For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
54
views
Article has an altmetric score of 1
25
references
 Top references
cited by
16
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      216
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Remote ischemic preconditioning STAT3-dependently ameliorates pulmonary ischemia/reperfusion injury

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The lungs are highly susceptible to injury, including ischemia/reperfusion (I/R) injury. Pulmonary I/R injury can occur when correcting conditions such as primary pulmonary hypertension, and is also relatively common after lung transplantation or other cardiothoracic surgery. Methods to reduce pulmonary I/R injury are urgently needed to improve outcomes following procedures such as lung transplantation. Remote liver ischemic preconditioning (RLIPC) is an effective cardioprotective measure, reducing damage caused by subsequent cardiac I/R injury, but little is known about its potential role in pulmonary protection. Here, we analyzed the efficacy and mechanistic basis of RLIPC in a rat model of pulmonary I/R injury. RLIPC reduced lung I/R injury, lessening structural damage, inflammatory cytokine production and apoptosis. In addition, RLIPC preserved pulmonary function compared to controls following lung I/R injury. RLIPC stimulated phosphorylation of pulmonary STAT3, a component of the SAFE signaling pathway, but not phosphorylation of RISK pathway signaling proteins. Accordingly, STAT3 inhibition using AG490 eliminated the pulmonary protection afforded by RLIPC. Our data demonstrate for the first time that RLIPC protects against pulmonary I/R injury, via a signaling pathway requiring STAT3 phosphorylation.

          Related collections

          Most cited references25

          • Record: found
          • Abstract: found
          • Article: not found

          An official American Thoracic Society workshop report: features and measurements of experimental acute lung injury in animals.

          Gustavo Matute-Bello, Gregory Downey, Bethany B. Moore … (2011)
          Acute lung injury (ALI) is well defined in humans, but there is no agreement as to the main features of acute lung injury in animal models. A Committee was organized to determine the main features that characterize ALI in animal models and to identify the most relevant methods to assess these features. We used a Delphi approach in which a series of questionnaires were distributed to a panel of experts in experimental lung injury. The Committee concluded that the main features of experimental ALI include histological evidence of tissue injury, alteration of the alveolar capillary barrier, presence of an inflammatory response, and evidence of physiological dysfunction; they recommended that, to determine if ALI has occurred, at least three of these four main features of ALI should be present. The Committee also identified key "very relevant" and "somewhat relevant" measurements for each of the main features of ALI and recommended the use of least one "very relevant" measurement and preferably one or two additional separate measurements to determine if a main feature of ALI is present. Finally, the Committee emphasized that not all of the measurements listed can or should be performed in every study, and that measurements not included in the list are by no means "irrelevant." Our list of features and measurements of ALI is intended as a guide for investigators, and ultimately investigators should choose the particular measurements that best suit the experimental questions being addressed as well as take into consideration any unique aspects of the experimental design.
          Article 0 comments Cited 735 times – based on 0 reviews     Review now
          Article has an altmetric score of 10
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The lung is a site of platelet biogenesis and a reservoir for hematopoietic progenitors

            Emma Lefrancais, Guadalupe Ortiz-Muñoz, Axelle Caudrillier … (2017)
            Platelets are critical for hemostasis, thrombosis, and inflammatory responses 1,2 , yet the events leading to mature platelet production remain incompletely understood 3 . The bone marrow (BM) is proposed to be a major site of platelet production although indirect evidence points towards a potential pulmonary contribution to platelet biogenesis 4-7 . By directly imaging the lung microcirculation in mice 8 , we discovered that a large number of megakaryocytes (MKs) circulate through the lungs where they dynamically release platelets. MKs releasing platelets in the lung are of extrapulmonary origin, such as the BM, where we observed large MKs migrating out of the BM space. The lung contribution to platelet biogenesis is substantial with approximately 50% of total platelet production or 10 million platelets per hour. Furthermore, we identified populations of mature and immature MKs along with hematopoietic progenitors that reside in the extravascular spaces of the lung. Under conditions of thrombocytopenia and relative stem cell deficiency in the BM 9 , these progenitors can migrate out of the lung, repopulate the BM, completely reconstitute blood platelet counts, and contribute to multiple hematopoietic lineages. These results position the lung as a primary site of terminal platelet production and an organ with considerable hematopoietic potential.
            Article 0 comments Cited 453 times – based on 0 reviews     Review now
            Article has an altmetric score of 1275
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.

              Beth A. Rose, Thomas I Force, Yibin Wang (2010)
              Among the myriad of intracellular signaling networks that govern the cardiac development and pathogenesis, mitogen-activated protein kinases (MAPKs) are prominent players that have been the focus of extensive investigations in the past decades. The four best characterized MAPK subfamilies, ERK1/2, JNK, p38, and ERK5, are the targets of pharmacological and genetic manipulations to uncover their roles in cardiac development, function, and diseases. However, information reported in the literature from these efforts has not yet resulted in a clear view about the roles of specific MAPK pathways in heart. Rather, controversies from contradictive results have led to a perception that MAPKs are ambiguous characters in heart with both protective and detrimental effects. The primary object of this review is to provide a comprehensive overview of the current progress, in an effort to highlight the areas where consensus is established verses the ones where controversy remains. MAPKs in cardiac development, cardiac hypertrophy, ischemia/reperfusion injury, and pathological remodeling are the main focuses of this review as these represent the most critical issues for evaluating MAPKs as viable targets of therapeutic development. The studies presented in this review will help to reveal the major challenges in the field and the limitations of current approaches and point to a critical need in future studies to gain better understanding of the fundamental mechanisms of MAPK function and regulation in the heart.
              Article 0 comments Cited 256 times – based on 0 reviews     Review now
              Article has an altmetric score of 9
                Bookmark
                All references

                Author and article information

                Contributors
                Nanfu Luo: Role: ConceptualizationRole: Data curationRole: Formal analysisRole: Investigation
                Jin Liu: Role: ConceptualizationRole: Formal analysisRole: Writing – review & editing
                Yan Chen: Role: ConceptualizationRole: Formal analysisRole: InvestigationRole: Writing – review & editing
                Huan Li: Role: ConceptualizationRole: Formal analysisRole: InvestigationRole: Writing – review & editing
                Zhaoyang Hu: Role: ConceptualizationRole: Data curationRole: Formal analysisRole: Funding acquisitionRole: InvestigationRole: MethodologyRole: SupervisionRole: ValidationRole: Writing – original draftRole: Writing – review & editing
                Geoffrey W. Abbott:
                ORCID: http://orcid.org/0000-0003-4552-496X
                Role: ResourcesRole: SupervisionRole: Writing – original draftRole: Writing – review & editing
                Tobias Eckle: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 16 May 2018
                Publication date Collection: 2018
                Volume: 13
                Issue: 5
                Electronic Location Identifier: e0196186
                Affiliations
                [1 ] Laboratory of Anesthesiology & Critical Care Medicine, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China
                [2 ] Bioelectricity Laboratory, Dept. of Physiology and Biophysics, School of Medicine, University of California, Irvine, California, United States of America
                University of Colorado Denver, UNITED STATES
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Author information
                http://orcid.org/0000-0003-4552-496X
                Article
                Publisher ID: PONE-D-17-42608
                DOI: 10.1371/journal.pone.0196186
                PMC ID: 5955491
                PubMed ID: 29768493
                SO-VID: cb4009af-9107-4750-8efc-17289c8e9061
                Copyright © © 2018 Luo et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 4 December 2017
                Date accepted : 3 March 2018
                Page count
                Figures: 6, Tables: 0, Pages: 16
                Funding
                Funded by: funder-id http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81670300
                Award Recipient :
                This study was supported by grant No. 81670300 (to ZH) from the National Natural Science Foundation of China, and University of California, Irvine School of Medicine Setup Funds (to GWA). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Medicine and Health Sciences
                Subject: Critical Care and Emergency Medicine
                Subject: Reperfusion
                Subject: Medicine and Health Sciences
                Subject: Surgical and Invasive Medical Procedures
                Subject: Transplantation
                Subject: Organ Transplantation
                Subject: Lung Transplantation
                Subject: Medicine and Health Sciences
                Subject: Surgical and Invasive Medical Procedures
                Subject: Respiratory System Procedures
                Subject: Lung Transplantation
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cell Processes
                Subject: Cell Death
                Subject: Apoptosis
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Diagnostic Medicine
                Subject: Signs and Symptoms
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Pathology and Laboratory Medicine
                Subject: Signs and Symptoms
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Vascular Medicine
                Subject: Ischemia
                Subject: Medicine and Health Sciences
                Subject: Critical Care and Emergency Medicine
                Subject: Trauma Medicine
                Subject: Reperfusion Injury
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Proteins
                Subject: Post-Translational Modification
                Subject: Phosphorylation
                Subject: Biology and life sciences
                Subject: Cell biology
                Subject: Signal transduction
                Subject: Cell signaling
                Subject: STAT signaling
                Custom metadata
                Data Availability All relevant data are within the paper and its Supporting Information files.

                ScienceOpen disciplines: Uncategorized
                Data availability:
                ScienceOpen disciplines: Uncategorized

                Comments

                Comment on this article

                scite_
                0
                0
                0
                0
                Smart Citations
                0
                0
                0
                0
                Citing PublicationsSupportingMentioningContrasting
                View Citations

                See how this article has been cited at scite.ai

                scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

                Similar content216

                See all similar

                Cited by16

                See all cited by

                Most referenced authors399

                See all reference authors