Role of semaphorin 7a signaling in transforming growth factor β1-induced lung fibrosis and scleroderma-related interstitial lung disease.
Role of semaphorin 7a signaling in transforming growth factor β1-induced lung fibrosis and scleroderma-related interstitial lung disease.
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DOI：
10.1002/art.30386
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发表时间：
2011-08
影响因子：
--
通讯作者：
Herzog, Erica
中科院分区：
文献类型：
--
作者：
Gan, Ye;Reilkoff, Ronald;Peng, Xueyan;Russell, Thomas;Chen, Qingsheng;Mathai, Susan K.;Homer, Robert;Gulati, Mridu;Siner, Jonathan;Elias, Jack;Bucala, Richard;Herzog, Erica
Semaphorin (Sema) 7a regulates TGF- β1 induced fibrosis. Using a murine model of pulmonary fibrosis in which an inducible, bioactive form of the human TGF- β1 gene is overexpressed in the lung, we tested the hypothesis that Sema-7a exerts its pro-fibrotic effects in part by promoting the tissue accumulation of CD45+ fibrocytes. Fibrosis and fibrocytes were evaluated in TGF- β1 transgenic mice in which the Sema-7a locus had been disrupted. The effect of replacement or deletion of Sema-7a on bone marrow derived cells was ascertained using bone marrow transplantation. The role of the Sema-7a receptor β1 integrin was assessed using neutralizing antibodies. The applicability of these findings to TGF-β1-driven fibrosis in humans was examined in patients with scleroderma-related interstitial lung disease. The appearance of fibrocytes in the lungs in TGF- β1 transgenic mice requires Sema-7a. Replacement of Sema-7a in bone marrow derived cells restores lung fibrosis and fibrocytes. Immunoneutralization of β1 integrin reduces pulmonary fibrocytes and fibrosis. Peripheral blood mononuclear cells from patients with scleroderma-related interstitial lung disease show increased mRNA for Sema-7a and the β1 integrin, with Sema-7a located on collagen producing fibrocytes and CD19+ lymphocytes. Peripheral blood fibrocyte outgrowth is enhanced in these patients. Stimulation of normal human peripheral blood mononuclear cells with recombinant Sema-7a enhances fibrocyte differentiation; these effects are attenuated by β1 integrin neutralization. Interventions that reduce Sema-7a expression or prevent the Sema-7a - β1 integrin interaction may be ameliorative in TGF- β1-driven or fibrocyte-associated autoimmune fibroses.
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影响因子：
3.7
作者：
Murray LA;Rosada R;Moreira AP;Joshi A;Kramer MS;Hesson DP;Argentieri RL;Mathai S;Gulati M;Herzog EL;Hogaboam CM
通讯作者：
Hogaboam CM
DOI：
10.1016/j.bbrc.2006.11.149
发表时间：
2007-02-02
影响因子：
3.1
作者：
Mehrad, Borna;Burdick, Marie D.;Strieter, Robert M.
通讯作者：
Strieter, Robert M.
影响因子：
32.4
作者：
Czopik, Agnieszka K.;Bynoe, Margaret S.;Medzhitov, Ruslan
通讯作者：
Medzhitov, Ruslan
DOI：
10.1073/pnas.062010399
发表时间：
2002-03-19
影响因子：
11.1
作者：
Dong, CM;Zhu, SK;Goldschmidt-Clermont, PJ
通讯作者：
Goldschmidt-Clermont, PJ
DOI：
10.1016/j.jtcvs.2004.10.035
发表时间：
2005-05-01
影响因子：
6
作者：
D'Ovidio, F;Mura, M;Keshavjee, S
通讯作者：
Keshavjee, S