Differentiation of Vascular Stem Cells Contributes to Ectopic Calcification of Atherosclerotic Plaque

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F16%3A00064082" target="_blank" >RIV/00159816:_____/16:00064082 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1002/stem.2315" target="_blank" >http://dx.doi.org/10.1002/stem.2315</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/stem.2315" target="_blank" >10.1002/stem.2315</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Differentiation of Vascular Stem Cells Contributes to Ectopic Calcification of Atherosclerotic Plaque

Popis výsledku v původním jazyce

The cellular and molecular basis of vascular calcification (VC) in atherosclerosis is not fully understood. Here, we investigate role of resident/circulating progenitor cells in VC and contribution of inflammatory plaque environment to this process. VSCs and MSCs isolated from atherosclerotic ApoE-/- mice showed significantly more in vitro osteogenesis and chondrogenesis than cells generated from control C57BL/6 mice. To assess their ability to form bone in vivo, cells were primed chondrogenically or cultured in control medium on collagen glycosaminoglycan scaffolds in vitro prior to subcutaneous implantation in ApoE-/- and C57BL/6 mice using a crossover study design. Atherosclerotic ApoE-/- MSCs and VSCs formed bone when implanted in C57BL/6 mice. In ApoE-/- mice, these cells generated more mature bone than C57BL/6 cells. The atherosclerotic in vivo environment alone promoted bone formation by implanted C57BL/6 cells. Un-primed C57BL/6 VSCs were unable to form bone in either mouse strain. Treatment of ApoE-/- VSC chondrogenic cultures with interleukin (IL)-6 resulted in significantly increased glycosaminoglycan deposition and expression of characteristic chondrogenic genes at 21 days. In conclusion, resident vascular cells from atherosclerotic environment respond to the inflammatory milieu and undergo calcification. IL-6 may have a role in aberrant differentiation of VSCs contributing to vascular calcification in atherosclerosis.

Název v anglickém jazyce

Differentiation of Vascular Stem Cells Contributes to Ectopic Calcification of Atherosclerotic Plaque

Popis výsledku anglicky

The cellular and molecular basis of vascular calcification (VC) in atherosclerosis is not fully understood. Here, we investigate role of resident/circulating progenitor cells in VC and contribution of inflammatory plaque environment to this process. VSCs and MSCs isolated from atherosclerotic ApoE-/- mice showed significantly more in vitro osteogenesis and chondrogenesis than cells generated from control C57BL/6 mice. To assess their ability to form bone in vivo, cells were primed chondrogenically or cultured in control medium on collagen glycosaminoglycan scaffolds in vitro prior to subcutaneous implantation in ApoE-/- and C57BL/6 mice using a crossover study design. Atherosclerotic ApoE-/- MSCs and VSCs formed bone when implanted in C57BL/6 mice. In ApoE-/- mice, these cells generated more mature bone than C57BL/6 cells. The atherosclerotic in vivo environment alone promoted bone formation by implanted C57BL/6 cells. Un-primed C57BL/6 VSCs were unable to form bone in either mouse strain. Treatment of ApoE-/- VSC chondrogenic cultures with interleukin (IL)-6 resulted in significantly increased glycosaminoglycan deposition and expression of characteristic chondrogenic genes at 21 days. In conclusion, resident vascular cells from atherosclerotic environment respond to the inflammatory milieu and undergo calcification. IL-6 may have a role in aberrant differentiation of VSCs contributing to vascular calcification in atherosclerosis.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EI - Biotechnologie a bionika

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2016

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Stem Cells

ISSN

1066-5099

e-ISSN

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Svazek periodika

34

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

913-923

Kód UT WoS článku

000374697700010

EID výsledku v databázi Scopus

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