Lineage tracing of cells involved in atherosclerosis

Atherosclerosis

Volumn 251, Issue , 2016, Pages 445-453

  Albarrán Juárez, Julián ^a   Kaur, Harmandeep ^a   Grimm, Myriam ^a   Offermanns, Stefan ^a,b   Wettschureck, Nina ^a,b  

^a MAX PLANCK INSTITUTE FOR HEART AND LUNG RESEARCH   (Germany)

^b GOETHE UNIVERSITY   (Germany)

Author keywords

Atherosclerosis; Gene expression; Lineage tracing; Macrophage; Smooth muscle cell; Transdifferentiation

Indexed keywords

CHLORDANE; CYCLOOXYGENASE 2; MESSENGER RNA; VASCULAR CELL ADHESION MOLECULE 1; CD68 PROTEIN, MOUSE; DIFFERENTIATION ANTIGEN; LEUKOCYTE ANTIGEN;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; ATHEROSCLEROTIC PLAQUE; BLOOD; BONE MARROW; CELL LEVEL; CELL SUSPENSION; CELL TRANSDIFFERENTIATION; CONTROLLED STUDY; FLOW CYTOMETRY; HISTOPATHOLOGY; MACROPHAGE; MALE; MOUSE; NONHUMAN; PERITONEAL CAVITY; PRIORITY JOURNAL; VASCULAR SMOOTH MUSCLE; ANIMAL; ATHEROSCLEROSIS; BONE MARROW CELL; C57BL MOUSE; CELL LINEAGE; CHROMOSOMAL MAPPING; CYTOLOGY; GENE EXPRESSION REGULATION; METABOLISM; PATHOPHYSIOLOGY; PHENOTYPE; SMOOTH MUSCLE CELL; TRANSGENIC MOUSE;

ANIMALS; ANTIGENS, CD; ANTIGENS, DIFFERENTIATION, MYELOMONOCYTIC; ATHEROSCLEROSIS; CELL LINEAGE; CHROMOSOME MAPPING; GENE EXPRESSION REGULATION; MACROPHAGES; MALE; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MUSCLE, SMOOTH, VASCULAR; MYELOID CELLS; MYOCYTES, SMOOTH MUSCLE; PHENOTYPE;

EID: 85006705703     PISSN: 00219150     EISSN: 18791484     Source Type: Journal    
DOI: 10.1016/j.atherosclerosis.2016.06.012     Document Type: Article

References (26)

1. [1] Allahverdian, S., Chehroudi, A.C., McManus, B.M., Abraham, T., Francis, G.A., Contribution of intimal smooth muscle cells to cholesterol accumulation and macrophage-like cells in human atherosclerosis. Circulation 129 (2014), 1551–1559.
2. [2] Amanzada, A., Malik, I.A., Blaschke, M., Khan, S., Rahman, H., Ramadori, G., Moriconi, F., Identification of CD68(+) neutrophil granulocytes in in vitro model of acute inflammation and inflammatory bowel disease. Int. J. Clin. Exp. Pathol. 6 (2013), 561–570.
3. [3] Bennett, M.R., Sinha, S., Owens, G.K., Vascular smooth muscle cells in atherosclerosis. Circ. Res. 118 (2016), 692–702.
4. [4] Caplice, N.M., Bunch, T.J., Stalboerger, P.G., Wang, S., Simper, D., Miller, D.V., Russell, S.J., Litzow, M.R., Edwards, W.D., Smooth muscle cells in human coronary atherosclerosis can originate from cells administered at marrow transplantation. Proc. Natl. Acad. Sci. U. S. A. 100 (2003), 4754–4759.
5. [5] Clausen, B.E., Burkhardt, C., Reith, W., Renkawitz, R., Forster, I., Conditional gene targeting in macrophages and granulocytes using LysMcre mice. Transgenic Res. 8 (1999), 265–277.
6. [6] Cross, M., Mangelsdorf, I., Wedel, A., Renkawitz, R., Mouse lysozyme M gene: isolation, characterization, and expression studies. Proc. Natl. Acad. Sci. U. S. A. 85 (1988), 6232–6236.
7. [7] Feil, S., Fehrenbacher, B., Lukowski, R., Essmann, F., Schulze-Osthoff, K., Schaller, M., Feil, R., Transdifferentiation of vascular smooth muscle cells to macrophage-like cells during atherogenesis. Circ. Res. 115 (2014), 662–667.
8. [8] Gomez, D., Owens, G.K., Smooth muscle cell phenotypic switching in atherosclerosis. Cardiovasc. Res. 95 (2012), 156–164.
9. [9] Grimm, M., Tischner, D., Troidl, K., Albarran Juarez, J., Sivaraj, K.K., Ferreiros Bouzas, N., Geisslinger, G., Binder, C.J., Wettschureck, N., S1P2/G12/13 signaling negatively regulates macrophage activation and indirectly shapes the atheroprotective B1-cell population. Arterioscler. Thromb. Vasc. Biol. 36 (2016), 37–48.
10. [10] Lee, R.T., Libby, P., The unstable atheroma. Arterioscler. Thromb. Vasc. Biol. 17 (1997), 1859–1867.
11. [11] Ley, K., Miller, Y.I., Hedrick, C.C., Monocyte and macrophage dynamics during atherogenesis. Arterioscler. Thromb. Vasc. Biol. 31 (2011), 1506–1516.
12. [12] Livak, K.J., Wills, Q.F., Tipping, A.J., Datta, K., Mittal, R., Goldson, A.J., Sexton, D.W., Holmes, C.C., Methods for qPCR gene expression profiling applied to 1440 lymphoblastoid single cells. Methods 59 (2013), 71–79.
13. [13] Mallat, Z., Besnard, S., Duriez, M., Deleuze, V., Emmanuel, F., Bureau, M.F., Soubrier, F., Esposito, B., Duez, H., Fievet, C., Staels, B., Duverger, N., Scherman, D., Tedgui, A., Protective role of interleukin-10 in atherosclerosis. Circ. Res. 85 (1999), e17–24.
14. [14] Moore, K.J., Tabas, I., Macrophages in the pathogenesis of atherosclerosis. Cell 145 (2011), 341–355.
15. [15] Moore, K.J., Sheedy, F.J., Fisher, E.A., Macrophages in atherosclerosis: a dynamic balance. Nat. Rev. Immunol. 13 (2013), 709–721.
16. [16] Muzumdar, M.D., Tasic, B., Miyamichi, K., Li, L., Luo, L., A global double-fluorescent Cre reporter mouse. Genesis 45 (2007), 593–605.
17. [17] Piedrahita, J.A., Zhang, S.H., Hagaman, J.R., Oliver, P.M., Maeda, N., Generation of mice carrying a mutant apolipoprotein E gene inactivated by gene targeting in embryonic stem cells. Proc. Natl. Acad. Sci. U. S. A. 89 (1992), 4471–4475.
18. [18] Rong, J.X., Shapiro, M., Trogan, E., Fisher, E.A., Transdifferentiation of mouse aortic smooth muscle cells to a macrophage-like state after cholesterol loading. Proc. Natl. Acad. Sci. U. S. A. 100 (2003), 13531–13536.
19. [19] Schindelin, J., Arganda-Carreras, I., Frise, E., Kaynig, V., Longair, M., Pietzsch, T., Preibisch, S., Rueden, C., Saalfeld, S., Schmid, B., Tinevez, J.Y., White, D.J., Hartenstein, V., Eliceiri, K., Tomancak, P., Cardona, A., Fiji: an open-source platform for biological-image analysis. Nat. Methods 9 (2012), 676–682.
20. [20] Schreiber, H.A., Loschko, J., Karssemeijer, R.A., Escolano, A., Meredith, M.M., Mucida, D., Guermonprez, P., Nussenzweig, M.C., Intestinal monocytes and macrophages are required for T cell polarization in response to Citrobacter rodentium. J. Exp. Med. 210 (2013), 2025–2039.
21. [21] Shankman, L.S., Gomez, D., Cherepanova, O.A., Salmon, M., Alencar, G.F., Haskins, R.M., Swiatlowska, P., Newman, A.A., Greene, E.S., Straub, A.C., Isakson, B., Randolph, G.J., Owens, G.K., KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis. Nat. Med. 21 (2015), 628–637.
22. [22] Swirski, F.K., Nahrendorf, M., Do vascular smooth muscle cells differentiate to macrophages in atherosclerotic lesions?. Circ. Res. 115 (2014), 605–606.
23. [23] Tabas, I., Garcia-Cardena, G., Owens, G.K., Recent insights into the cellular biology of atherosclerosis. J. Cell Biol. 209 (2015), 13–22.
24. [24] Virmani, R., Kolodgie, F.D., Burke, A.P., Farb, A., Schwartz, S.M., Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler. Thromb. Vasc. Biol. 20 (2000), 1262–1275.
25. [25] Wamhoff, B.R., Hoofnagle, M.H., Burns, A., Sinha, S., McDonald, O.G., Owens, G.K., A G/C element mediates repression of the SM22alpha promoter within phenotypically modulated smooth muscle cells in experimental atherosclerosis. Circ. Res. 95 (2004), 981–988.
26. [26] Wirth, A., Benyo, Z., Lukasova, M., Leutgeb, B., Wettschureck, N., Gorbey, S., Orsy, P., Horvath, B., Maser-Gluth, C., Greiner, E., Lemmer, B., Schutz, G., Gutkind, J.S., Offermanns, S., G12-G13-LARG-mediated signaling in vascular smooth muscle is required for salt-induced hypertension. Nat. Med. 14 (2008), 64–68.