دورية أكاديمية
Lipocalin-2 is increased in amyotrophic lateral sclerosis.
العنوان: | Lipocalin-2 is increased in amyotrophic lateral sclerosis. |
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المؤلفون: | Petrozziello T; Sean M. Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts., Mills AN; Sean M. Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts., Farhan SMK; Analytic and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.; Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, Massachusetts., Mueller KA; Sean M. Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts., Granucci EJ; Sean M. Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts., Glajch KE; Sean M. Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts., Chan J; Biostatistics Center, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts., Chew S; Sean M. Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts., Berry JD; Sean M. Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts., Sadri-Vakili G; Sean M. Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts. |
المصدر: | Muscle & nerve [Muscle Nerve] 2020 Aug; Vol. 62 (2), pp. 272-283. Date of Electronic Publication: 2020 May 29. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: John Wiley & Sons Country of Publication: United States NLM ID: 7803146 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4598 (Electronic) Linking ISSN: 0148639X NLM ISO Abbreviation: Muscle Nerve Subsets: MEDLINE |
أسماء مطبوعة: | Publication: <2005-> : Hoboken, NJ : John Wiley & Sons Original Publication: New York, NY : John Wiley & Sons |
مواضيع طبية MeSH: | Amyotrophic Lateral Sclerosis/*genetics , Inflammation/*metabolism , Lipocalin-2/*genetics , Motor Cortex/*metabolism , Spinal Cord/*metabolism, Adult ; Aged ; Aged, 80 and over ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/physiopathology ; Blotting, Western ; Case-Control Studies ; Cell Death ; Cell Line, Tumor ; Cytokines/drug effects ; Cytokines/metabolism ; Enzyme-Linked Immunosorbent Assay ; Female ; Fluorescent Antibody Technique ; Humans ; In Vitro Techniques ; Lipocalin-2/antagonists & inhibitors ; Lipocalin-2/metabolism ; Lipocalin-2/pharmacology ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Real-Time Polymerase Chain Reaction |
مستخلص: | Background: The exact mechanisms underlying neuroinflammation and how they contribute to amyotrophic lateral sclerosis (ALS) pathogenesis remain unclear. One possibility is the secretion of neurotoxic factors, such as lipocalin-2 (LCN2), that lead to neuronal death. Methods: LCN2 levels were measured in human postmortem tissue using Western blot, quantitative real time polymerase chain reaction, and immunofluorescence, and in plasma by enzyme-linked immunosorbent assay. SH-SY5Y cells were used to test the pro-inflammatory effects of LCN2. Results: LCN2 is increased in ALS postmortem motor cortex, spinal cord, and plasma. Furthermore, we identified several LCN2 variants in ALS patients that may contribute to disease pathogenesis. Lastly, while LCN2 treatment caused cell death and increased pro-inflammatory markers, treatment with an anti-LCN2 antibody prevented these responses in vitro. Conclusions: LCN2 upregulation in ALS postmortem samples and plasma may be an upstream event for triggering neuroinflammation and neuronal death. (© 2020 Wiley Periodicals, Inc.) |
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فهرسة مساهمة: | Keywords: amyotrophic lateral sclerosis; biomarker; cell death; lipocalin-2; neuroinflammation |
المشرفين على المادة: | 0 (Cytokines) 0 (LCN2 protein, human) 0 (Lipocalin-2) |
تواريخ الأحداث: | Date Created: 20200506 Date Completed: 20200925 Latest Revision: 20200925 |
رمز التحديث: | 20221213 |
DOI: | 10.1002/mus.26911 |
PMID: | 32369618 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1097-4598 |
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DOI: | 10.1002/mus.26911 |