دورية أكاديمية
أعرض في EDS

Protein Quality Control Activation and Microtubule Remodeling in Hypertrophic Cardiomyopathy.

التفاصيل البيبلوغرافية
العنوان: Protein Quality Control Activation and Microtubule Remodeling in Hypertrophic Cardiomyopathy.
المؤلفون: Dorsch LM; Department of Physiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Cardiovascular Sciences, 1081 HV Amsterdam, The Netherlands. l.dorsch@vumc.nl., Schuldt M; Department of Physiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Cardiovascular Sciences, 1081 HV Amsterdam, The Netherlands., dos Remedios CG; Sydney Heart Bank, Discipline of Anatomy, Bosch Institute, University of Sydney, Sydney 2006, Australia., Schinkel AFL; Department of Cardiology, Thoraxcenter, Erasmus Medical Center, 3015 GD Rotterdam, The Netherlands., de Jong PL; Department of Cardiothoracic Surgery, Thoraxcenter, Erasmus Medical Center, 3015 GD Rotterdam, The Netherlands., Michels M; Department of Cardiology, Thoraxcenter, Erasmus Medical Center, 3015 GD Rotterdam, The Netherlands., Kuster DWD; Department of Physiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Cardiovascular Sciences, 1081 HV Amsterdam, The Netherlands., Brundel BJJM; Department of Physiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Cardiovascular Sciences, 1081 HV Amsterdam, The Netherlands., van der Velden J; Department of Physiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Cardiovascular Sciences, 1081 HV Amsterdam, The Netherlands.; Netherlands Heart Institute, 3511 EP Utrecht, The Netherlands.
المصدر: Cells [Cells] 2019 Jul 18; Vol. 8 (7). Date of Electronic Publication: 2019 Jul 18.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI
مواضيع طبية MeSH: Unfolded Protein Response*, Cardiomyopathy, Hypertrophic/*metabolism , Microtubules/*metabolism, Adult ; Aged ; Cardiomyopathy, Hypertrophic/genetics ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Chaperonin 60/metabolism ; Female ; HSP70 Heat-Shock Proteins/metabolism ; Humans ; Male ; Microtubules/genetics ; Middle Aged ; Mitochondrial Proteins/metabolism ; Mutation ; Myocytes, Cardiac/metabolism ; Sarcomeres/genetics ; Sarcomeres/metabolism ; Tubulin/metabolism
مستخلص: Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disorder. It is mainly caused by mutations in genes encoding sarcomere proteins. Mutant forms of these highly abundant proteins likely stress the protein quality control (PQC) system of cardiomyocytes. The PQC system, together with a functional microtubule network, maintains proteostasis. We compared left ventricular (LV) tissue of nine donors (controls) with 38 sarcomere mutation-positive (HCM SMP ) and 14 sarcomere mutation-negative (HCM SMN ) patients to define HCM and mutation-specific changes in PQC. Mutations in HCM SMP result in poison polypeptides or reduced protein levels (haploinsufficiency, HI). The main findings were 1) several key PQC players were more abundant in HCM compared to controls, 2) after correction for sex and age, stabilizing heat shock protein (HSP)B1, and refolding, HSPD1 and HSPA2 were increased in HCM SMP compared to controls, 3) α-tubulin and acetylated α-tubulin levels were higher in HCM compared to controls, especially in HCM HI , 4) myosin-binding protein-C (cMyBP-C) levels were inversely correlated with α-tubulin, and 5) α-tubulin levels correlated with acetylated α-tubulin and HSPs. Overall, carrying a mutation affects PQC and α-tubulin acetylation. The haploinsufficiency of cMyBP-C may trigger HSPs and α-tubulin acetylation. Our study indicates that proliferation of the microtubular network may represent a novel pathomechanism in cMyBP-C haploinsufficiency-mediated HCM.
Competing Interests: The authors declare no conflict of interest.
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فهرسة مساهمة: Keywords: autophagy; cardiomyopathy; haploinsufficiency; heat shock proteins; hypertrophy; microtubules; poison polypeptide; protein quality control; sarcomere mutation
المشرفين على المادة: 0 (Carrier Proteins)
0 (Chaperonin 60)
0 (HSP70 Heat-Shock Proteins)
0 (HSPA2 protein, human)
0 (HSPD1 protein, human)
0 (Mitochondrial Proteins)
0 (Tubulin)
0 (myosin-binding protein C)
تواريخ الأحداث: Date Created: 20190721 Date Completed: 20200210 Latest Revision: 20231013
رمز التحديث: 20231013
مُعرف محوري في PubMed: PMC6678711
DOI: 10.3390/cells8070741
PMID: 31323898
قاعدة البيانات: MEDLINE
الوصف
تدمد:2073-4409
DOI:10.3390/cells8070741