dsc43men

Property	Value
?:abstract	Despite past extensive studies, the mechanisms underlying pulmonary fibrosis (PF) still remain poorly understood Here, we demonstrated that lungs originating from different types of patients with PF, including coronavirus disease 2019, systemic sclerosis-associated interstitial lung disease, and idiopathic PF, and from mice following bleomycin (BLM)-induced PF are characterized by the altered methyl-CpG-binding domain 2 (MBD2) expression in macrophages Depletion of Mbd2 in macrophages protected mice against BLM-induced PF Mbd2 deficiency significantly attenuated transforming growth factor-beta1 (TGF-beta1) production and reduced M2 macrophage accumulation in the lung following BLM induction Mechanistically, Mbd2 selectively bound to the Ship promoter in macrophages, by which it repressed Ship expression and enhanced PI3K/Akt signaling to promote the macrophage M2 program Therefore, intratracheal administration of liposomes loaded with Mbd2 siRNA protected mice from BLM-induced lung injuries and fibrosis Together, our data support the possibility that MBD2 could be a viable target against PF in clinical settings Despite past extensive studies, the mechanisms underlying pulmonary fibrosis (PF) still remain poorly understood. Herein we demonstrated that lungs originated from different types of PF patients including coronavirus disease 2019, systemic sclerosis associated interstitial lung disease and idiopathic pulmonary fibrosis, and mice following bleomycin (BLM)-induced PF are characterized by the altered methyl-CpG-binding domain 2 (MBD2) expression in macrophages. Depletion of Mbd2 in macrophages protected mice against BLM-induced PF. Mbd2 deficiency significantly attenuated transforming growth factor ß1 (TGF-ß1) production and reduced M2 macrophage accumulation in the lung following BLM induction. Mechanistically, Mbd2 selectively bound to the Ship promoter in macrophages, by which it repressed Ship expression and enhanced PI3K/Akt signaling to promote macrophage M2 program. Therefore, intratracheal administration of liposomes loaded with Mbd2 siRNA protected mice from BLM-induced lung injuries and fibrosis. Together, our data support that MBD2 could be a viable target against pulmonary fibrosis in clinical settings.
is ?:annotates of	<https://research.tib.eu/covid-19/entity/dsc43men_hasAnnotation_C0016059> <https://research.tib.eu/covid-19/entity/dsc43men_hasAnnotation_C0023828> <https://research.tib.eu/covid-19/entity/dsc43men_hasAnnotation_C0273115> <https://research.tib.eu/covid-19/entity/dsc43men_hasAnnotation_C1417050> <https://research.tib.eu/covid-19/entity/dsc43men_hasAnnotation_C4277657> <https://research.tib.eu/covid-19/entity/dsc43men_hasAnnotation_C4284302>
?:creator	<https://research.tib.eu/covid-19/entity/Wang%2C_Y.%3B_Zhang%2C_L.%3B_Wu%2C_G._R.%3B_Zhou%2C_Q.%3B_Yue%2C_H.%3B_Rao%2C_L._Z.%3B_Yuan%2C_T.%3B_Mo%2C_B.%3B_Wang%2C_F._X.%3B_Chen%2C_L._M.%3B_Sun%2C_F.%3B_Song%2C_J.%3B_Xiong%2C_F.%3B_Zhang%2C_S.%3B_Yu%2C_Q.%3B_Yang%2C_P.%3B_Xu%2C_Y.%3B_Zhao%2C_J.%3B_Zhang%2C_H.%3B_Xiong%2C_W.%3B_Wang%2C_C._Y.> <https://research.tib.eu/covid-19/entity/Wang%2C_Yi%3B_Zhang%2C_Lei%3B_Wu%2C_Guo-Rao%3B_Zhou%2C_Qing%3B_Yue%2C_Huihui%3B_Rao%2C_Li-Zong%3B_Yuan%2C_Ting%3B_Mo%2C_Biwen%3B_Wang%2C_Fa-Xi%3B_Chen%2C_Long-Min%3B_Sun%2C_Fei%3B_Song%2C_Jia%3B_Xiong%2C_Fei%3B_Zhang%2C_Shu%3B_Yu%2C_Qilin%3B_Yang%2C_Ping%3B_Xu%2C_Yongjian%3B_Zhao%2C_Jianping%3B_Zhang%2C_Huilan%3B_Xiong%2C_Weining%3B_Wang%2C_Cong-Yi>
?:journal	Sci._Adv Science_Advances
?:license	unk
?:publication_isRelatedTo_Disease	<https://research.tib.eu/covid-19/entity/COVID-19>
is ?:relation_isRelatedTo_publication of	<https://research.tib.eu/covid-19/entity/dsc43men_HAS_C0005740_CAUSES_C0016059> <https://research.tib.eu/covid-19/entity/dsc43men_HAS_C0005740_CAUSES_C0034069> <https://research.tib.eu/covid-19/entity/dsc43men_HAS_C0005740_CAUSES_C0273115> <https://research.tib.eu/covid-19/entity/dsc43men_HAS_C0034069_PRECEDES_C0206062> <https://research.tib.eu/covid-19/entity/dsc43men_HAS_C0034069_PRECEDES_C1800706>
?:source	WHO
?:title	MBD2 serves as a viable target against pulmonary fibrosis by inhibiting macrophage M2 program
?:type	<https://research.tib.eu/covid-19/vocab/Publication>
?:who_covidence_id	#1066781 #960993
?:year	2020 2021

Property

Value

?:abstract

Despite past extensive studies, the mechanisms underlying pulmonary fibrosis (PF) still remain poorly understood Here, we demonstrated that lungs originating from different types of patients with PF, including coronavirus disease 2019, systemic sclerosis-associated interstitial lung disease, and idiopathic PF, and from mice following bleomycin (BLM)-induced PF are characterized by the altered methyl-CpG-binding domain 2 (MBD2) expression in macrophages Depletion of Mbd2 in macrophages protected mice against BLM-induced PF Mbd2 deficiency significantly attenuated transforming growth factor-beta1 (TGF-beta1) production and reduced M2 macrophage accumulation in the lung following BLM induction Mechanistically, Mbd2 selectively bound to the Ship promoter in macrophages, by which it repressed Ship expression and enhanced PI3K/Akt signaling to promote the macrophage M2 program Therefore, intratracheal administration of liposomes loaded with Mbd2 siRNA protected mice from BLM-induced lung injuries and fibrosis Together, our data support the possibility that MBD2 could be a viable target against PF in clinical settings
Despite past extensive studies, the mechanisms underlying pulmonary fibrosis (PF) still remain poorly understood. Herein we demonstrated that lungs originated from different types of PF patients including coronavirus disease 2019, systemic sclerosis associated interstitial lung disease and idiopathic pulmonary fibrosis, and mice following bleomycin (BLM)-induced PF are characterized by the altered methyl-CpG-binding domain 2 (MBD2) expression in macrophages. Depletion of Mbd2 in macrophages protected mice against BLM-induced PF. Mbd2 deficiency significantly attenuated transforming growth factor ß1 (TGF-ß1) production and reduced M2 macrophage accumulation in the lung following BLM induction. Mechanistically, Mbd2 selectively bound to the Ship promoter in macrophages, by which it repressed Ship expression and enhanced PI3K/Akt signaling to promote macrophage M2 program. Therefore, intratracheal administration of liposomes loaded with Mbd2 siRNA protected mice from BLM-induced lung injuries and fibrosis. Together, our data support that MBD2 could be a viable target against pulmonary fibrosis in clinical settings.

is ?:annotates of