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- W2028008068 abstract "As miRNAs are associated with normal cellular processes, deregulation of miRNAs is thought to play a causative role in many complex diseases. Nevertheless, the precise contribution of miRNAs in fibrotic lung diseases, especially the idiopathic form (IPF), remains poorly understood. Given the poor response rate of IPF patients to current therapy, new insights into the pathogenic mechanisms controlling lung fibroblasts activation, the key cell type driving the fibrogenic process, are essential to develop new therapeutic strategies for this devastating disease. To identify miRNAs with potential roles in lung fibrogenesis, we performed a genome-wide assessment of miRNA expression in lungs from two different mouse strains known for their distinct susceptibility to develop lung fibrosis after bleomycin exposure. This led to the identification of miR-199a-5p as the best miRNA candidate associated with bleomycin response. Importantly, miR-199a-5p pulmonary expression was also significantly increased in IPF patients (94 IPF versus 83 controls). In particular, levels of miR-199a-5p were selectively increased in myofibroblasts from injured mouse lungs and fibroblastic foci, a histologic feature associated with IPF. Therefore, miR-199a-5p profibrotic effects were further investigated in cultured lung fibroblasts: miR-199a-5p expression was induced upon TGFβ exposure, and ectopic expression of miR-199a-5p was sufficient to promote the pathogenic activation of pulmonary fibroblasts including proliferation, migration, invasion, and differentiation into myofibroblasts. In addition, we demonstrated that miR-199a-5p is a key effector of TGFβ signaling in lung fibroblasts by regulating CAV1, a critical mediator of pulmonary fibrosis. Remarkably, aberrant expression of miR-199a-5p was also found in unilateral ureteral obstruction mouse model of kidney fibrosis, as well as in both bile duct ligation and CCl4-induced mouse models of liver fibrosis, suggesting that dysregulation of miR-199a-5p represents a general mechanism contributing to the fibrotic process. MiR-199a-5p thus behaves as a major regulator of tissue fibrosis with therapeutic potency to treat fibroproliferative diseases." @default.
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- W2028008068 date "2013-02-14" @default.
- W2028008068 modified "2023-10-18" @default.
- W2028008068 title "miR-199a-5p Is Upregulated during Fibrogenic Response to Tissue Injury and Mediates TGFbeta-Induced Lung Fibroblast Activation by Targeting Caveolin-1" @default.
- W2028008068 cites W1537353085 @default.
- W2028008068 cites W1648301895 @default.
- W2028008068 cites W1782190153 @default.
- W2028008068 cites W1913982549 @default.
- W2028008068 cites W1976077409 @default.
- W2028008068 cites W1981269419 @default.
- W2028008068 cites W1981533568 @default.
- W2028008068 cites W1983251505 @default.
- W2028008068 cites W1983611264 @default.
- W2028008068 cites W1989626257 @default.
- W2028008068 cites W1991663093 @default.
- W2028008068 cites W1992508898 @default.
- W2028008068 cites W1993489616 @default.
- W2028008068 cites W1995105009 @default.
- W2028008068 cites W1996137961 @default.
- W2028008068 cites W2007701028 @default.
- W2028008068 cites W2008204899 @default.
- W2028008068 cites W2009001235 @default.
- W2028008068 cites W2012511861 @default.
- W2028008068 cites W2013114941 @default.
- W2028008068 cites W2014162043 @default.
- W2028008068 cites W2016613783 @default.
- W2028008068 cites W2019821950 @default.
- W2028008068 cites W2028324150 @default.
- W2028008068 cites W2030698703 @default.
- W2028008068 cites W2044662583 @default.
- W2028008068 cites W2054110511 @default.
- W2028008068 cites W2061558045 @default.
- W2028008068 cites W2061638986 @default.
- W2028008068 cites W2062410538 @default.
- W2028008068 cites W2062750166 @default.
- W2028008068 cites W2064307892 @default.
- W2028008068 cites W2067512788 @default.
- W2028008068 cites W2083896648 @default.
- W2028008068 cites W2091096046 @default.
- W2028008068 cites W2099677690 @default.
- W2028008068 cites W2103198823 @default.
- W2028008068 cites W2107272258 @default.
- W2028008068 cites W2108683967 @default.
- W2028008068 cites W2111833940 @default.
- W2028008068 cites W2112192177 @default.
- W2028008068 cites W2112871329 @default.
- W2028008068 cites W2115813327 @default.
- W2028008068 cites W2123106337 @default.
- W2028008068 cites W2125536613 @default.
- W2028008068 cites W2130410032 @default.
- W2028008068 cites W2130704025 @default.
- W2028008068 cites W2130979840 @default.
- W2028008068 cites W2132093971 @default.
- W2028008068 cites W2136592357 @default.
- W2028008068 cites W2138664009 @default.
- W2028008068 cites W2146483998 @default.
- W2028008068 cites W2151603591 @default.
- W2028008068 cites W2152956716 @default.
- W2028008068 cites W2154087214 @default.
- W2028008068 cites W2158102355 @default.
- W2028008068 cites W2159864284 @default.
- W2028008068 cites W2160467221 @default.
- W2028008068 cites W2160905065 @default.
- W2028008068 cites W2165467938 @default.
- W2028008068 cites W2169354377 @default.
- W2028008068 cites W2169928292 @default.
- W2028008068 cites W2170748626 @default.
- W2028008068 cites W2171260596 @default.
- W2028008068 cites W2230393028 @default.
- W2028008068 cites W4211067148 @default.
- W2028008068 cites W4234164547 @default.
- W2028008068 cites W4237473415 @default.
- W2028008068 cites W4251765607 @default.
- W2028008068 cites W4255712601 @default.
- W2028008068 doi "https://doi.org/10.1371/journal.pgen.1003291" @default.
- W2028008068 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3573122" @default.