Glast-expressing progenitor cells contribute to heterotopic ossification.
Glast-expressing progenitor cells contribute to heterotopic ossification.
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DOI：
10.1016/j.bone.2012.12.008
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发表时间：
2013-03
期刊：
影响因子：
4.1
通讯作者：
Kessler, John A.
中科院分区：
文献类型：
--
作者：
Kan, Lixin;Peng, Chian-Yu;McGuire, Tammy L.;Kessler, John A.
关键词：
异位骨化（HO），获得性或遗传性，是在正常骨骼外形成真骨。虽然在正常发育过程中有助于骨形成的细胞谱系是明确的，但有助于HO的细胞的精确谱系尚不清楚。本研究利用基于Cre-lox的遗传谱系追踪来检查表达FoxD 1或Glast的细胞对HO的贡献。这两个谱系广泛地贡献于不同的正常组织，FoxD 1-cre标记的细胞有助于正常骨形成。尽管正常组织的标记模式相似，FoxD 1-cre标记的细胞对正常骨有显著贡献，但只有Glast-creERT标记的祖细胞在所有阶段对HO有显著贡献，这表明通常有助于生理性骨形成的细胞群，如Foxd 1-cre标记的细胞，可能不参与病理性HO。此外，将Glast表达细胞鉴定为引起HO的前体应有助于分子靶向该群体以预防和治疗HO。
Heterotopic ossification (HO), acquired or hereditary, is the formation of true bone outside of the normal skeleton. Although the lineages of cells contributing to bone formation during normal development are well defined, the precise lineages of cells that contribute to HO are not clear. This study utilized Cre-lox based genetic lineage tracing to examine the contribution to HO of cells that expressed either FoxD1 or Glast. Both lineages contributed broadly to different normal tissues, and FoxD1-cre labeled cells contributed to normal bone formation. Despite the similarity in labeling patterns of normal tissues, and the significant contribution of FoxD1-cre labeled cells to normal bone, only Glast-creERT labeled progenitors contributed significantly to HO at all stages, suggesting the cell populations that normally contribute to physiological bone formation, such as the Foxd1-cre labeled cells, may not participate in pathological HO. Further, identification of Glast-expressing cells as precursors that give rise to HO should help with molecular targeting of this population both for the prevention and for the treatment of HO.
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DOI：
10.1007/s00429-006-0109-x
发表时间：
2006-11-01
期刊：
ANATOMY AND EMBRYOLOGY
影响因子：
--
作者：
Berger, Urs V.;Hediger, Matthias A.
通讯作者：
Hediger, Matthias A.
影响因子：
4.6
作者：
Herrera, E;Marcus, R;Mason, C
通讯作者：
Mason, C
影响因子：
5.3
作者：
Isabel Carreres, Maria;Escalante, Augusto;Herrera, Eloisa
通讯作者：
Herrera, Eloisa
影响因子：
3.6
作者：
Anthony TE;Heintz N
通讯作者：
Heintz N
影响因子：
25
作者：
Madisen L;Zwingman TA;Sunkin SM;Oh SW;Zariwala HA;Gu H;Ng LL;Palmiter RD;Hawrylycz MJ;Jones AR;Lein ES;Zeng H
通讯作者：
Zeng H