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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Tuesday, 2015 January 20
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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PubMed Results

Items 1 - 3 of 3

1.	Nat Med. 2014 Nov;20(11):1238-40. doi: 10.1038/nm.3747. Osteoclast progenitors promote bone vascularization and osteogenesis. Kusumbe AP1, Adams RH1. Comment on PDGF-BB secreted by preosteoclasts induces angiogenesis during coupling with osteogenesis. [Nat Med. 2014] PDGF-BB secreted by preosteoclasts induces angiogenesis during coupling with osteogenesis.Xie H, Cui Z, Wang L, Xia Z, Hu Y, Xian L, Li C, Xie L, Crane J, Wan M, et al. Nat Med. 2014 Nov; 20(11):1270-8. Epub 2014 Oct 5.
	PMID: 25375923 [PubMed - indexed for MEDLINE]
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2.	Nat Med. 2014 Nov;20(11):1279-88. doi: 10.1038/nm.3654. Epub 2014 Oct 12. Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures. Movérare-Skrtic S1, Henning P1, Liu X2, Nagano K3, Saito H3, Börjesson AE1, Sjögren K1, Windahl SH1, Farman H1, Kindlund B1, Engdahl C1, Koskela A4, Zhang FP5, Eriksson EE6, Zaman F7, Hammarstedt A8, Isaksson H9, Bally M10, Kassem A11, Lindholm C1, Sandberg O12, Aspenberg P12, Sävendahl L6, Feng JQ13, Tuckermann J14, Tuukkanen J4, Poutanen M15, Baron R16, Lerner UH17, Gori F16, Ohlsson C1. Abstract The WNT16 locus is a major determinant of cortical bone thickness and nonvertebral fracture risk in humans. The disability, mortality and costs caused by osteoporosis-induced nonvertebral fractures are enormous. We demonstrate here that Wnt16-deficient mice develop spontaneous fractures as a result of low cortical thickness and high cortical porosity. In contrast, trabecular bone volume is not altered in these mice. Mechanistic studies revealed that WNT16 is osteoblast derived and inhibits human and mouse osteoclastogenesis both directly by acting on osteoclast progenitors and indirectly by increasing expression of osteoprotegerin (Opg) in osteoblasts. The signaling pathway activated by WNT16 in osteoclast progenitors is noncanonical, whereas the pathway activated in osteoblasts is both canonical and noncanonical. Conditional Wnt16 inactivation revealed that osteoblast-lineage cells are the principal source of WNT16, and its targeted deletion in osteoblasts increases fracture susceptibility. Thus, osteoblast-derived WNT16 is a previously unreported key regulator of osteoclastogenesis and fracture susceptibility. These findings open new avenues for the specific prevention or treatment of nonvertebral fractures, a substantial unmet medical need.
	PMID: 25306233 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2014 Nov;20(11):1270-8. doi: 10.1038/nm.3668. Epub 2014 Oct 5. PDGF-BB secreted by preosteoclasts induces angiogenesis during coupling with osteogenesis. Xie H1, Cui Z2, Wang L3, Xia Z1, Hu Y1, Xian L4, Li C4, Xie L4, Crane J4, Wan M4, Zhen G4, Bian Q4, Yu B5, Chang W4, Qiu T4, Pickarski M6, Duong le T6, Windle JJ7, Luo X8, Liao E8, Cao X4. Comment in Osteoclast progenitors promote bone vascularization and osteogenesis. [Nat Med. 2014] Osteoclast progenitors promote bone vascularization and osteogenesis.Kusumbe AP, Adams RH. Nat Med. 2014 Nov; 20(11):1238-40. Abstract Osteogenesis during bone modeling and remodeling is coupled with angiogenesis. A recent study showed that a specific vessel subtype, strongly positive for CD31 and endomucin (CD31(hi)Emcn(hi)), couples angiogenesis and osteogenesis. Here, we found that platelet-derived growth factor-BB (PDGF-BB) secreted by preosteoclasts induces CD31(hi)Emcn(hi) vessel formation during bone modeling and remodeling. Mice with depletion of PDGF-BB in the tartrate-resistant acid phosphatase-positive cell lineage show significantly lower trabecular and cortical bone mass, serum and bone marrow PDGF-BB concentrations, and fewer CD31(hi)Emcn(hi) vessels compared to wild-type mice. In the ovariectomy (OVX)-induced osteoporotic mouse model, serum and bone marrow levels of PDGF-BB and numbers of CD31(hi)Emcn(hi) vessels are significantly lower compared to sham-operated controls. Treatment with exogenous PDGF-BB or inhibition of cathepsin K to increase the number of preosteoclasts, and thus the endogenous levels of PDGF-BB, increases CD31(hi)Emcn(hi) vessel number and stimulates bone formation in OVX mice. Thus, pharmacotherapies that increase PDGF-BB secretion from preosteoclasts offer a new therapeutic target for treating osteoporosis by promoting angiogenesis and thus bone formation. PMCID: PMC4224644 [Available on 2015/5/1]
	PMID: 25282358 [PubMed - indexed for MEDLINE]
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