Journal: Diabetes & metabolism

Article Title: Fenofibrate decreases plasma ceramide in type 2 diabetes patients: A novel marker of CVD?

doi: 10.1016/j.diabet.2017.04.003

Figure Lengend Snippet: Fig. 2. Associations between ceramide (Cer) and sphingomyelin (SM) in the circulation: changes in Cer/SM ratio after fenofibrate treatment (A); Pearson correlation of changes in plasma Cer and SM after fenofibrate treatment (B); effect of fenofibrate on secretory acid sphingomyelinase (S-ASM) concentrations (C); and Pearson correlation of changes in Cer/SM ratio and S-ASM concentrations after fenofibrate treatment (D). *** P < 0.001.

Article Snippet: A pool of reference standard solutions, including sphingosine1-phosphate (S1P; d18:1), nine ceramide (Cer) species and nine sphingomyelin (SM) species (Avanti Polar Lipids, Alabaster, AL, USA; Table S2; see supplementary material associated with this article online), was prepared with serial dilutions of methanol to obtain seven standard solutions, ranging from 1–500 nmol/L, 2– 1000 nmol/L and 0.04–20 mmol/L for Cer, S1P and SM, respectively.

Techniques: Clinical Proteomics

Journal: Diabetes & metabolism

Article Title: Fenofibrate decreases plasma ceramide in type 2 diabetes patients: A novel marker of CVD?

doi: 10.1016/j.diabet.2017.04.003

Figure Lengend Snippet: Fig. 3. Pearson correlations between changes in plasma ceramide (Cer) after treatment and basal plasma Cer (A), basal plasma sphingomyelin (SM) (B), basal plasma sphingosine-1-phosphate (S1P) (C), and basal plasma secretory acid sphingomyelinase (S-ASM) concentrations (D).

Article Snippet: A pool of reference standard solutions, including sphingosine1-phosphate (S1P; d18:1), nine ceramide (Cer) species and nine sphingomyelin (SM) species (Avanti Polar Lipids, Alabaster, AL, USA; Table S2; see supplementary material associated with this article online), was prepared with serial dilutions of methanol to obtain seven standard solutions, ranging from 1–500 nmol/L, 2– 1000 nmol/L and 0.04–20 mmol/L for Cer, S1P and SM, respectively.

Techniques: Clinical Proteomics

Journal: International Journal of Molecular Medicine

Article Title: Histone deacetylase-4 and histone deacetylase-8 regulate interleukin-1β-induced cartilage catabolic degradation through MAPK/JNK and ERK pathways

doi: 10.3892/ijmm.2018.3410

Figure Lengend Snippet: IL-1β promoted the expression of ADAMTS-4 and ADAMTS-5 through the activation of MAPK signaling. (A) Of the 3 MAPK isoforms, ERK1/2 and JNK were markedly phosphorylated following treatment with IL-1β. The gene expression of (B) ADAMTS-5 and (C) ADAMTS-4 was facilitated by C6 (ERK activator) or Ani (JNK activator). The IL-1β-induced gene expression of (B) ADAMTS-5 and (C) ADAMTS-4 was inhibited by FR (ERK inhibitor) or SP (JNK inhibitor). Data present the means ± standard deviation, n=3. * P<0.05. IL, interleukin; ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs; MAPK, mitogen-activated protein kinase; ERK, extracellular signal-regulated kinase; JNK, c-Jun N-terminal kinase; DMSO, dimethyl sulfoxide; C6, Ceramide C6; Ani, Anisomycin; FR, FR180204; SP, SP600125; p, phosphorylated; t, total.

Article Snippet: For the kinase assays, rACs were pretreated with specific inhibitors of ERK (FR180204 at 50 μ M) and JNK (SP600125 at 10 μ M; both from Selleck Chemicals, Houston, TX, USA) and exposed to IL-1β, or treated with the specific activators of ERK (ceramide C6 at 50 μ M; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) or JNK (anisomycin at 1 μ M; Selleck Chemicals) alone. rACs treated with DMSO were used as a vehicle control and with IL-1β were used as a positive control.

Techniques: Expressing, Activation Assay, Gene Expression, Standard Deviation

Journal: International Journal of Molecular Medicine

Article Title: Histone deacetylase-4 and histone deacetylase-8 regulate interleukin-1β-induced cartilage catabolic degradation through MAPK/JNK and ERK pathways

doi: 10.3892/ijmm.2018.3410

Figure Lengend Snippet: HDAC regulates the osteoarthritis-related genes and protein expression of rACs via ERK1/2 and JNK. (A) IL-1β-induced ERK1/2 phosphorylation was blocked by TSA, and not blocked by PCI; JNK phosphorylation was blocked by TSA and PCI. (B) HDAC inhibitors (TSA or PCI) suppressed HDAC expression at both mRNA and protein level, and prevented the upregulation of osteoarthritis-related genes (col X, COX2, ADAMTS-5 and ADAMTS-4) expression induced by IL-1β. Results are presented with respect to GAPDH expression. (C) siRNAs (targeting HDAC4 or HDAC8) suppressed HDAC expression at both mRNA and protein level, and prevented the upregulation of osteoarthritis-related gene expression induced by IL-1β. Results are expressed with respect to GAPDH expression. Data represent the means ± standard deviation, n=3. * P<0.05. HDAC, histone deacetylase; ERK, extracellular signal-regulated kinase; JNK, c-Jun N-terminal kinase; IL, interleukin; TSA, Trichostatin A; DMSO, dimethyl sulfoxide; PCI, PCI-34051; col X, type X collagen; COX2, cyclooxygenase; ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs; siRNA, small interfering RNA; p, phosphorylated; t, total. rACs, rat articular chondrocytes.

Article Snippet: For the kinase assays, rACs were pretreated with specific inhibitors of ERK (FR180204 at 50 μ M) and JNK (SP600125 at 10 μ M; both from Selleck Chemicals, Houston, TX, USA) and exposed to IL-1β, or treated with the specific activators of ERK (ceramide C6 at 50 μ M; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) or JNK (anisomycin at 1 μ M; Selleck Chemicals) alone. rACs treated with DMSO were used as a vehicle control and with IL-1β were used as a positive control.

Techniques: Expressing, Phospho-proteomics, Gene Expression, Standard Deviation, Histone Deacetylase Assay, Small Interfering RNA

Journal: International Journal of Molecular Medicine

Article Title: Histone deacetylase-4 and histone deacetylase-8 regulate interleukin-1β-induced cartilage catabolic degradation through MAPK/JNK and ERK pathways

doi: 10.3892/ijmm.2018.3410

Figure Lengend Snippet: Possible signaling pathways associated with ADAMTS, col X, and COX-2 regulation by IL-1β in chondrocytes. ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs; col X, type X collagen; COX2, cyclooxygenase; IL, interleukin; HDAC, histone deacetylase; ERK, extracellular signal-regulated kinase; JNK, c-Jun N-terminal kinase; IL, interleukin; TSA, Trichostatin A; PCI, PCI-34051.

Article Snippet: For the kinase assays, rACs were pretreated with specific inhibitors of ERK (FR180204 at 50 μ M) and JNK (SP600125 at 10 μ M; both from Selleck Chemicals, Houston, TX, USA) and exposed to IL-1β, or treated with the specific activators of ERK (ceramide C6 at 50 μ M; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) or JNK (anisomycin at 1 μ M; Selleck Chemicals) alone. rACs treated with DMSO were used as a vehicle control and with IL-1β were used as a positive control.

Techniques: Protein-Protein interactions, Histone Deacetylase Assay

Journal: The Journal of clinical endocrinology and metabolism

Article Title: Plasma Sphingolipid Profile of Healthy Black and White Adults Differs Based on Their Parental History of Type 2 Diabetes.

doi: 10.1210/clinem/dgad595

Figure Lengend Snippet: Figure 2. Relative composition (Mole %) of individual species of 3 major classes of sphingolipids, namely, ceramide, MHC, and sphingomyelin. A-C, Relative composition (Mole %) of ceramide (A), monohexosylceramide (MHC, B), and sphingomyelin (C) individual species with a fatty acid chain length from C14 to C26 with saturated or monounsaturated species from healthy subjects with no family history of diabetes (FH−). Very long-chain species (C28-C34) are pooled together as VLC. D-F, Relative composition (Mole %) of ceramide (D), monohexosylceramide (MHC, E), and sphingomyelin (F) individual species with a fatty acid chain length from C14 to C26 with saturated or monounsaturated species from healthy subjects with a family history of diabetes (FH+). Very long-chain species (C28-C34) are pooled together as VLC.

Article Snippet: For analysis, frozen samples were placed in borosilicate glass tubes and spiked with 250 pmol of sphingomyelin, ceramide, and monohexosylceramide (d18:1/12:0 species), and sphingosine, dihydro-sphingosine (dh-sphingosine), sphingosine-1phosphate (S1P), dihydro-S1P (dh-S1P) (d17:0 sphinganine/ d17:1 sphingosine) as internal standard (Avanti Polar Lipids).

Techniques:

Journal: The Journal of clinical endocrinology and metabolism

Article Title: Plasma Sphingolipid Profile of Healthy Black and White Adults Differs Based on Their Parental History of Type 2 Diabetes.

doi: 10.1210/clinem/dgad595

Figure Lengend Snippet: Figure 1. Sphingolipid (SPL) profile of human plasma. A, Concentration (pmol/mL of plasma) of major classes of SPL such as ceramide (Cer), monohexosylceramide (MHC), and sphingomyelin (SM) from healthy subjects with no family history of diabetes (FH−) and with a family history of diabetes (FH+; POP-ABC). Significant differences were observed in the levels of Cer, MHC, and SM. B, Concentration of major long-chain bases SPL species such as sphingosine (So), dihydro-sphingosine (dh-So), sphingosine 1-phosphate (S1P), and dihydro-S1P (dh-S1P) from healthy subjects with no family history of diabetes (FH−) and with a family history of diabetes (FH+). Significant differences were observed in the levels of So and dh-S1P. ** P < .01, *** P < .001; Control, n = 100; POP-ABC, n = 140.

Article Snippet: For analysis, frozen samples were placed in borosilicate glass tubes and spiked with 250 pmol of sphingomyelin, ceramide, and monohexosylceramide (d18:1/12:0 species), and sphingosine, dihydro-sphingosine (dh-sphingosine), sphingosine-1phosphate (S1P), dihydro-S1P (dh-S1P) (d17:0 sphinganine/ d17:1 sphingosine) as internal standard (Avanti Polar Lipids).

Techniques: Clinical Proteomics, Concentration Assay, Control