Characterization of human PDGFR-β-positive pericytes from IPF and non-IPF lungs.
Characterization of human PDGFR-β-positive pericytes from IPF and non-IPF lungs.
复制标题
来自 IPF 和非 IPF 肺的人类 PDGFR-β 阳性周细胞的特征。
DOI:
10.1152/ajplung.00289.2018
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发表时间:
2018
期刊:
影响因子:
--
通讯作者:
Schnapp,LynnM
中科院分区:
文献类型:
--
作者:
Wilson,CaroleL;Stephenson,SarahE;Higuero,JeanPaul;Feghali-Bostwick,Carol;Hung,ChiF;Schnapp,LynnM
Pericytes are key regulators of the microvasculature through their close interactions with the endothelium. However, pericytes play additional roles in tissue homeostasis and repair, in part by transitioning into myofibroblasts. Accumulation of myofibroblasts is a hallmark of fibrotic diseases such as idiopathic pulmonary fibrosis (IPF). To understand the contribution and role of pericytes in human lung fibrosis, we isolated these cells from non-IPF control and IPF lung tissues based on expression of platelet-derived growth factor receptor-β (PDGFR-β), a common marker of pericytes. When cultured in a specialized growth medium, PDGFR-β+ cells retain the morphology and marker profile typical of pericytes. We found that IPF pericytes migrated more rapidly and invaded a basement membrane matrix more readily than control pericytes. Exposure of cells to transforming growth factor-β, a major fibrosis-inducing cytokine, increased expression of α-smooth muscle actin and extracellular matrix genes in both control and IPF pericytes. Given that pericytes are uniquely positioned in vivo to respond to danger signals of both systemic and tissue origin, we stimulated human lung pericytes with agonists having pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). Both control and IPF lung pericytes increased expression of proinflammatory chemokines in response to specific PAMPs and DAMPs released from necrotic cells. Our results suggest that control and IPF lung pericytes are poised to react to tissue damage, as well as microbial and fibrotic stimuli. However, IPF pericytes are primed for migration and matrix invasion, features that may contribute to the function of these cells in lung fibrosis.
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影响因子:
23.9
作者:
Guimarães-Camboa N;Cattaneo P;Sun Y;Moore-Morris T;Gu Y;Dalton ND;Rockenstein E;Masliah E;Peterson KL;Stallcup WB;Chen J;Evans SM
通讯作者:
Evans SM
影响因子:
2.4
作者:
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通讯作者:
M. Dragunow
DOI:
10.1016/j.ajpath.2014.09.013
发表时间:
2015
期刊:
The American journal of pathology
影响因子:
--
作者:
K. Yuan;M. Orcholski;Cristina Panaroni;Eric M. Shuffle;N. Huang;Xinguo Jiang;W. Tian;Eszter K Vladar;Lingli Wang;M. Nicolls;Joy Y Wu;V. A. de Jesus Perez
通讯作者:
K. Yuan;M. Orcholski;Cristina Panaroni;Eric M. Shuffle;N. Huang;Xinguo Jiang;W. Tian;Eszter K Vladar;Lingli Wang;M. Nicolls;Joy Y Wu;V. A. de Jesus Perez
影响因子:
2.9
作者:
Pieper, Christian;Marek, Jasmin Jacqueline;Galla, Hans-Joachim
通讯作者:
Galla, Hans-Joachim
影响因子:
4.1
作者:
Bichsel, Colette A.;Hall, Sean R. R.;Geiser, Thomas
通讯作者:
Geiser, Thomas