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The DOI matches its Crossref record, with a small difference in title or year; 4 of the 4 references it cites were found in a registry or an index.

Disabled-2 Determines Commitment of a Pre-adipocyte Population in Juvenile Mice

Tao, Wensi, Moore, Robert, Meng, Yue, Yeasky, Toni M., Smith, Elizabeth R., Xu, Xiang-Xi·2016·Scientific Reports
DOI 10.1038/srep35947PMC PMC5078790
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Abstract

Disabled-2 (Dab2) is a widely expressed clathrin binding endocytic adaptor protein and known for the endocytosis of the low-density lipoprotein (LDL) family receptors. Dab2 also modulates endosomal Ras/MAPK (Erk1/2) activity by regulating the disassembly of Grb2/Sos1 complexes associated with clathrin-coated vesicles. We found that the most prominent phenotype of Dab2 knockout mice was their striking lean body composition under a high fat and high caloric diet, although the weight of the mutant mice was indistinguishable from wild-type littermates on a regular chow. The remarkable difference in resistance to high caloric diet-induced weight gain of the dab2-deleted mice was presented only in juvenile but not in mature mice. Investigation using Dab2-deficient embryonic fibroblasts and mesenchymal stromal cells indicated that Dab2 promoted adipogenic differentiation by modulation of MAPK (Erk1/2) activity, which otherwise suppresses adipogenesis through the phosphorylation of PPARγ. The results suggest that Dab2 is required for the excessive calorie-induced differentiation of an adipocyte progenitor cell population that is present in juvenile but depleted in mature animals. The finding provides evidence for a limited pre-adipocyte population in juvenile mammals and the requirement of Dab2 in the regulation of Ras/MAPK signal in the commitment of the precursor cells to adipose tissues.

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  • Dab2 is essential for the expansion of adipocyte cell number.

    “The research results suggest Dab2 is essential for the expansion of adipocyte cell number.”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Tao et al., 2016b

    The Results section reports fewer adipocytes in Dab2-deficient mice fed a high-fat diet, supporting a role for Dab2 in cell-number expansion. The Discussion limits this effect to young mice and says older mice did not differ from controls in their response to the diet; the claim omits those age and diet conditions. (LLM, conf=0.87)

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  • The resistance to high fat diet-induced weight gain in adipose lineage Dab2-deleted mice is adipocyte cell autonomous.

    “Restricted Dab2 deletion in adipose lineage using aP2-Cre supports that this phenotype is adipocyte cell autonomous”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Tao et al., 2016b

  • Dab2 is required for adipocyte differentiation.

    “Based on analyses of cell lines and primary stromal mesenchymal stem cells and cells of the adipose vascular stromal fraction, the mechanism was determined to be a requirement of Dab2 in adipocyte differentiation (Figure 4; Tao et al., 2016b).”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Tao et al., 2016b

  • In pre-adipocytes, Dab2 is required to suppress Ras/MAPK activity.

    “In the pre-adipocytes, Dab2 is required to suppress the activity of Ras/MAPK”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Tao et al., 2016b

  • In adipose tissues, Dab2 is expressed in pericytes attached to vascular structures.

    “In adipose tissues, Dab2 is found to express in pericytes attached to the vascular structures (Tao et al., 2016b).”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Tao et al., 2016b

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Research works printed but not linked: 57

  1. Spiegelman, B. M. & Flier, J. S. Obesity and the regulation of energy balance. Cell 104, 531–543 (2001). · DOI · Paper page
  2. Stubbs, R. J. & Tolkamp, B. J. Control of energy balance in relation to energy intake and energy expenditure in animals and man: an ecological perspective. Br. J. Nutr. 95, 657–676 (2006). · DOI
  3. Jo, J. et al. Hypertrophy and/or Hyperplasia: Dynamics of Adipose Tissue Growth. PLoS Comput. Biol. 5, e1000324 (2009). · DOI
  4. Sun, K., Kusminski, C. M. & Scherer, P. E. Adipose tissue remodeling and obesity. J. Clin. Invest. 121, 2094–2101 (2011). · DOI · Paper page
  5. Kopelman, P. G. Obesity as a medical problem. Nature 404, 635–643 (2000). · DOI · Paper page
  6. Cristancho, A. G. & Lazar, M. A. Forming functional fat: a growing understanding of adipocyte differentiation. Nat. Rev. Mol. Cell. Biol. 12, 722–734 (2011). · DOI · Paper page
  7. Rosen, E. D. & Spiegelman, B. M. Molecular regulation of adipogenesis. Annu. Rev. Cell Dev. Biol. 16, 145–171 (2000). · DOI
  8. Rosen, E. D. & MacDougald, O. A. Adipocyte differentiation from the inside out. Nat. Rev. Mol. Cell. Biol. 7, 885–896 (2006). · DOI · Paper page
  9. Evans, R. M., Barish, G. D. & Wang, Y. X. PPARs and the complex journey to obesity. Nat. Med. 10, 355–361 (2004). · DOI
  10. Rosen, E. D. et al. PPAR gamma is required for the differentiation of adipose tissue in vivo and in vitro. Mol. Cell 4, 611–617 (1999). · DOI
  11. Lowell, B. B. PPARgamma: an essential regulator of adipogenesis and modulator of fat cell function. Cell 99, 239–242 (1999). · DOI
  12. Bost, F. et al. The extracellular signal-regulated kinase isoform ERK1 is specifically required for in vitro and in vivo adipogenesis. Diabetes 54, 402–411 (2005). · DOI
  13. Bost, F., Aouadi, M., Caron, L. & Binétruy, B. The role of MAPKs in adipocyte differentiation and obesity. Biochimie. 87, 51–56 (2005). · DOI
  14. Adams, M., Reginato, M. J., Shao, D., Lazar M. A. & Chatterjee, V. K. Transcriptional activation by peroxisome proliferator-activated receptor gamma is inhibited by phosphorylation at a consensus mitogen-activated protein kinase site. J. Biol. Chem. 272, 5128–5132 (1997). · DOI
  15. Hu, E., Kim, J. B., Sarraf, P. & Spiegelman, B. M. Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARgamma. Science 274, 2100–2103 (1996). · DOI
  16. Kim, K. A., Kim, J. H., Wang, Y. & Sul, H. S. Pref-1 (preadipocyte factor 1) activates the MEK/extracellular signal-regulated kinase pathway to inhibit adipocyte differentiation. Mol. Cell. Biol. 27, 2294–2308 (2007). · DOI
  17. Burgermeister, E. & Seger, R. MAPK kinases as nucleo-cytoplasmic shuttles for PPARgamma. Cell Cycle 6, 1539–1548 (2007). · DOI
  18. Hosooka, T. et al. Dok1 mediates high-fat diet-induced adipocyte hypertrophy and obesity through modulation of PPAR-gamma phosphorylation. Nat Med. 14, 188–193 (2008). · DOI
  19. Lee, S. J. et al. A functional role for the p62-ERK1 axis in the control of energy homeostasis and adipogenesis. EMBO Rep. 11, 226–232 (2010). · DOI
  20. Moore, R., Cai, K. Q., Tao, W., Smith, E. R. & Xu, X. X. Differential requirement for Dab2 in the development of embryonic and extra-embryonic tissues. BMC Dev. Biol. 13, 39 (2013). · DOI · Paper page
  21. Traub, L. M. Sorting it out: AP-2 and alternate clathrin adaptors in endocytic cargo selection. J. Cell Biol. 163, 203–208 (2003). · DOI
  22. Xu, X. X., Yi, T., Tang, B. & Lambeth, J. D. Disabled-2 (Dab2) is an SH3 domain-binding partner of Grb2. Oncogene 16, 1561–1569 (1998). · DOI
  23. Zhou, J. & Hsieh, J. T. The inhibitory role of DOC-2/DAB2 in growth factor receptor-mediated signal cascade. DOC-2/DAB2-mediated inhibition of ERK phosphorylation via binding to Grb2. J. Biol. Chem. 276, 27793–27798 (2001). · DOI · Paper page
  24. Yang, D. H. et al. Disabled-2 is essential for endodermal cell positioning and structure formation during mouse embryogenesis. Dev. Biol. 251, 27–44 (2002). · DOI · Paper page
  25. Yang, D. H., Cai, K. Q., Roland, I. H., Smith, E. R. & Xu, X. X. Disabled-2 is an epithelial surface positioning gene. J. Biol. Chem. 282, 13114–13122 (2007). · DOI · Paper page
  26. Morris, S. M., Tallquist, M. D., Rock, C. O. & Cooper, J. A. Dual roles for the Dab2 adaptor protein in embryonic development and kidney transport. EMBO J. 21, 1555–1564 (2002). · DOI · Paper page
  27. Hayashi, S., Lewis, P., Pevny, L. & McMahon, A. P. Efficient gene modulation in mouse epiblast using a Sox2Cre transgenic mouse strain. Mech. Dev. 119, S97–S101 (2002). · DOI
  28. Garcia, C. K. et al. Autosomal recessive hypercholesterolemia caused by mutations in a putative LDL receptor adaptor protein. Science 292, 1394–1398 (2001). · DOI · Paper page
  29. He, W. et al. Adipose-specific peroxisome proliferator-activated receptor gamma knockout causes insulin resistance in fat and liver but not in muscle. Proc. Natl. Acad. Sci. USA 100, 15712–15717 (2003). · DOI
  30. Uysal, K. T., Scheja, L., Wiesbrock, S. M., Bonner-Weir, S. & Hotamisligil, G. S. Improved glucose and lipid metabolism in genetically obese mice lacking aP2. Endocrinology 141, 3388–3396 (2000). · DOI
  31. Cawthorn, W. P., Scheller, E. L. & MacDougald, O. A. Adipose tissue stem cells meet preadipocyte commitment: going back to the future. J. Lipid Res. 53, 227–246 (2012). · DOI
  32. Djian, P., Roncari, D. A. & Hollenberg, C. H. Adipocyte precursor clones vary in capacity for differentiation. Metabolism 34, 880–883 (1985). · DOI
  33. Hausman, G. J. & Hausman, D. B. Search for the preadipocyte progenitor cell. J. Clin. Invest. 116, 3103–3106 (2006). · DOI
  34. Gesta, S., Tseng, Y. H. & Kahn, C. R. Developmental origin of fat: tracking obesity to its source. Cell 131, 242–256 (2007). · DOI · Paper page
  35. Kahn, C. R. Medicine. Can we nip obesity in its vascular bud? Science 322, 542–543 (2008). · DOI
  36. Tang, W. et al. White fat progenitor cells reside in the adipose vasculature. Science 322, 583–586 (2008). · DOI · Paper page
  37. McCormick, F. Signal transduction: How receptors turn Ras on. Nature 363, 15–16 (1993). · DOI · Paper page
  38. Rozakis-Adcock, M., Fernley, R., Wade, J., Pawson, T. & Bowtell, D. The SH2 and SH3 domains of mammalian Grb2 couple the EGF receptor to the Ras activator mSos1. Nature 363, 83–85 (1993). · DOI
  39. Cherniack, A. D., Klarlund, J. K., Conway, B. R. & Czech, M. P. Disassembly of Son-of-sevenless proteins from Grb2 during p21ras desensitization by insulin. J. Biol. Chem. 270, 1485–1488 (1995). · DOI
  40. Waters, S. B. et al. Desensitization of Ras activation by a feedback disassociation of the SOS-Grb2 complex. J. Biol. Chem. 270, 20883–20886 (1995). · DOI
  41. Ceresa, B. P. & Schmid, S. L. Regulation of signal transduction by endocytosis. Curr. Opin. Cell Biol. 12, 204–210 (2000). · DOI
  42. Fehrenbacher, N., Bar-Sagi, D. & Philips, M. Ras/MAPK signaling from endomembranes. Mol. Oncol. 3, 297–307 (2009). · DOI · Paper page
  43. Vieira, A. V., Lamaze, C. & Schmid, S. L. Control of EGF receptor signaling by clathrin-mediated endocytosis. Science 274, 2086–2089 (1996). · DOI · Paper page
  44. Arner, P. & Spalding, K. L. Fat cell turnover in humans. Biochem. Biophys. Res. Commun. 396, 101–104 (2010). · DOI
  45. Spalding, K. L. et al. Dynamics of fat cell turnover in humans. Nature 453, 783–787 (2008). · DOI · Paper page
  46. Knittle, J. L. & Hirsch, J. Effect of early nutrition on the development of rat epididymal fat pads: cellularity and metabolism. J. Clin. Invest. 47, 2091–2098 (1968). · DOI
  47. Peckham, S. C., Entenman, C. & Carroll, H. W. The influence of a hypercalric diet on gross body and adipose tissue composition in the rat. J. Nutr. 77, 187–197 (1962). · DOI
  48. Steinberg, M. D., Zingg, W. & Angel, A. Studies of the number and volume of fat cells in adipose tissue. J. Pediatr. 61, 299–300 (1962). · DOI
  49. Tsujikawa, M. & Kimura, S. Effect of early feeding on cellularity of rat adipose tissue. J. Nutr. Sci. Vitaminol. (Tokyo) 26, 475–482 (1980). · DOI
  50. Efrat, M., Tepper, S. & Birk, R. Z. From fat cell biology to public health preventive strategies - pinpointing the critical period for obesity prevention. J. Pediatr. Endocrinol. Metab. 26, 197–209 (2013). · DOI
  51. Berry, R., Jeffery, E. & Rodeheffer, M. S. Weighing in on adipocyte precursors. Cell Metab. 19, 8–20 (2014). · DOI
  52. Billon, N., Monteiro, M. C. & Dani, C. Developmental origin of adipocytes: new insights into a pending question. Biol. Cell 100, 563–575 (2008). · DOI
  53. Wang, Q. A., Tao, C., Gupta, R. K. & Scherer, P. E. Tracking adipogenesis during white adipose tissue development, expansion and regeneration. Nat. Med. 19, 1338–1344 (2013). · DOI · Paper page
  54. Lee, Y. H., Petkova, A. P., Mottillo, E. P. & Granneman, J. G. In vivo identification of bipotential adipocyte progenitors recruited by β3-adrenoceptor activation and high-fat feeding. Cell Metab. 15, 480–491 (2012). · DOI
  55. Soleimani, M. & Nadri, S. A protocol for isolation and culture of mesenchymal stem cells from mouse bone marrow. Nat. Protoc. 4, 102–106 (2009). · DOI
  56. Church, C. D., Berry, R. & Rodeheffer, M. S. Isolation and study of adipocyte precursors. Methods Enzymol. 537, 31–46 (2014). · DOI
  57. Hausman, D. B., Park, H. J. & Hausman, G. J. Isolation and culture of preadipocytes from rodent white adipose tissue. Methods Mol. Biol. 456, 201–219 (2008). · DOI

Cited by

Sorted by citations

Metadata

Authors
Tao, W., Moore, R., Meng, Y., Yeasky, T. M., Smith, E. R., & Xu, X.-X.
Venue
Scientific Reports
Publisher
Springer Science and Business Media LLC
Published
2016-10-25
Volume
6
Issue
1
ISSN
2045-2322
DOI
10.1038/srep35947
PMC
PMC5078790
Cited by
13
References
4
Language
en
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