Mohammad A Uddin, Mohammad S Akhter, Khadeja-Tul Kubra, Nektarios Barabutis
{"title":"盲肠结扎及脓毒症穿刺模型小鼠肺内NEK家族激酶的诱导","authors":"Mohammad A Uddin, Mohammad S Akhter, Khadeja-Tul Kubra, Nektarios Barabutis","doi":"10.1080/21688370.2021.1929787","DOIUrl":null,"url":null,"abstract":"<p><p>Endothelial barrier dysfunction (EBD) is the hallmark of Acute Respiratory Distress Syndrome (ARDS), a potentially lethal respiratory disorder associated with the COVID-19 - related deaths. Herein, we employed a cecal ligation and puncture (CLP) murine model of sepsis, to evaluate the effects of sepsis-induced EBD in the expression of the never in mitosis A (NIMA)-related kinases (NEKs). Members of that family of kinases regulate the activity and expression of the tumor suppressor P53, previously shown to modulate the actin cytoskeleton remodeling. Our results introduce the induction of NEK2, NEK3, NEK4, NEK7, and NEK9 in a CLP model of sepsis. Hence, we suggest that NEKs are involved in inflammatory processes and are holding the potential to serve as novel therapeutic targets for pathologies related to EBD, including ARDS and sepsis. Further studies will delineate the underlying molecular events and their interrelations with P53.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":"9 4","pages":"1929787"},"PeriodicalIF":3.6000,"publicationDate":"2021-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/21688370.2021.1929787","citationCount":"7","resultStr":"{\"title\":\"Induction of the NEK family of kinases in the lungs of mice subjected to cecal ligation and puncture model of sepsis.\",\"authors\":\"Mohammad A Uddin, Mohammad S Akhter, Khadeja-Tul Kubra, Nektarios Barabutis\",\"doi\":\"10.1080/21688370.2021.1929787\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Endothelial barrier dysfunction (EBD) is the hallmark of Acute Respiratory Distress Syndrome (ARDS), a potentially lethal respiratory disorder associated with the COVID-19 - related deaths. Herein, we employed a cecal ligation and puncture (CLP) murine model of sepsis, to evaluate the effects of sepsis-induced EBD in the expression of the never in mitosis A (NIMA)-related kinases (NEKs). Members of that family of kinases regulate the activity and expression of the tumor suppressor P53, previously shown to modulate the actin cytoskeleton remodeling. Our results introduce the induction of NEK2, NEK3, NEK4, NEK7, and NEK9 in a CLP model of sepsis. Hence, we suggest that NEKs are involved in inflammatory processes and are holding the potential to serve as novel therapeutic targets for pathologies related to EBD, including ARDS and sepsis. Further studies will delineate the underlying molecular events and their interrelations with P53.</p>\",\"PeriodicalId\":23469,\"journal\":{\"name\":\"Tissue Barriers\",\"volume\":\"9 4\",\"pages\":\"1929787\"},\"PeriodicalIF\":3.6000,\"publicationDate\":\"2021-10-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/21688370.2021.1929787\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Tissue Barriers\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/21688370.2021.1929787\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/6/20 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tissue Barriers","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/21688370.2021.1929787","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/6/20 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
Induction of the NEK family of kinases in the lungs of mice subjected to cecal ligation and puncture model of sepsis.
Endothelial barrier dysfunction (EBD) is the hallmark of Acute Respiratory Distress Syndrome (ARDS), a potentially lethal respiratory disorder associated with the COVID-19 - related deaths. Herein, we employed a cecal ligation and puncture (CLP) murine model of sepsis, to evaluate the effects of sepsis-induced EBD in the expression of the never in mitosis A (NIMA)-related kinases (NEKs). Members of that family of kinases regulate the activity and expression of the tumor suppressor P53, previously shown to modulate the actin cytoskeleton remodeling. Our results introduce the induction of NEK2, NEK3, NEK4, NEK7, and NEK9 in a CLP model of sepsis. Hence, we suggest that NEKs are involved in inflammatory processes and are holding the potential to serve as novel therapeutic targets for pathologies related to EBD, including ARDS and sepsis. Further studies will delineate the underlying molecular events and their interrelations with P53.
期刊介绍:
Tissue Barriers is the first international interdisciplinary journal that focuses on the architecture, biological roles and regulation of tissue barriers and intercellular junctions. We publish high quality peer-reviewed articles that cover a wide range of topics including structure and functions of the diverse and complex tissue barriers that occur across tissue and cell types, including the molecular composition and dynamics of polarized cell junctions and cell-cell interactions during normal homeostasis, injury and disease state. Tissue barrier formation in regenerative medicine and restoration of tissue and organ function is also of interest. Tissue Barriers publishes several categories of articles including: Original Research Papers, Short Communications, Technical Papers, Reviews, Perspectives and Commentaries, Hypothesis and Meeting Reports. Reviews and Perspectives/Commentaries will typically be invited. We also anticipate to publish special issues that are devoted to rapidly developing or controversial areas of research. Suggestions for topics are welcome. Tissue Barriers objectives: Promote interdisciplinary awareness and collaboration between researchers working with epithelial, epidermal and endothelial barriers and to build a broad and cohesive worldwide community of scientists interesting in this exciting field. Comprehend the enormous complexity of tissue barriers and map cross-talks and interactions between their different cellular and non-cellular components. Highlight the roles of tissue barrier dysfunctions in human diseases. Promote understanding and strategies for restoration of tissue barrier formation and function in regenerative medicine. Accelerate a search for pharmacological enhancers of tissue barriers as potential therapeutic agents. Understand and optimize drug delivery across epithelial and endothelial barriers.