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. 2025 Jun 2;39(11):e70692. doi: 10.1096/fj.202501754

Correction to “Intracellular Sphingosine‐1‐Phosphate Induces Lipolysis Through Direct Activation of Protein Kinase C Zeta”

PMCID: PMC12416992  PMID: 40452382

1.

S. Weske, M. K. Nowak, and A. Zaufel, et al., “Intracellular Sphingosine‐1‐Phosphate Induces Lipolysis Through Direct Activation of Protein Kinase C Zeta,” FASEB Journal. 39, no. 7 (2025): e70528, https://doi.org/10.1096/fj.202403272R.

In the originally published version of this article, Figures 1 and 2 were mistakenly swapped. Accordingly, the figure legends must also be reassigned: the legend originally published for Figure 1 should be assigned to Figure 2 and vice versa. In addition, the legend for Figure 2, panels (E)‐(J), including the statistical information, pertains to Figure 1.

FIGURE 1.

FIGURE 1

S1P induces lipolysis through PKCzeta in differentiated 3T3‐L1 adipocytes. (A) Glycerol release per mg protein after 16 h treatment of differentiated 3T3‐L1 cells with S1P (0.1, 1, 10 or 50 μM) or vehicle controls (0.1% MeOH or 0.02% BSA) (n = 4 per group). (B) Glycerol release per mg protein after 16 h treatment of differentiated 3T3‐L1 cells with 10 μM S1P, 10 μM AUY954, 10 μM CYM5520, 10 μM CYM5541, or vehicle control (0.1% DMSO). (n = 4–5 per group). (C) Adipocyte‐associated S1P, sphingosine, and ceramide in 3T3‐L1 adipocytes after a 30 min incubation with 10 μM S1P as measured by LC–MS/MS and calculated based on an average cell volume of 4380 μm3. (n = 5 per group). (D) Glycerol release per mg protein after 16 h treatment of differentiated 3T3‐L1 cells with 10 μM S1P or vehicle control (0.02% BSA) in the presence or absence of the 25 μM ceramide synthase inhibitor Fumonisin B1. (n = 5 per group). (E) Gylcerol release per mg protein after 16h treatment of differentiated 3T3‐L1 cells with vehicle (0.02% BSA) vs 10 μM S1P or vehicle (0.1% DMSO) versus 1 μM Isoproterenol in the presence or absence of 100 μM of the adenylate cyclase inhibitor SQ22536. (n = 4 per group). (F) Glycerol release per mg protein after 16 h treatment of differentiated 3T3‐L1 cells with 10 μM S1P or vehicle control (0.02% BSA) in presence or absence of the 100 nM PI3K Inhibitor Wortmannin. (n = 3–8 per group). (G) Relative kinase activity of recombinant PKC zeta treated with 10 μM S1P or vehicle (MeOH) for 10 min as determined by in vitro phosphorylation assay. (n = 3 per group). (H) Glycerol release per mg protein after 16 h treatment of differentiated 3T3‐L1 cells with 10 μM S1P or vehicle control (0.02% BSA) in presence or absence of the 3 μM PKC inhibitor bisindolylmaleimid I (Bis). (n = 3–8 per group). (I) Glycerol release per mg protein after 16 h treatment of differentiated 3T3‐L1 cells with 10 μM S1P or vehicle (0.02% BSA) in the presence or absence of 10 M PKC zeta pseudo‐substrate inhibitor (PSI). (n = 4 per group). (J) Representative Western Blots for T410 phosphorylated PKC zeta, total PKC zeta and GAPDH in differentiated 3T3‐L1 adipocytes treated with 10 μM S1P or vehicle (0.02% BSA) for 15 min. (n = 4 per condition). Quantification of phospho‐PKC zeta T410 normalized GAPDH. Data are presented as mean ± SEM. A one‐way ANOVA with Tukey's multiple‐comparisons test or paired/unpaired t‐test was used for statistical analysis. *p < 0.05; **p < 0.01; ***p < 0.001.

FIGURE 2.

FIGURE 2

S1P induces lipolysis through a PKCzeta/MAPK/HSL pathway in differentiated 3T3‐L1 cells. (A) Glycerol release per mg protein after 16 h treatment of differentiated 3T3‐L1 cells with vehicle (0.02% BSA), 10 μM S1P (in 0.02% BSA) in the presence or absence of 10 μM PD98059 or 25 μM small molecular HSL inhibitor (smHSLi). (n = 4 per group). (B) Representative Western Blots for p‐p44/42 MAPK and p‐HSL Ser660 in differentiated 3T3‐L1 adipocytes treated with 10 μM S1P or vehicle (0.02% BSA) in the presence or absence of 3 μM bisindolylmaleimide I (Bis) for 15 min (n = 4–5 per condition). Quantification of p‐p44/42 MAPK and p‐HSL Ser660 normalized to GAPDH. (C) Glycerol release per mg protein after 16 h treatment of differentiated 3T3‐L1 cells with vehicle or 1 μM S1P lyase inhibitor VD‐78. (n = 5 per group). (D) Glycerol release per mg protein after 16 h treatment of primary mouse adipocytes with vehicle or 1 μM S1P lyase inhibitor VD‐78 (n = 6 per group). Data are presented as mean ± SEM. A one‐way ANOVA with Tukey's multiple‐comparisons test or paired t‐test was used for statistical analysis. *p < 0.05; **p < 0.01.

We apologize for this error.

The corrected versions of Figures 1 and 2 and their corresponding legends are provided below.


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