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| Untersuchte Arbeit: Seite: 83, Zeilen: 1-12 |
Quelle: Boyce and Xing 2009 Seite(n): 3, 4, Zeilen: 3: last lines; 4: 1ff |
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| [De fet, ara tenim clar que els osteoclasts no són simplement cèl·lules que reabsorbeixen os sinó que també regulen el] funcionament dels osteoblasts [227, 228], l’alliberament de les cèl·lules hematopoètiques des de la medul·la òssia fins a la sang [229] i d’immunomodul·ladors en estat patològics [230].
6.3. Regulació de la formació i activació dels osteoclasts amb el sistema OPG/RANKL/RANK Els osteoclasts deriven de precursors mononuclears mieloides que també poden donar lloc a macròfags. L’expressió de M-CSF pels osteoblasts es necessària perquè les cèl·lules progenitores es diferenciïn a osteoclasts, però a part calen altres factors com RANKL i RANK als osteoclasts. El primer en descriure-ho fou Yoshida H et al [231] que van observar en un model de ratolins sense M-CSF l’existència d’osteopetrosi degut a l’absència d’osteoclasts. 227. Zhao, C., et al., Bidirectional ephrinB2-EphB4 signaling controls bone homeostasis. Cell Metab, 2006. 4(2): p. 111-21. 228. Lee, S.H., et al., v-ATPase V0 subunit d2-deficient mice exhibit impaired osteoclast fusion and increased bone formation. Nat Med, 2006. 12(12): p. 1403-9. 229. Kollet, O., et al., Osteoclasts degrade endosteal components and promote mobilization of hematopoietic progenitor cells. Nat Med, 2006. 12(6): p. 657-64. 230. Xing, L., E.M. Schwarz, and B.F. Boyce, Osteoclast precursors, RANKL/RANK, and immunology. Immunol Rev, 2005. 208: p. 19-29. 231. Yoshida, H., et al., The murine mutation osteopetrosis is in the coding region of the macrophage colony stimulating factor gene. Nature, 1990. 345(6274): p. 442-4. |
More recently, it has become increasingly clear that osteoclasts are not simply bone resorbing cells, but that they also regulate osteoblast functions positively and negatively (22,23), mediate the egression of hematopoietic stems from the marrow into the blood (24), and function as immunomodulators in pathologic states (25).
[page 4] Regulation of Osteoclast Formation and Activation by OPG, RANKL and RANK Osteoclasts are derived from mononuclear precursors in the myeloid lineage of hematopoietic cells that also give rise to macrophages. [...] M-CSF expression by osteoblastic stromal cells is required for progenitor cells to differentiate into osteoclasts, but M-CSF on its own is unable to complete this process. This requirement for M-CSF was discovered by the observation that op/op mice, which do not express functional M-CSF, have osteopetrosis because they lack osteoclasts (26). 22. Zhao C, Irie N, Takada Y, Shimoda K, Miyamoto T, Nishiwaki T, Suda T, Matsuo K. Bidirectional ephrinB2-EphB4 signaling controls bone homeostasis. Cell Metabolism 2006;4:111–121. [PubMed: 16890539] 23. Lee SH, Rho J, Jeong D, Sul JY, Kim T, Kim N, Kang JS, Miyamoto T, Suda T, Lee SK, et al. v- ATPase V0 subunit d2-deficient mice exhibit impaired osteoclast fusion and increased bone formation. Nat Med 2006;12:1403–1409. [PubMed: 17128270] 24. Kollet O, Dar A, Shivtiel S, Kalinkovich A, Lapid K, Sztainberg Y, Tesio M, Samstein RM, Goichberg P, Spiegel A, et al. Osteoclasts degrade endosteal components and promote mobilization of hematopoietic progenitor cells. Nat Med 2006;12:657–664. [PubMed: 16715089] 25. Xing L, Schwarz EM, Boyce BF. Osteoclast precursors, RANKL/RANK, and immunology. Immunol Rev 2005;208:19–29. [PubMed: 16313338] 26. Yoshida H, Hayashi S, Kunisada T, Ogawa M, Nishikawa S, Okamura H, Sudo T, Shultz LD. The murine mutation osteopetrosis is in the coding region of the macrophage colony stimulating factor gene. Nature 1990;345:442–444. [PubMed: 2188141] |
The source is not mentioned, but the text has been taken from the source after translating it. Also all references to the literature have been taken from the source. |
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