Phytosphingosine Stimulates the Differentiation of Human Keratinocytes and Inhibits TPA-Induced Inflammatory Epidermal Hyperplasia in Hairless Mouse Skin

Kim, Sujong; Hong, In–Sun; Hwang, Jung Sun; Choi, Jin Kyu; Rho, Ho Sik; Kim, Duck Hee; Chang, Ih-Seop; Lee, Seung Hun; Lee, Mi Ock; Hwang, Jae Sung

doi:10.2119/2006-00001.kim

Cited by 60 publications

(50 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Phytosphingosine (C18:0) is structurally similar to dihydrosphingosine with the exception of a hydroxyl group at C4. Phytosphingosine also mediates a variety of cellular processes and has anti-proliferative and anti-inflammatory properties [9,10]. …”

Section: Introductionmentioning

confidence: 99%

Sphingoid Bases Are Taken Up by Escherichia coli and Staphylococcus aureus and Induce Ultrastructural Damage

Fischer¹,

Walters²,

Drake³

et al. 2012

Skin Pharmacol Physiol

View full text Add to dashboard Cite

Sphingoid bases found in the outer layers of the skin exhibit antimicrobial activity against gram-positive and gram-negative bacteria. We investigated the uptake of several sphingoid bases by Escherichia coli and Staphylococcus aureus, and assessed subsequent ultrastructural damage. E. coli and S. aureus were incubated with d-sphingosine, dihydrosphingosine, or phytosphingosine at ten times their MIC for 0.5 and 4 h, respectively, to kill 50% of viable bacteria. Treated bacterial cells were immediately prepared for SEM, TEM, and analyzed for lipid content by QTLC. E. coli and S. aureus treated with sphingoid bases were distorted and their surfaces were concave and rugate. Significant differences were observed in the visual surface area relative to controls for both E. coli and S. aureus when treated with dihydrosphingosine and sphingosine (p < 0.0001) but not phytosphingosine. While sphingoid base-treated S. aureus exhibited disruption and loss of cell wall and membrane, E. coli cytoplasmic membranes appeared intact and the outer envelope uncompromised. Both E. coli and S. aureus cells contained unique internal inclusion bodies, likely associated with cell death. QTLC demonstrated extensive uptake of sphingoid bases by the bacteria. Hence, sphingoid bases induce both extracellular and intracellular damage and cause intracellular inclusions that may reflect lipid uptake.

show abstract

Section: Introductionmentioning

confidence: 99%

Sphingoid Bases Are Taken Up by Escherichia coli and Staphylococcus aureus and Induce Ultrastructural Damage

Fischer¹,

Walters²,

Drake³

et al. 2012

Skin Pharmacol Physiol

View full text Add to dashboard Cite

show abstract

“…Among these metabolites, phytosphingosine and dipalmitoylphosphatidic acid have anti-inflammatory effects [63,64]. The increased level of thromboxane B2, an inactive product of thromboxane A2, may improve the high coagulation state of MG patients, while the decrease in biliverdin IX indicated less hemoglobin breakdown.…”

Section: Resultsmentioning

confidence: 99%

Serum proteomic, peptidomic and metabolomic profiles in myasthenia gravis patients during treatment with Qiangji Jianli Fang

Wang

Chen

et al. 2012

Chin Med

View full text Add to dashboard Cite

BackgroundQiangji Jianli Fang (QJF) has been used for treatment of myasthenia gravis (MG) in China. However, our understanding of the effects of QJF against MG at the molecular level is limited. This study aims to investigate the effects of QJF treatment of MG patients on the protein, peptide and metabolite levels in serum.MethodsHigh-throughput proteomic, peptidomic and metabolomic techniques were applied to investigate serum samples from 21 healthy individuals and 47 MG patients before and after QJF treatment via two-dimensional gel electrophoresis, matrix-assisted laser desorption/ionization time of flight mass spectrometry and liquid chromatography Fourier transform mass spectrometry, respectively.ResultsAfter QJF treatment, the expression levels of peptides m/z 1865.019, 2021.128 and 1211.668 of complement C3f increased (P = 0.004, P = 0.001 and P = 0.043, respectively), while that of peptide m/z 1739.931 of component C4b decreased (P = 0.043), in the serum of MG patients. The levels of γ-aminobutyric acid (P = 0.000) and coenzyme Q4 (P = 0.000) resumed their normal states.ConclusionQJF could inhibit the activity of the complement system and restore the normal levels of metabolites.

show abstract

“…22) In addition to its anticancer effects, phytosphingosine stimulates the differentiation of human keratinocytes and inhibits inflammatory epidermal hyperplasia in the skin of hairless mice. 23) Phytosphingosine also activates the transcriptional activity of peroxisome proliferator-activated receptors (PPARs), which play important roles in skin barrier homeostasis and epidermal differentiation. 23) Sphingolipids and its metabolites regulate the growth and melanogenesis of human melanocytes.…”

Section: Discussionmentioning

confidence: 99%

“…23) Phytosphingosine also activates the transcriptional activity of peroxisome proliferator-activated receptors (PPARs), which play important roles in skin barrier homeostasis and epidermal differentiation. 23) Sphingolipids and its metabolites regulate the growth and melanogenesis of human melanocytes. Ceramide, S1P, and sphingosylphosphorylcholine decrease melanogenesis and reduce melanin synthesis by downregulating tyrosinase expression.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of N,N,N-trimethyl phytosphingosine-iodide on melanogenesis via ERK activation-mediated MITF degradation

Lee

Bang

Chung

et al. 2016

Bioscience, Biotechnology, and Biochemistry

View full text Add to dashboard Cite

N,N,N-trimethyl phytosphingosine-iodide (TMP) was recently developed as an antitumor agent. We examined the effects of TMP on melanogenesis and its related signaling pathways in normal human melanocytes. Our results showed that melanin is significantly reduced in a dose-dependent manner in both cells following liposomal TMP treatment. We also investigated changes in the phosphorylation of extracellular signal-regulated kinase (ERK), which is related to the degradation of microphthalmia-associated transcription factor (MITF). Our results indicated that liposomal TMP treatment leads to the phosphorylation of ERK, which reduces both MITF and tyrosinase protein levels. Treatment with PD98059, an ERK pathway-specific inhibitor, restored liposomal TMP-induced reductions in melanin, abrogated reductions in tyrosinase activity, and downregulated MITF and tyrosinase protein. In conclusion, these results suggest that the inhibitory effects of TMP on melanogenesis are due to MITF and tyrosinase downregulation via ERK activation.

show abstract

Phytosphingosine Stimulates the Differentiation of Human Keratinocytes and Inhibits TPA-Induced Inflammatory Epidermal Hyperplasia in Hairless Mouse Skin

Cited by 60 publications

References 39 publications

Sphingoid Bases Are Taken Up by Escherichia coli and Staphylococcus aureus and Induce Ultrastructural Damage

Sphingoid Bases Are Taken Up by Escherichia coli and Staphylococcus aureus and Induce Ultrastructural Damage

Serum proteomic, peptidomic and metabolomic profiles in myasthenia gravis patients during treatment with Qiangji Jianli Fang

Inhibitory effects of N,N,N-trimethyl phytosphingosine-iodide on melanogenesis via ERK activation-mediated MITF degradation

Contact Info

Product

Resources

About