Regulation of fibroblast lipid storage and myofibroblast phenotypes during alveolar septation in mice.
Regulation of fibroblast lipid storage and myofibroblast phenotypes during alveolar septation in mice.
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小鼠肺泡间隔期间成纤维细胞脂质储存和肌成纤维细胞表型的调节。
DOI：
10.1152/ajplung.00144.2014
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
McCoy,DiannM
中科院分区：
文献类型：
--
作者：
McGowan,StephenE;McCoy,DiannM
Signaling through platelet-derived growth factor receptor-α (PDGFRα) is required for alveolar septation and participates in alveolar regeneration after pneumonectomy. In both adipose tissue and skeletal muscle, bipotentpdgfrα-expressing progenitors expressing delta-like ligand-1 or sex-determining region Y box 9 (Sox9) may differentiate into either lipid storage cells or myofibroblasts. We analyzed markers of mesenchymal progenitors and differentiation in lung fibroblasts (LF) with different levels (absent, low, or high) ofpdgfrα gene expression. A larger proportion ofpdgfrα-expressing than nonexpressing LF contained Sox9. Neutral lipids, CD166, and Tcf21 were more abundant in LF with a lower compared with a higher level ofpdgfrα gene expression. PDGF-A increased Sox9 in primary LF cultures, suggesting that active signaling through PDGFRα is required to maintain Sox9. As alveolar septation progresses frompostnatal day(P)8to P12, fewerpdgfrα-expressing LF contain Sox9, whereas more of these LF contain myocardin-like transcription factor-A, showing that Sox9 diminishes as LF become myofibroblasts. At P8, neutral lipid droplets predominate in LF with the lower level ofpdgfrα gene expression, whereastransgelin(tagln) was predominantly expressed in LF with higherpdgfrα gene expression. Targeted deletion ofpdgfrα in LF, which expressedtagln, reduced Sox9 in α-actin (α-SMA, ACTA2)-containing LF, whereas it increased the abundance of cell surface delta-like protein-1 (as well as peroxisome proliferator-activated receptor-γ andtcf21 mRNA in LF, which also expressed stem cell antigen-1). Thuspdgfrα deletion differentially alters delta-like protein-1 and Sox9, suggesting that targeting different downstream pathways in PDGF-A-responsive LF could identify strategies that promote lung regeneration without initiating fibrosis.
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DOI：
10.1165/rcmb.2011-0316oc
发表时间：
2012-12
影响因子：
6.4
作者：
B. Varisco;N. Ambalavanan;J. Whitsett;J. Hagood
通讯作者：
B. Varisco;N. Ambalavanan;J. Whitsett;J. Hagood
DOI：
10.1152/ajplung.00011.2013
发表时间：
2013-08-01
影响因子：
4.9
作者：
McGowan, Stephen E.;McCoy, Diann M.
通讯作者：
McCoy, Diann M.
影响因子：
29.4
作者：
Pelczar P;Zibat A;van Dop WA;Heijmans J;Bleckmann A;Gruber W;Nitzki F;Uhmann A;Guijarro MV;Hernando E;Dittmann K;Wienands J;Dressel R;Wojnowski L;Binder C;Taguchi T;Beissbarth T;Hogendoorn PC;Antonescu CR;Rubin BP;Schulz-Schaeffer W;Aberger F;van den Brink GR;Hahn H
通讯作者：
Hahn H
DOI：
10.1016/j.bbrc.2012.04.149
发表时间：
2012-06-01
影响因子：
3.1
作者：
Xu Z;Ji G;Shen J;Wang X;Zhou J;Li L
通讯作者：
Li L
影响因子：
3.3
作者：
HANTOS, Z;DAROCZY, B;NAGY, S
通讯作者：
NAGY, S