PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11381097

Circulating skeletal stem cells.

S A Kuznetsov·M H Mankani·S Gronthos·K Satomura·P Bianco·P G Robey
View original source ↗Export metadata ↓

Abstract

We report the isolation of adherent, clonogenic, fibroblast-like cells with osteogenic and adipogenic potential from the blood of four mammalian species. These cells phenotypically resemble but are distinguishable from skeletal stem cells found in bone marrow (stromal stem cells, "mesenchymal stem cells"). The osteogenic potential of the blood-borne cells was proven by an in vivo transplantation assay in which either polyclonal or single colony-derived strains were transplanted into the subcutis of immunocompromised mice, and the donor origin of the fully differentiated bone cells was proven using species-specific probes. This is the first definitive proof of the existence of circulating skeletal stem cells in mammals.

Explore related subjects

AdipocytesAnimalsBone DevelopmentBone and BonesCell AdhesionCell DifferentiationCell LineageCell SizeCells, CulturedClone CellsFibroblastsGuinea PigsHematopoietic Stem Cell TransplantationHematopoietic Stem CellsHumansImmunohistochemistryImmunophenotypingMesodermMiceRabbitsRepetitive Sequences, Nucleic AcidSkinSpecies SpecificityStromal CellsJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S A Kuznetsov, M H Mankani, S Gronthos, K Satomura, P Bianco, P G Robey. 2001-05-28. Circulating skeletal stem cells.. https://doi.org/10.1083/jcb.153.5.1133

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Insulin stimulation of pyruvate dehydrogenase in adipocytes involves two distinct signalling pathways.

In isolated rat adipocytes, the insulin stimulation of pyruvate dehydrogenase can be partially inhibited by inhibitors of PI3K (phosphoinositide 3-kinase) and MEK1/2 (mitogen-activated protein kinase/extracellular signal-regulated kinase kinase). In combination, U0126 and wortmannin completely block the insulin stimulation of pyruvate dehydrogenase. It is concluded that the effect of insulin on pyruvate dehydrogenase in rat adipocytes involves two distinct signalling pathways: one is sensitive to wortmannin and the other to U0126. The synthetic phosphoinositolglycan PIG41 can activate pyruvate dehydrogenase but the activation is only approx. 30% of the maximal effect of insulin. This modest activation can be completely blocked by wortmannin alone, suggesting that PIG41 acts through only one of the pathways leading to the activation of pyruvate dehydrogenase.

Adipocytes↗
PubMed2002

Short-time deoxynivalenol treatment induces metabolic disturbances in the rat.

Deoxynivalenol (DON) is produced by several Fusarium species and may contaminate feeds causing reduced food consumption and utilisation, reduced body weight gain and other unfavourable changes in animals. To verify if its adverse influence involves also hormonal and metabolic changes, the effect of DON on blood insulin, glucagon, leptin and metabolic parameters in growing Wistar rats was studied. Animals were treated subcutaneously with DON in the amount of 1 mg/kg b.w. After 3 days a significant increase in blood insulin, glucose and free fatty acids were observed in these animals in comparison to the control group. DON treatment caused an increment in glycogen depots and a reduction in triglycerides content in the muscle. Studies on isolated adipocytes revealed that DON (20 micromol/l) slightly stimulated basal lipogenesis, whereas insulin-induced lipid synthesis and lipolysis were unchanged. Results obtained after subcutaneous DON administration indicate that its adverse effects in animals may partially result from metabolic disturbances evoked by this mycotoxin.

Adipocytes↗
PubMed2002

Adipocyte-specific gene expression and adipogenic steatosis in the mouse liver due to peroxisome proliferator-activated receptor gamma1 (PPARgamma1) overexpression.

Peroxisome proliferator activated-receptor (PPAR) isoforms, alpha and gamma, function as important coregulators of energy (lipid) homeostasis. PPARalpha regulates fatty acid oxidation primarily in liver and to a lesser extent in adipose tissue, whereas PPARgamma serves as a key regulator of adipocyte differentiation and lipid storage. Of the two PPARgamma isoforms, PPARgamma1 and PPARgamma2 generated by alternative splicing, PPARgamma1 isoform is expressed in liver and other tissues, whereas PPARgamma2 isoform is expressed exclusively in adipose tissue where it regulates adipogenesis and lipogenesis. Since the function of PPARgamma1 in liver is not clear, we have, in this study, investigated the biological impact of overexpression of PPARgamma1 in mouse liver. Adenovirus-PPARgamma1 injected into the tail vein induced hepatic steatosis in PPARalpha(-/-) mice. Northern blotting and gene expression profiling results showed that adipocyte-specific genes and lipogenesis-related genes are highly induced in PPARalpha(-/-) livers with PPARgamma1 overexpression. These include adipsin, adiponectin, aP2, caveolin-1, fasting-induced adipose factor, fat-specific gene 27 (FSP27), CD36, Delta(9) desaturase, and malic enzyme among others, implying adipogenic transformation of hepatocytes. Of interest is that hepatic steatosis per se, induced either by feeding a diet deficient in choline or developing in fasted PPARalpha(-/-) mice, failed to induce the expression of these PPARgamma-regulated adipogenesis-related genes in steatotic liver. These results suggest that a high level of PPARgamma in mouse liver is sufficient for the induction of adipogenic transformation of hepatocytes with adipose tissue-specific gene expression and lipid accumulation. We conclude that excess PPARgamma activity can lead to the development of a novel type of adipogenic hepatic steatosis.

Adipocytes↗