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Although prior studies suggest that hypoxia may increase pulmonary vascular permeability, the mechanisms responsible for that effect remain uncertain. Neprilysin (neutral endopeptidase) is a cell surface metallopeptidase that degrades several vasoactive peptides including substance P and bradykinin. We hypothesized that hypoxia could reduce lung neprilysin expression, leading to increased vascular leak. Weanling rats were exposed to normobaric hypoxia (inspired O\u003Cjats:sub>2\u003C\u002Fjats:sub> fraction = 0.1). Lung neprilysin activity was significantly decreased after 24 and 48 h of hypoxia ( P < 0.006). The decrease in enzyme activity was associated with decreased lung neprilysin protein content and decreased lung neprilysin mRNA expression. Immunohistochemistry showed a predominantly perivascular distribution of neprilysin, with clear reductions in neprilysin immunoreactivity after exposure to hypoxia. Exposure to hypoxia for 24 h also caused marked increases in vascular leak ( P = 0.008), which were reversed by the administration of recombinant neprilysin. The hypoxia-induced increase in leak was also reversed by substance P and bradykinin receptor antagonists. We conclude that in young rats hypoxia decreases lung neprilysin expression, which contributes to increased pulmonary vascular leak via substance P and bradykinin receptors. \u003C\u002Fjats:p>",{"EN":595},"Hypoxia decreases lung neprilysin expression and increases pulmonary vascular leak",{"VOID":597},"11557598",{"VOID":599},"10.1152\u002Fajplung.2001.281.4.l941",[210],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajplung.2001.281.4.L941",[603,622],{"id":604,"sortIndex":25,"researcher":24,"roles":605,"affiliations":606,"properties":615,"displayName":619,"givenName":24,"familyName":24},"53e275a7-c8e8-4f18-b9ad-cf5dd34e3063",[],[607],{"id":608,"sortIndex":25,"affiliation":609,"properties":24},"6c15b82a-5916-424a-9ff3-3b61d2a96345",{"id":608,"createTime":24,"updateTime":24,"relativeEntities":610,"slug":24,"properties":611,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":614,"statistic":24},[],{"title":612},{"VI":613},"Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado, 80262",[],{"orcid":616,"title":618,"openalex":620},{"VOID":617},"https:\u002F\u002Forcid.org\u002F0000-0002-9855-0021",{"EN":619},"Todd C. 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Pulmonary hypertension (PH) is a rare disease in which pathophysiology is characterized by an increase in proinflammatory mediators, chronic endothelial dysfunctions, and a high migration rate of smooth muscle cells (SMC). Over the course of the last decade, various treatments have been proposed to relax the pulmonary arteries, none of which have been effective in resolving PH. Our hypothesis is that artery-relaxing drugs are not the long-term solution, but rather the inhibition of tissue inflammation, which underlies human pulmonary artery (HPA) dysfunctions that lead to abnormal vasoconstriction. The goal of the present study was to assess the anti-inflammatory effects of resolvin E\u003Cjats:sub>1\u003C\u002Fjats:sub> (RvE\u003Cjats:sub>1\u003C\u002Fjats:sub>) with concomitant effects on SMC migration and on HPA reactivity. The role and mode of action of RvE\u003Cjats:sub>1\u003C\u002Fjats:sub> and its precursor, monoacylglyceride eicosapentaenoic acid were assessed on HPA under proinflammatory conditions, involving a combined pretreatment with 10 ng\u002Fml TNF-α and 10 ng\u002Fml IL-6. Our results show that TNF-α and IL-6 treatment induced hyperreactivity and Ca\u003Cjats:sup>2+\u003C\u002Fjats:sup> hypersensitivity in response to pharmaco-mechanical stimuli, including 80 mM KCl, 1 μM phorbol 12–13-dibutyrate, and 30 nM U-46619. Furthermore, the proinflammatory treatment increased the migration rate of SMC isolated from HPA. The phosphorylation level of regulatory contractile proteins (CPI-17, MYPT-1), and proinflammatory signaling pathways (c-Fos, c-Jun, NF-κB) were also significantly increased compared with control conditions. Conversely, 300 nM RvE\u003Cjats:sub>1\u003C\u002Fjats:sub> was able to normalize all of the above abnormal events triggered by proinflammation. In conclusion, RvE\u003Cjats:sub>1\u003C\u002Fjats:sub> can resolve human arterial hyperreactivity via the resolution of inflammatory markers. \u003C\u002Fjats:p>",{"EN":783},"Resolvin E\u003Csub>1\u003C\u002Fsub> normalizes contractility, Ca\u003Csup>2+\u003C\u002Fsup> sensitivity and smooth muscle cell migration rate in TNF-α- and IL-6-pretreated human pulmonary 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Our objectives to further investigate the pathogenesis of ALI and VILI and the mechanism of lung protection in these syndromes were: 1) to determine if plasma measurements of soluble TNF receptor I (sTNFRI) and II (sTNFRII) would predict the development of ALI and mortality in a small single center trial; 2) to test the predictive value of these markers and of TNF-α in a larger, broader group of patients with ALI; 3) to test the hypothesis that low tidal volume ventilation (LTVV) would be associated with a decrease in plasma levels of TNF-α, sTNFRI, and sTNFRII. In the single center study, sTNFRI and II levels were higher in patients at risk for and with ALI, but they did not predict the development of the syndrome. In the multicenter trial sTNFRI and II were strongly associated with mortality (OR 5.76\u002F1 log10 increment in receptor level; 95% CI 2.63–12.6 and OR 2.58; 95% CI 1.05–6.31, respectively) and morbidity measured as fewer nonpulmonary organ failure-free and ventilator-free days. The LTVV strategy was associated with an attenuation of plasma sTNFRI levels. In vitro, stimulated A549 cells release sTNFRI but not sTNRFII. In conclusion, plasma levels of sTNFRI and II can serve as biomarkers for morbidity and mortality in patients with ALI. Furthermore, LTVV is associated with a specific decrease in sTNFRI levels. 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Inhibition of tumor necrosis factor-α-induced apoptosis by HO-1 overexpression was reversed by 1 H-(1,2,4)oxadiazolo(4,3- a)quinoxalin-1-one, an inhibitor of guanylate cyclase, which is a target enzyme for carbon monoxide. 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many lung diseases are associated with hypoxia, alveolar type II epithelial (ATII) cell impairment, and pulmonary surfactant dysfunction, the effects of O\u003Cjats:sub>2\u003C\u002Fjats:sub>limitation on metabolic pathways necessary to maintain cellular energy in ATII cells have not been studied extensively. This report presents results of targeted assays aimed at identifying specific metabolic processes that contribute to energy homeostasis using primary ATII cells and a model ATII cell line, mouse lung epithelial 15 (MLE-15), cultured in normoxic and hypoxic conditions. MLEs cultured in normoxia demonstrated a robust O\u003Cjats:sub>2\u003C\u002Fjats:sub>consumption rate (OCR) coupled to ATP generation and limited extracellular lactate production, indicating reliance on oxidative phosphorylation for ATP production. Pharmacological uncoupling of respiration increased OCR in normoxic cultures to 175% of basal levels, indicating significant spare respiratory capacity. However, when exposed to hypoxia for 20 h, basal O\u003Cjats:sub>2\u003C\u002Fjats:sub>consumption fell to 60% of normoxic rates, and cells maintained only ∼50% of normoxic spare respiratory capacity, indicating suppression of mitochondrial function, although intracellular ATP levels remained at near normoxic levels. Moreover, while hypoxic exposure stimulated glycogen synthesis and storage in MLE-15, glycolytic rate (as measured by lactate generation) was not significantly increased in the cells, despite enhanced expression of several enzymes related to glycolysis. These results were largely recapitulated in murine primary ATII, demonstrating MLE-15 suitability for modeling ATII metabolism. The ability of ATII cells to maintain ATP levels in hypoxia without enhancing glycolysis suggests that these cells are exceptionally efficient at conserving ATP to maintain bioenergetic homeostasis under O\u003Cjats:sub>2\u003C\u002Fjats:sub>limitation.\u003C\u002Fjats:p>","\u003Cjats:p>Mặc dù nhiều bệnh lý phổi liên quan đến tình trạng thiếu oxy, sự suy giảm tế bào biểu mô loại II phế nang (ATII), và rối loạn chức năng hoạt chất bề mặt phổi, tác động của sự hạn chế O\u003Cjats:sub>2\u003C\u002Fjats:sub> đến các con đường chuyển hóa cần thiết để duy trì năng lượng của tế bào trong các tế bào ATII vẫn chưa được nghiên cứu kỹ lưỡng. Bài báo này trình bày kết quả của các thử nghiệm có mục tiêu nhằm xác định các quá trình chuyển hóa cụ thể góp phần vào cân bằng năng lượng sử dụng các tế bào ATII nguyên phát và một dòng tế bào ATII mẫu, tế bào biểu mô phổi chuột 15 (MLE-15), được nuôi cấy trong điều kiện bình thường (normoxic) và thiếu oxy (hypoxic). Các tế bào MLE nuôi cấy trong điều kiện bình thường thể hiện tỷ lệ tiêu thụ O\u003Cjats:sub>2\u003C\u002Fjats:sub> mạnh mẽ (OCR) kèm theo sự sản xuất ATP và sản xuất lactate ngoại bào hạn chế, cho thấy sự phụ thuộc vào phosphoryl hóa oxy hóa để sản xuất ATP. Việc không gắn kết dược lý của quá trình hô hấp đã làm tăng OCR trong các nền văn hóa bình thường lên 175% so với mức cơ bản, cho thấy khả năng dự trữ hô hấp đáng kể. Tuy nhiên, khi tiếp xúc với điều kiện thiếu oxy trong 20 giờ, mức tiêu thụ O\u003Cjats:sub>2\u003C\u002Fjats:sub> cơ bản giảm còn 60% so với tỷ lệ bình thường, và các tế bào chỉ duy trì khoảng 50% khả năng dự trữ hô hấp bình thường, cho thấy sự ức chế chức năng ty thể, mặc dù mức ATP nội bào vẫn giữ gần mức bình thường. Hơn nữa, trong khi sự tiếp xúc với điều kiện thiếu oxy kích thích tổng hợp và lưu trữ glycogen trong MLE-15, tốc độ glycolysis (như được đo bằng sản xuất lactate) không được tăng đáng kể trong các tế bào, mặc dù có sự tăng cường biểu hiện của một số enzyme liên quan đến glycolysis. Những kết quả này chủ yếu được tái hiện trong các tế bào ATII nguyên phát của chuột, chứng minh rằng MLE-15 phù hợp để mô hình hóa chuyển hóa ATII. Khả năng của các tế bào ATII duy trì mức ATP trong điều kiện thiếu oxy mà không tăng cường glycolysis cho thấy rằng các tế bào này cực kỳ hiệu quả trong việc bảo tồn ATP để giữ cân bằng năng lượng sinh học trong điều kiện hạn chế O\u003Cjats:sub>2\u003C\u002Fjats:sub>.\u003C\u002Fjats:p>",{"EN":3086,"VI":3087},"Alveolar type II cells maintain bioenergetic homeostasis in hypoxia through metabolic and molecular adaptation","Các tế bào biểu mô loại II phế nang duy trì cân bằng năng lượng sinh học trong điều kiện thiếu oxy thông qua thích nghi về chuyển hóa và phân tử",{"VOID":3089},"24682450",{"VOID":3091},"10.1152\u002Fajplung.00298.2013","2024-09-24T00:28:45.302+00:00",[210],[3095],"VI","https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajplung.00298.2013",[3098,3115,3132,3151],{"id":3099,"sortIndex":25,"researcher":24,"roles":3100,"affiliations":3101,"properties":3110,"displayName":3112,"givenName":24,"familyName":24},"094cb9a0-4d36-475f-b110-81d0db63a098",[],[3102],{"id":3103,"sortIndex":25,"affiliation":3104,"properties":24},"2856831b-173f-486e-a81e-fbcc99517768",{"id":3103,"createTime":24,"updateTime":24,"relativeEntities":3105,"slug":24,"properties":3106,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3109,"statistic":24},[],{"title":3107},{"EN":3108},"Department of Pediatrics, Medical University of South Carolina, Charleston, South Carolia; and",[],{"title":3111,"openalex":3113},{"EN":3112},"Robyn G. 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cầu đa nhân trung tính, Tổn thương phổi cấp tính, Thiếu máu\u002Ftái tưới máu, Oxit carbon, Resolvin D1, Tương tác PMN-tiểu cầu, Leukotrien, Thromboxan, Bảo vệ phổi, Cysteinyl LTs",{"VOID":3367},"4233292",{"VOID":3369},"W2141593309",{"EN":3371,"VI":3372},"\u003Cjats:p>Polymorphonuclear leukocyte (PMN)-mediated acute lung injury from ischemia\u002Freperfusion (I\u002FR) remains a major cause of morbidity and mortality in critical care medicine. Here, we report that inhaled low-dose carbon monoxide (CO) and intravenous resolvin D1 (RvD1) in mice each reduced PMN-mediated acute lung injury from I\u002FR. Inhaled CO (125–250 ppm) and RvD1 (250–500 ng) each reduced PMN lung infiltration and gave additive lung protection. In mouse whole blood, CO and RvD1 attenuated PMN-platelet aggregates, reducing leukotrienes (LTs) and thromboxane B\u003Cjats:sub>2\u003C\u002Fjats:sub>(TxB\u003Cjats:sub>2\u003C\u002Fjats:sub>) in I\u002FR lungs. With human whole blood, CO (125–250 ppm) decreased PMN-platelet aggregates, expression of adhesion molecules, and cysteinyl LTs, as well as TxB\u003Cjats:sub>2\u003C\u002Fjats:sub>. RvD1 (1–100 nM) also dose dependently reduced platelet activating factor-stimulated PMN-platelet aggregates in human whole blood. In nonhuman primate (baboon) lung infection with Streptococcus pneumoniae, inhaled CO reduced urinary cysteinyl LTs. These results demonstrate lung protection by low-dose inhaled CO as well as RvD1 that each reduced PMN-mediated acute tissue injury, PMN-platelet interactions, and production of both cysteinyl LTs and TxB\u003Cjats:sub>2\u003C\u002Fjats:sub>. Together they suggest a potential therapeutic role of low-dose inhaled CO in organ protection, as demonstrated using mouse I\u002FR-initiated lung injury, baboon infections, and human whole blood.\u003C\u002Fjats:p>","\u003Cjats:p>Bạch cầu đa nhân trung tính (PMN) đóng vai trò trung gian gây tổn thương cấp tính ở phổi do thiếu máu\u002Ftái tưới máu (I\u002FR) vẫn tiếp tục là nguyên nhân chính gây tử vong trong y học chăm sóc đặc biệt. Trong nghiên cứu này, chúng tôi báo cáo rằng việc hít oxit carbon (CO) liều thấp và tiêm tĩnh mạch resolvin D1 (RvD1) ở chuột có thể làm giảm tổn thương phổi cấp tính do PMN gây ra từ I\u002FR. Việc hít CO (125–250 ppm) và RvD1 (250–500 ng) đều làm giảm sự thâm nhập của PMN vào phổi và cải thiện bảo vệ phổi. Trong mẫu máu toàn phần của chuột, CO và RvD1 giảm mạnh tổng hợp PMN-tiểu cầu, từ đó giảm leukotrien (LTs) và thromboxan B\u003Cjats:sub>2\u003C\u002Fjats:sub>(TxB\u003Cjats:sub>2\u003C\u002Fjats:sub>) trong phổi chịu tác động I\u002FR. Với mẫu máu toàn phần của người, CO (125–250 ppm) làm giảm tổng hợp PMN-tiểu cầu, sự biểu hiện của phân tử bám dính, cytokine LTs cũng như TxB\u003Cjats:sub>2\u003C\u002Fjats:sub>. RvD1 (1–100 nM) cũng giảm phụ thuộc liều tổng hợp PMN-tiểu cầu kích thích bởi yếu tố hoạt hóa tiểu cầu trong mẫu máu người. Trong nghiên cứu trên động vật không phải người (khỉ đầu chó) bị nhiễm Streptococcus pneumoniae ở phổi, CO hít vào làm giảm đáng kể LTs cysteinyl trong nước tiểu. Những kết quả này chứng minh việc bảo vệ phổi bằng CO hít liều thấp cũng như RvD1 giảm tổn thương mô cấp tính bởi PMN, tương tác PMN-tiểu cầu và sản xuất LTs cysteinyl và TxB\u003Cjats:sub>2\u003C\u002Fjats:sub>. Cùng nhau, chúng gợi ý một vai trò điều trị tiềm năng của CO hít liều thấp trong bảo vệ cơ quan, như đã chứng minh qua các mô hình tổn thương phổi khởi tạo I\u002FR trên chuột, nhiễm trùng khỉ đầu chó và mẫu máu toàn phần của người.\u003C\u002Fjats:p>",{"EN":3374,"VI":3375},"Cell-cell interactions and bronchoconstrictor eicosanoid reduction with inhaled carbon monoxide and resolvin D1","Tương tác tế bào-tế bào và giảm eicosanoid gây co thắt phế quản thông qua oxit carbon hít vào và resolvin D1",{"VOID":3377},"25217660",{"VOID":3379},"10.1152\u002Fajplung.00166.2014",[210],[3095],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajplung.00166.2014",[3384,3403,3418,3433,3450,3467,3486,3501,3525],{"id":3385,"sortIndex":25,"researcher":24,"roles":3386,"affiliations":3387,"properties":3396,"displayName":3400,"givenName":24,"familyName":24},"b837b630-2029-4299-994c-d556b820c5bc",[],[3388],{"id":3389,"sortIndex":25,"affiliation":3390,"properties":24},"7b46a6f4-6911-4fe3-8ebb-ebaabb1baa22",{"id":3389,"createTime":24,"updateTime":24,"relativeEntities":3391,"slug":24,"properties":3392,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3395,"statistic":24},[],{"title":3393},{"VI":3394},"Center for Experimental Therapeutics and Reperfusion Injury, Harvard Institutes of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts",[],{"orcid":3397,"title":3399,"openalex":3401},{"VOID":3398},"https:\u002F\u002Forcid.org\u002F0000-0001-8724-0071",{"EN":3400},"Masakazu Shinohara",{"VOID":3402},"A5048441665",{"id":3404,"sortIndex":118,"researcher":24,"roles":3405,"affiliations":3406,"properties":3413,"displayName":3415,"givenName":24,"familyName":24},"a784e7bc-7b53-43b5-9d40-85fc101bfa41",[],[3407],{"id":3389,"sortIndex":25,"affiliation":3408,"properties":24},{"id":3389,"createTime":24,"updateTime":24,"relativeEntities":3409,"slug":24,"properties":3410,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3412,"statistic":24},[],{"title":3411},{"VI":3394},[],{"title":3414,"openalex":3416},{"EN":3415},"Megumi Kibi",{"VOID":3417},"A5006940721",{"id":3419,"sortIndex":119,"researcher":24,"roles":3420,"affiliations":3421,"properties":3428,"displayName":3430,"givenName":24,"familyName":24},"3b3336dc-5e40-4c3e-8f2a-5fd6df2a7c80",[],[3422],{"id":3389,"sortIndex":25,"affiliation":3423,"properties":24},{"id":3389,"createTime":24,"updateTime":24,"relativeEntities":3424,"slug":24,"properties":3425,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3427,"statistic":24},[],{"title":3426},{"VI":3394},[],{"title":3429,"openalex":3431},{"EN":3430},"Ian R. 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