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Angaben zur Quelle [Bearbeiten]

Autor     Brendan F. Boyce, Lianping Xing
Titel    Functions of RANKL/RANK/OPG in bone modeling and remodeling
Zeitschrift    Archives of Biochemistry and Biophysics
Verlag    Elsevier
Ausgabe    473
Jahr    2009
Nummer    2
Seiten    139-146
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2413418/pdf/nihms50780.pdf

Literaturverz.   

no
Fußnoten    yes
Fragmente    2


Fragmente der Quelle:
[1.] Analyse:Mcm/Fragment 083 01 - Diskussion
Zuletzt bearbeitet: 2014-12-11 01:47:34 Hindemith
Boyce and Xing 2009, Fragment, Mcm, SMWFragment, Schutzlevel, ZuSichten, ÜbersetzungsPlagiat

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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]

Anmerkungen

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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(Hindemith)

[2.] Analyse:Mcm/Fragment 088 01 - Diskussion
Zuletzt bearbeitet: 2014-12-11 02:05:57 Hindemith
Boyce and Xing 2009, Fragment, Mcm, SMWFragment, Schutzlevel, ZuSichten, ÜbersetzungsPlagiat

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Ha demostrat ser un potent inhibidor de l’osteoclastogenesi in vitro a través de la inhibició del sistema RANKL [242, 243].

6.5. RANK

És una proteïna de membrana homotrimèrica membre de la superfamília del receptor TNF.

Sembla trobar-se expressada en menys teixit que RANKL a nivell proteic, però a part de trobar-la en els osteoclasts en formació i cèl·lules dendrítiques, també s’expressa a les glàndules mamaries i algunes cèl·lules cancerígenes (mama/pròstata) [244].

6.6. OPG

L’OPG és secretada per varis tipus cel·lulars a més dels osteoblasts, fins i tot les cèl·lules del cor, ronyons, fetge i melsa.

Estudis recents refereixen que les cèl·lules B serien responsables del 64% del total de la producció OPG del moll d’os. Aquesta afirmació sorgí arrel d’estudis on els ratolins deficients en cèl·lules B mostraren de forma constant osteoporosi [245].

La majoria de factors que comporten la inducció osteoblàstica de RANKL també regulen l’expressió osteoblàstica de OPG [246].


242. Takayanagi, H., et al., RANKL maintains bone homeostasis through c- Fos-dependent induction of interferon-beta. Nature, 2002. 416(6882): p. 744-9.

243. Takayanagi, H., et al., T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-gamma. Nature, 2000. 408(6812): p. 600-5.

244. Chen, G., et al., Expression of RANKL/RANK/OPG in primary and metastatic human prostate cancer as markers of disease stage and functional regulation. Cancer, 2006. 107(2): p. 289-98.

245. Li, Y., et al., B cells and T cells are critical for the preservation of bone homeostasis and attainment of peak bone mass in vivo. Blood, 2007. 109(9): p. 3839-48.

246. Hofbauer, L.C. and M. Schoppet, Clinical implications of the osteoprotegerin/RANKL/RANK system for bone and vascular diseases. JAMA, 2004. 292(4): p. 490-5.

It has been reported to be a strong suppressor of osteoclastogenesis in vitro through inhibition of RANKL signaling (54,56). [...]

[...]

RANK

RANK is a homotrimeric transmembrane protein member of the TNF receptor superfamily. It appears to be expressed in fewer tissues than RANKL at the protein level, but in addition to OCPs, mature osteoclasts and dendritic cells, it is expressed in mammary glands (50) and some cancer cells, including breast and prostate cancers (51,62), two tumors with high bone

[page 7]

metastatic potential. [...]


OPG

OPG is secreted by many cell types in addition to osteoblasts, including those in the heart, kidney, liver, and spleen. A recent study reports that B cells may be responsible for 64% of total bone marrow OPG production and B cell-deficient mice are consistently osteoporotic, consistent with B cells being a major source of OPG in the bone marrow of normal mice (65). Most of the factors that induce RANKL expression by osteoblasts also regulate OPG expression (66).


50. Fata JE, Kong YY, Li J, Sasaki T, Irie-Sasaki J, Moorehead RA, Elliott R, Scully S, Voura EB, Lacey DL. The Osteoclast Differentiation Factor Osteoprotegerin-Ligand Is Essential for Mammary Gland Development. Cell 2000;103:41–50. [PubMed: 11051546]

51. Kim NS, Kim HJ, Koo BK, Kwon MC, Kim YW, Cho Y, Yokota Y, Penninger JM, Kong YY. Receptor activator of NF-kappaB ligand regulates the proliferation of mammary epithelial cells via Id2. Mol Cell Biol 2006;26:1002–1013. [PubMed: 16428453]

[53. Takayanagi H, Kim S, Matsuo K, Suzuki H, Suzuki T, Sato K, Yokochi T, Oda H, Nakamura K, Ida N, et al. RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-beta. [see comment]. Nature 2002;416:744–749. [PubMed: 11961557] ]

54. Takayanagi H, Ogasawara K, Hida S, Chiba T, Murata S, Sato K, Takaoka A, Yokochi T, Oda H, Tanaka K, et al. T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-gamma. Nature 2000;408:600–605. [PubMed: 11117749]

56. Takayanagi H, Kim S, Taniguchi T. Signaling crosstalk between RANKL and interferons in osteoclast differentiation. Arthritis Res 2002;4 Suppl 3:S227–232. [PubMed: 12110142]

62. Chen G, Sircar K, Aprikian A, Potti A, Goltzman D, Rabbani SA. Expression of RANKL/RANK/ OPG in primary and metastatic human prostate cancer as markers of disease stage and functional regulation. Cancer 2006;107:289–298. [PubMed: 16752412]

65. Li Y, Toraldo G, Li A, Yang X, Zhang H, Qian WP, Weitzmann MN. B cells and T cells are critical for the preservation of bone homeostasis and attainment of peak bone mass in vivo. Blood 2007;109:3839–3848. [PubMed: 17202317]

66. Hofbauer LC, Schoppet M. Clinical implications of the osteoprotegerin/RANKL/RANK system for bone and vascular diseases. Jama 2004;292:490–495. [PubMed: 15280347]

Anmerkungen

The source is not mentioned although the entire page has been translated from it.

Note that in one instance a different paper of Takayanagi et al. has been referenced in the dissertation than had been referenced in the source. Using the numbering of the source 53 has been used instead of 54.

Sichter
(Hindemith)

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