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Characterization of ANGPTL4 function in macrophages and adipocytes using Angptl4-knockout and Angptl4-hypomorphic mice

Oteng, Antwi-Boasiako, Ruppert, PhilipM.M., Boutens, Lily, Dijk, Wieneke, van Dierendonck, XantheA.M.H., Olivecrona, Gunilla, Stienstra, Rinke, Kersten, Sander·2019·Journal of Lipid Research
DOI 10.1194/jlr.m094128
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Fig. 1 Angptl4 expression is induced in primary macrophages by lipid stimulation or PPAR agonists. A: Angptl4 expression in peritoneal macrophages treated with 0.5 mM oleic acid for 6 h. B: Angptl4 expression in peritoneal macrophages (left) and BMDMs (right) treated for 6 h with 0.5 mM intralipid. C: Heat map of top 10 most upregulated and top 10 most downregulated genes in BMDMs treated for 5 h with 250 uM oleic acid or BSA (vehicle control). Data are from a previously published dataset (GSE77104) (43). D: Angptl4 expression in BMDMs treated for 6 h with 1  M of PPAR agonists, Wy14643 (PPAR  ), GW501516 (PPAR  ), L165041 (PPAR  ), and rosiglitazone (PPAR  ), or vehicle (DMSO). mRNA expression was normalized to 36b4. Data are mean ± SD from three biological replicates; * P < 0.05, ** P < 0.01, and *** P < 0.001 relative to vehicle control.
Fig. 1 Angptl4 expression is induced in primary macrophages by lipid stimulation or PPAR agonists. A: Angptl4 expression in peritoneal macrophages treated with 0.5 mM oleic acid for 6 h. B: Angptl4 expression in peritoneal macrophages (left) and BMDMs (right) treated for 6 h with 0.5 mM intralipid. C: Heat map of top 10 most upregulated and top 10 most downregulated genes in BMDMs treated for 5 h with 250 uM oleic acid or BSA (vehicle control). Data are from a previously published dataset (GSE77104) (43). D: Angptl4 expression in BMDMs treated for 6 h with 1  M of PPAR agonists, Wy14643 (PPAR  ), GW501516 (PPAR  ), L165041 (PPAR  ), and rosiglitazone (PPAR  ), or vehicle (DMSO). mRNA expression was normalized to 36b4. Data are mean ± SD from three biological replicates; * P < 0.05, ** P < 0.01, and *** P < 0.001 relative to vehicle control.CC-BY · From the PDF
Fig. 2 ANGPTL4 deficiency promotes macrophage lipid uptake and magnifies the induction of lipid-sensitive genes. A: Oil Red O staining of lipid droplets in RAW264.7 macrophages treated with 0.5 mM intralipid for 6 h in the presence or absence of 0.5  g/ml recombinant ANGPTL4. B: Oil Red O staining of lipid droplets in peritoneal macrophages treated for 6 h with lymph (final triglyceride concentration of 2 mM) in the presence or absence of 0.5  g/ml recombinant ANGPTL4. C: Microarray heat map showing expression profile of lipid-sensitive genes in peritoneal macrophages treated for 6 h with 0.5 mM intralipid in the presence or absence of recombinant ANGPTL4. D: Bodipy staining of Angptl4 +/+ and Angptl4  /  BMDMs cultured with regular culture medium (Cntl) or for 6 h with 0.5 mM intralipid with or without orlistat. E, F: mRNA expression of lipid-sensitive genes in Angptl4 +/+ and Angptl4  /  BMDMs treated for 6 h with 0.5 mM intralipid (E) or peritoneal macrophages treated for 6 h with lymph (final triglyceride concentration of 2 mM) (F). mRNA expression was normalized to 36b4. Data are mean ± SD from three biological replicates; * P < 0.05, ** P < 0.01, and *** P < 0.001 relative to untreated WT; and # P < 0.05, ## P < 0.01, and ### P < 0.001 relative to WT + intralipid/lymph.
Fig. 2 ANGPTL4 deficiency promotes macrophage lipid uptake and magnifies the induction of lipid-sensitive genes. A: Oil Red O staining of lipid droplets in RAW264.7 macrophages treated with 0.5 mM intralipid for 6 h in the presence or absence of 0.5  g/ml recombinant ANGPTL4. B: Oil Red O staining of lipid droplets in peritoneal macrophages treated for 6 h with lymph (final triglyceride concentration of 2 mM) in the presence or absence of 0.5  g/ml recombinant ANGPTL4. C: Microarray heat map showing expression profile of lipid-sensitive genes in peritoneal macrophages treated for 6 h with 0.5 mM intralipid in the presence or absence of recombinant ANGPTL4. D: Bodipy staining of Angptl4 +/+ and Angptl4  /  BMDMs cultured with regular culture medium (Cntl) or for 6 h with 0.5 mM intralipid with or without orlistat. E, F: mRNA expression of lipid-sensitive genes in Angptl4 +/+ and Angptl4  /  BMDMs treated for 6 h with 0.5 mM intralipid (E) or peritoneal macrophages treated for 6 h with lymph (final triglyceride concentration of 2 mM) (F). mRNA expression was normalized to 36b4. Data are mean ± SD from three biological replicates; * P < 0.05, ** P < 0.01, and *** P < 0.001 relative to untreated WT; and # P < 0.05, ## P < 0.01, and ### P < 0.001 relative to WT + intralipid/lymph.CC-BY · From the PDF
Fig. 3 ANGPTL4 deficiency increases respiration in BMDMs but does not influence LPL abundance. A: Real-time changes in OCR in BMDMs from Angptl4 +/+ and Angptl4  /  mice in the presence or absence of recombinant ANGPTL4, treated with 0.5 mM intralipid for 6 h, and assessed in unbuffered medium during sequential injections with oligomycin, FCCP, and antimycin A + rotenone. B: Basal (left) and maximal (right) OCR in BMDMs from Angptl4 +/+ and Angptl4  /  mice in the presence or absence of recombinant ANGPTL4 (0.5  g/ml) incubated with 0.5 mM intralipid for 6 h. Measurements were done in quintuplicates in unbuffered medium. Data are mean ± SD; *** P < 0.001. C: Immunoblot of LPL in Angptl4 +/+ and Angptl4  /  BMDMs treated for 6 h with or without 0.5 mM intralipid in the presence or absence of endonuclease-H. D: Immunoblot of LPL from culture medium of Angptl4 +/+ and Angptl4  /  BMDMs treated with or without heparin. E: Immunoblot of LPL in Angptl4 +/+ and Angptl4  /  BMDMs treated with or without ER to Golgi transport inhibitors monensin (Mon; 10  M for 3 h) and Brefeldin A (BFA; 5  g/ml for 4 h), proteasomal degradation inhibitor MG132 (40  M for 4 h), and lysosomal degradation inhibitors, e64d (20  M for 24 h) and leupeptin (Leup; 5  M for 16 h). HSP90 or Coomassie staining serve as loading control.
Fig. 3 ANGPTL4 deficiency increases respiration in BMDMs but does not influence LPL abundance. A: Real-time changes in OCR in BMDMs from Angptl4 +/+ and Angptl4  /  mice in the presence or absence of recombinant ANGPTL4, treated with 0.5 mM intralipid for 6 h, and assessed in unbuffered medium during sequential injections with oligomycin, FCCP, and antimycin A + rotenone. B: Basal (left) and maximal (right) OCR in BMDMs from Angptl4 +/+ and Angptl4  /  mice in the presence or absence of recombinant ANGPTL4 (0.5  g/ml) incubated with 0.5 mM intralipid for 6 h. Measurements were done in quintuplicates in unbuffered medium. Data are mean ± SD; *** P < 0.001. C: Immunoblot of LPL in Angptl4 +/+ and Angptl4  /  BMDMs treated for 6 h with or without 0.5 mM intralipid in the presence or absence of endonuclease-H. D: Immunoblot of LPL from culture medium of Angptl4 +/+ and Angptl4  /  BMDMs treated with or without heparin. E: Immunoblot of LPL in Angptl4 +/+ and Angptl4  /  BMDMs treated with or without ER to Golgi transport inhibitors monensin (Mon; 10  M for 3 h) and Brefeldin A (BFA; 5  g/ml for 4 h), proteasomal degradation inhibitor MG132 (40  M for 4 h), and lysosomal degradation inhibitors, e64d (20  M for 24 h) and leupeptin (Leup; 5  M for 16 h). HSP90 or Coomassie staining serve as loading control.CC-BY · From the PDF
Fig. 4 Hypomorphic ANGPTL4 mice show reduced ANGPTL4 expression and reduced regulation on LPL. A: Schematic map of the Angptl4 locus by knockout first-allele strategy. B: Full ANGPTL4 protein (upper scheme) and predicted sequence of truncated ANGPTL4 (lower scheme) based on sequence analysis of the knockout first-allele mice. mRNA expression of all seven exons of Angptl4 in epididymal adipose tissue (C) and primary adipocytes (D) of Angptl4  /  and Angptl4 hyp mice relative to WT mice. Western blot showing full-length and N-terminal ANGPTL4, and LPL in adipose tissue (E) and primary adipocytes (F) of the Angptl4  /  , Angptl4 hyp , and WT mice. mRNA expression was normalized to 36b4. Data are mean ± SEM. N = 7-11 mice per group. s.e., short exposure; l.e., long exposure.
Fig. 4 Hypomorphic ANGPTL4 mice show reduced ANGPTL4 expression and reduced regulation on LPL. A: Schematic map of the Angptl4 locus by knockout first-allele strategy. B: Full ANGPTL4 protein (upper scheme) and predicted sequence of truncated ANGPTL4 (lower scheme) based on sequence analysis of the knockout first-allele mice. mRNA expression of all seven exons of Angptl4 in epididymal adipose tissue (C) and primary adipocytes (D) of Angptl4  /  and Angptl4 hyp mice relative to WT mice. Western blot showing full-length and N-terminal ANGPTL4, and LPL in adipose tissue (E) and primary adipocytes (F) of the Angptl4  /  , Angptl4 hyp , and WT mice. mRNA expression was normalized to 36b4. Data are mean ± SEM. N = 7-11 mice per group. s.e., short exposure; l.e., long exposure.CC-BY · From the PDF
Fig. 5 Similar regulation on plasma metabolites and LPL between Angptl4 hyp and Angptl4  /  mice after 24 h fast. A: Plasma levels of triglycerides, glucose, cholesterol, NEFAs, and  -hydroxybutyrate in fed (closed bars) and fasted (opened bars) mice. B: mRNA expression from N-terminal (left column) and C-terminal (right column) regions of Angptl4 in epididymal adipose tissues of fed (closed bars) and fasted (opened) mice. C: Western blot of LPL and ANGPTL4 in epididymal adipose tissues from the three groups of mice in fed and fasted state. mRNA expression was normalized to 36b4. Data are mean ± SEM. N = 7-11 mice per group. * P < 0.05, ** P < 0.01, and *** P < 0.001 represent significance in fasted group relative to WT fasted mice; # P < 0.05 represents significance in fed group relative to WT fed mice; and §§ P < 0.01 relative to WT fed mice. s.e., short exposure; l.e., long exposure.
Fig. 5 Similar regulation on plasma metabolites and LPL between Angptl4 hyp and Angptl4  /  mice after 24 h fast. A: Plasma levels of triglycerides, glucose, cholesterol, NEFAs, and  -hydroxybutyrate in fed (closed bars) and fasted (opened bars) mice. B: mRNA expression from N-terminal (left column) and C-terminal (right column) regions of Angptl4 in epididymal adipose tissues of fed (closed bars) and fasted (opened) mice. C: Western blot of LPL and ANGPTL4 in epididymal adipose tissues from the three groups of mice in fed and fasted state. mRNA expression was normalized to 36b4. Data are mean ± SEM. N = 7-11 mice per group. * P < 0.05, ** P < 0.01, and *** P < 0.001 represent significance in fasted group relative to WT fasted mice; # P < 0.05 represents significance in fed group relative to WT fed mice; and §§ P < 0.01 relative to WT fed mice. s.e., short exposure; l.e., long exposure.CC-BY · From the PDF
Fig. 6 Angptl4 hyp mice have less severe pathological phenotypes in response to 20 weeks of high fat diet compared with Angptl4  /  mice. A: Plasma levels of SAA after 2, 4, and 20 weeks of high fat diet. B: Relative hepatic expression of pro-inflammatory markers in three groups of mice. C: Pictures showing levels of ascites formation in the peritoneum of Angptl4 hyp mice. Arrows pointing toward ascites. D: H&E staining depicting mesenteric panniculitis in Angptl4 hyp mice. E: Images showing Touton giant cells in the mesenteric lymph nodes of Angptl4 hyp and Angptl4  /  mice but not WT mice. Images are 200× magnification; insert is 400× magnification. mRNA expression was normalized to 36b4. Data are mean ± SEM. N = 7-11 mice per group. * P < 0.05, ** P < 0.01, and *** P < 0.001 relative to WT.
Fig. 6 Angptl4 hyp mice have less severe pathological phenotypes in response to 20 weeks of high fat diet compared with Angptl4  /  mice. A: Plasma levels of SAA after 2, 4, and 20 weeks of high fat diet. B: Relative hepatic expression of pro-inflammatory markers in three groups of mice. C: Pictures showing levels of ascites formation in the peritoneum of Angptl4 hyp mice. Arrows pointing toward ascites. D: H&E staining depicting mesenteric panniculitis in Angptl4 hyp mice. E: Images showing Touton giant cells in the mesenteric lymph nodes of Angptl4 hyp and Angptl4  /  mice but not WT mice. Images are 200× magnification; insert is 400× magnification. mRNA expression was normalized to 36b4. Data are mean ± SEM. N = 7-11 mice per group. * P < 0.05, ** P < 0.01, and *** P < 0.001 relative to WT.CC-BY · From the PDF
Fig. 7 Increased LPL activity and improved glucose tolerance in Angptl4 hyp mice after 20 weeks of high fat diet. A: LPL activity in epididymal adipose tissue of Angptl4 hyp , Angptl4  /  , and WT mice. B: Plasma concentrations of triglycerides, cholesterol, glycerol, and NEFAs in the three groups of mice. Plasma glucose levels (C) and glucose tolerance test (D) in the three groups of mice. Data are mean ± SEM. N = 7-11 mice per group. * P < 0.05, ** P < 0.01, and *** P < 0.001 relative to WT. No statistical analysis could be done on glucose tolerance in Angptl4  /  mice due to the use of different time points.
Fig. 7 Increased LPL activity and improved glucose tolerance in Angptl4 hyp mice after 20 weeks of high fat diet. A: LPL activity in epididymal adipose tissue of Angptl4 hyp , Angptl4  /  , and WT mice. B: Plasma concentrations of triglycerides, cholesterol, glycerol, and NEFAs in the three groups of mice. Plasma glucose levels (C) and glucose tolerance test (D) in the three groups of mice. Data are mean ± SEM. N = 7-11 mice per group. * P < 0.05, ** P < 0.01, and *** P < 0.001 relative to WT. No statistical analysis could be done on glucose tolerance in Angptl4  /  mice due to the use of different time points.CC-BY · From the PDF

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Metadata

Authors
Oteng, A.-B., Ruppert, P. M., Boutens, L., Dijk, W., van Dierendonck, X. M. H., Olivecrona, G., Stienstra, R., & Kersten, S.
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2019-10
Volume
60
Issue
10
Pages
1741-1754
ISSN
0022-2275
DOI
10.1194/jlr.m094128
Cited by
46
References
7
Language
en
Licence
Funders
  • Graduate School Voeding
  • Levensmiddelentechnologie
  • Agro-Biotechnologie en Gezondheid
  • CVON ENERGISE (CVON2014-02)

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