Objective Acute respiratory distress syndrome(ARDS)patients currently have relatively high mortality,which is associated with early lung fibrosis.This study aimed to investigate whether miR-17 suppression could allevi...Objective Acute respiratory distress syndrome(ARDS)patients currently have relatively high mortality,which is associated with early lung fibrosis.This study aimed to investigate whether miR-17 suppression could alleviate ARDS-associated lung fibrosis by regulating Mfn2.Methods A mouse model of ARDS-related lung fibrosis was constructed via intratracheal instillation of bleomycin.The expression level of miR-17 in lung tissues was detected via quantitative real time polymerase chain reaction(qRT-PCR).In the ARDS mouse model of lung fibrosis,the mitigating effects of miR-17 interference were evaluated via tail vein injection of the miR negative control or the miR-17 antagomir.The pathological changes in the lung tissue were examined via HE staining and Masson’s trichrome staining,and the underlying molecular mechanism was investigated via ELISA,qRT-PCR and Western blotting.Results Bleomycin-induced pulmonary fibrosis significantly increased collagen deposition and the levels of hydroxyproline(HYP)and miR-17.Interfering with miR-17 significantly reduced the levels of HYP and miR-17 and upregulated the expression of Mfn2.The intravenous injection of the miR-17 antagomir alleviated lung inflammation and reduced collagen deposition.In addition,interference with miR-17 could upregulate LC3B expression,downregulate p62 expression,and improve mitochondrial structure.Conclusion Interfering with miR-17 can improve pulmonary fibrosis in mice by promoting mitochondrial autophagy via Mfn2.展开更多
BACKGROUND In China,as the population grows older,the number of elderly people who have died from respiratory problems has increased.AIM To investigate whether enhanced recovery after surgery(ERAS)-based respiratory f...BACKGROUND In China,as the population grows older,the number of elderly people who have died from respiratory problems has increased.AIM To investigate whether enhanced recovery after surgery(ERAS)-based respiratory function training may help older patients who had abdominal surgery suffer fewer pulmonary problems,shorter hospital stays,and improved lung function.METHODS The data of 231 elderly individuals having abdominal surgery was retrospectively analyzed.Based on whether ERAS-based respiratory function training was provided,patients were divided into ERAS group(n=112)and control group(n=119).Deep vein thrombosis(DVT),pulmonary embolism(PE),and respiratory tract infection(RTI)were the primary outcome variables.Secondary outcome variables included the Borg score Scale,FEV1/FVC and postoperative hospital stay.RESULTS The percentage of 18.75%of ERAS group participants and 34.45%of control group participants,respectively,had respiratory infections(P=0.007).None of the individuals experienced PE or DVT.The ERAS group’s median postoperative hospital stay was 9.5 d(3-21 d)whereas the control groups was 11 d(4-18 d)(P=0.028).The Borg score decreased on the 4th d following surgery in the ERAS group compared to the 2nd d prior(P=0.003).The incidence of RTIs was greater in the control group than in the ERAS group among patients who spent more than 2 d in the hospital before surgery(P=0.029).CONCLUSION ERAS-based respiratory function training may reduce the risk of pulmonary complications in older individuals undergoing abdominal surgery.展开更多
Acute respiratory distress syndrome(ARDS)is one of the most fatal diseases worldwide.Pulmonary fibrosis occurs early in ARDS,and its severity plays a crucial role in ARDS mortality rate.Some studies suggested that fib...Acute respiratory distress syndrome(ARDS)is one of the most fatal diseases worldwide.Pulmonary fibrosis occurs early in ARDS,and its severity plays a crucial role in ARDS mortality rate.Some studies suggested that fibroproliferation is an essential mechanism in ARDS.Mitofusion2(Mfn2)overexpression plays a role in inhibiting cell proliferation.However,the role and potential mechanism of Mfn2 on the proliferation of fibroblasts is still unknown.In this study,we aimed at exploring the effect of Mfn2 on the human embryonic lung fibroblasts(HELF)and discussed its related mechanism.The HELF were treated with the Mfn2 overexpressing lentivirus(adv-Mfn2).The cell cycle was detected by flow cytometry.MTT,PCR and Western blotting were used to investigate the effect of Mfn2 on the proliferation of the HELF,collagen expression,the RAS-RAF-1-ERK1/2 pathway and the expression of cycle-related proteins(p21,p27,Rb,Raf-1,p-Raf-1,Erk1/2 and p-Erk1/2).The co-immunoprecipitation assay was used to explore the interaction between Mfn2 and Ras.The results showed that the overexpression of Mfn2 inhibited the proliferation of the HELF and induced the cell cycle arrest at the G0/G1 phase.Meanwhile,Mfn2 also inhibited the expression of collagen I,p-Erk and p-Raf-1.In addition,an interaction between Mfn2 and Ras existed in the HELF.This study suggests that the overexpression of Mfn2 can decrease the proliferation of HELF in ARDS,which was associated with the inhibition of the RAS-RAF-1-ERK1/2 pathway.The results may offer a potential therapeutic intervention for patients with ARDS.展开更多
基金supported by grants from the Natural Science Foundation of Hubei Province(No.2022CFB423,2023AFB1055)Hubei Province Health and Family Planning Scientific Research Project(No.WJ2023M030).
文摘Objective Acute respiratory distress syndrome(ARDS)patients currently have relatively high mortality,which is associated with early lung fibrosis.This study aimed to investigate whether miR-17 suppression could alleviate ARDS-associated lung fibrosis by regulating Mfn2.Methods A mouse model of ARDS-related lung fibrosis was constructed via intratracheal instillation of bleomycin.The expression level of miR-17 in lung tissues was detected via quantitative real time polymerase chain reaction(qRT-PCR).In the ARDS mouse model of lung fibrosis,the mitigating effects of miR-17 interference were evaluated via tail vein injection of the miR negative control or the miR-17 antagomir.The pathological changes in the lung tissue were examined via HE staining and Masson’s trichrome staining,and the underlying molecular mechanism was investigated via ELISA,qRT-PCR and Western blotting.Results Bleomycin-induced pulmonary fibrosis significantly increased collagen deposition and the levels of hydroxyproline(HYP)and miR-17.Interfering with miR-17 significantly reduced the levels of HYP and miR-17 and upregulated the expression of Mfn2.The intravenous injection of the miR-17 antagomir alleviated lung inflammation and reduced collagen deposition.In addition,interference with miR-17 could upregulate LC3B expression,downregulate p62 expression,and improve mitochondrial structure.Conclusion Interfering with miR-17 can improve pulmonary fibrosis in mice by promoting mitochondrial autophagy via Mfn2.
基金Supported by Project for Scientific Research by the Hongkou District Health Committee,No.Hong Wei 2002-08.
文摘BACKGROUND In China,as the population grows older,the number of elderly people who have died from respiratory problems has increased.AIM To investigate whether enhanced recovery after surgery(ERAS)-based respiratory function training may help older patients who had abdominal surgery suffer fewer pulmonary problems,shorter hospital stays,and improved lung function.METHODS The data of 231 elderly individuals having abdominal surgery was retrospectively analyzed.Based on whether ERAS-based respiratory function training was provided,patients were divided into ERAS group(n=112)and control group(n=119).Deep vein thrombosis(DVT),pulmonary embolism(PE),and respiratory tract infection(RTI)were the primary outcome variables.Secondary outcome variables included the Borg score Scale,FEV1/FVC and postoperative hospital stay.RESULTS The percentage of 18.75%of ERAS group participants and 34.45%of control group participants,respectively,had respiratory infections(P=0.007).None of the individuals experienced PE or DVT.The ERAS group’s median postoperative hospital stay was 9.5 d(3-21 d)whereas the control groups was 11 d(4-18 d)(P=0.028).The Borg score decreased on the 4th d following surgery in the ERAS group compared to the 2nd d prior(P=0.003).The incidence of RTIs was greater in the control group than in the ERAS group among patients who spent more than 2 d in the hospital before surgery(P=0.029).CONCLUSION ERAS-based respiratory function training may reduce the risk of pulmonary complications in older individuals undergoing abdominal surgery.
基金This project was supported by Wuhan Medical Science Foundation of China(No.WX17B07,No.WX19A09,and No.WJ2019H324).
文摘Acute respiratory distress syndrome(ARDS)is one of the most fatal diseases worldwide.Pulmonary fibrosis occurs early in ARDS,and its severity plays a crucial role in ARDS mortality rate.Some studies suggested that fibroproliferation is an essential mechanism in ARDS.Mitofusion2(Mfn2)overexpression plays a role in inhibiting cell proliferation.However,the role and potential mechanism of Mfn2 on the proliferation of fibroblasts is still unknown.In this study,we aimed at exploring the effect of Mfn2 on the human embryonic lung fibroblasts(HELF)and discussed its related mechanism.The HELF were treated with the Mfn2 overexpressing lentivirus(adv-Mfn2).The cell cycle was detected by flow cytometry.MTT,PCR and Western blotting were used to investigate the effect of Mfn2 on the proliferation of the HELF,collagen expression,the RAS-RAF-1-ERK1/2 pathway and the expression of cycle-related proteins(p21,p27,Rb,Raf-1,p-Raf-1,Erk1/2 and p-Erk1/2).The co-immunoprecipitation assay was used to explore the interaction between Mfn2 and Ras.The results showed that the overexpression of Mfn2 inhibited the proliferation of the HELF and induced the cell cycle arrest at the G0/G1 phase.Meanwhile,Mfn2 also inhibited the expression of collagen I,p-Erk and p-Raf-1.In addition,an interaction between Mfn2 and Ras existed in the HELF.This study suggests that the overexpression of Mfn2 can decrease the proliferation of HELF in ARDS,which was associated with the inhibition of the RAS-RAF-1-ERK1/2 pathway.The results may offer a potential therapeutic intervention for patients with ARDS.
