vascular progenitor cells that are especially suited for therapeutic strategies given their ease of