http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Shou‑Dong Chai,Zhen‑Kun Li,Rui Liu,Tao Liu,Ming‑Feng Dong,Pei‑Zhe Tang,Jian‑Tang Wang,Sheng‑Jun Ma 대한독성 유전단백체 학회 2020 Molecular & cellular toxicology Vol.16 No.3
Background Nisoldipine can effectively suppress pulmonary arterial smooth muscle cell proliferation and c-Fos expression. Objective To identify the mechanism of the anti-inflammatory effects in monocrotaline-induced pulmonary arterial hypertension (PAH), focusing on the c-Fos/NLRP3/caspase-1 pathway. Results In a mice model of monocrotaline-induced PAH, miRNA-155 expression was increased. In an in vitro model, overexpression of miRNA-155 promoted inflammation and induced c-Fos, NLRP3, and caspase-1 protein expression. The inhibition of c-Fos reduced the effects of miRNA-155 on inflammation in an in vitro model of monocrotaline-induced PAH. The inhibition of NLRP3 reduced the effects of miRNA-155 on inflammation in an in vitro model of monocrotaline-induced PAH. Conclusions miRNA-155 increased inflammation in monocrotaline-induced PAH through c-Fos/NLRP3/caspase-1.
Yao Xin-Tong,Li Pei-pei,Liu Jiang,Yang Yuan-Yuan,Luo Zhen-Ling,Jiang Hai-Tao,He Wen-Ge,Luo Hong-Hong,Deng Yi-Xuan,He Bai-Cheng 한국조직공학과 재생의학회 2023 조직공학과 재생의학 Vol.20 No.5
BACKGROUND: All-trans retinoic acid (ATRA) promotes the osteogenic differentiation induced by bone morphogenetic protein 9 (BMP9), but the intrinsic relationship between BMP9 and ATRA keeps unknown. Herein, we investigated the effect of Cyp26b1, a critical enzyme of ATRA degradation, on the BMP9-induced osteogenic differentiation in mesenchymal stem cells (MSCs), and unveiled possible mechanism through which BMP9 regulates the expression of Cyp26b1. METHODS: ATRA content was detected with ELISA and HPLC–MS/MS. PCR, Western blot, and histochemical staining were used to assay the osteogenic markers. Fetal limbs culture, cranial defect repair model, and micro–computed tomographic were used to evaluate the quality of bone formation. IP and ChIP assay were used to explore possible mechanism. RESULTS: We found that the protein level of Cyp26b1 was increased with age, whereas the ATRA content decreased. The osteogenic markers induced by BMP9 were increased by inhibiting or silencing Cyp26b1 but reduced by exogenous Cyp26b1. The BMP9-induced bone formation was enhanced by inhibiting Cyp26b1. The cranial defect repair was promoted by BMP9, which was strengthened by silencing Cyp26b1 and reduced by exogenous Cyp26b1. Mechanically, Cyp26b1 was reduced by BMP9, which was enhanced by activating Wnt/b-catenin, and reduced by inhibiting this pathway. b-catenin interacts with Smad1/5/9, and both were recruited at the promoter of Cyp26b1. CONCLUSIONS: Our findings suggested the BMP9-induced osteoblastic differentiation was mediated by activating retinoic acid signalling, viadown-regulating Cyp26b1. Meanwhile, Cyp26b1 may be a novel potential therapeutic target for the treatment of bone-related diseases or accelerating bone-tissue engineering.