In Mice Subjected to Chronic Stress, Exogenous cBIN1 Preserves Calcium-Handling Machinery and Cardiac Function.
AAV9, adeno-associated virus 9
ANOVA, analysis of variance
AR, adrenergic receptor
ATPase, adenosine triphosphatase
BW, body weight
CAMKII, Ca2+/calmodulin-dependent protein kinase
CMV, cytomegalovirus
Di-8-ANNEPs, 4-[2-[6-(Dioctylamino)-2-naphthalenyl]ethenyl]-1-(3-sulfopropyl)-pyridinium, inner salt
EC, excitation contraction
EDV, end diastolic volume
EF, ejection fraction
GFP, green fluorescent protein
HF, heart failure
HR, heart rate
HT, heterozygote
HW, heart weight
ISO, isoproterenol
LSD, least significant difference
LTCC, voltage-dependent L-type calcium channel
LV, left ventricular
LW, lung weight
PBS, phosphate-buffered saline
PKA, protein kinase A
PLN, phospholamban
RWT, relative wall thickness
RyR, ryanodine receptor
SD, standard deviation
SEM, standard error of the mean
SERCA2a, sarcoplasmic reticulum calcium ATPase pump 2a
SR, sarcoplasmic reticulum
STORM, stochastic optical reconstruction microscopy
TAC, transverse aortic constriction
TEM, transmission electron microscopy
WT, wild type
cBIN1, cardiac bridging integrator 1
diastolic dysfunction
heart failure
jSR, junctional sarcoplasmic reticulum
pressure overload
sympathetic overdrive
t-tubule
t-tubule, transverse-tubule
vg, vector genome
Journal
JACC. Basic to translational science
ISSN: 2452-302X
Titre abrégé: JACC Basic Transl Sci
Pays: United States
ID NLM: 101677259
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
02
10
2019
revised:
11
03
2020
accepted:
11
03
2020
entrez:
3
7
2020
pubmed:
3
7
2020
medline:
3
7
2020
Statut:
epublish
Résumé
Heart failure is an important, and growing, cause of morbidity and mortality. Half of patients with heart failure have preserved ejection fraction, for whom therapeutic options are limited. Here we report that cardiac bridging integrator 1 gene therapy to maintain subcellular membrane compartments within cardiomyocytes can stabilize intracellular distribution of calcium-handling machinery, preserving diastolic function in hearts stressed by chronic beta agonist stimulation and pressure overload. This study identifies that maintenance of intracellular architecture and, in particular, membrane microdomains at t-tubules, is important in the setting of sympathetic stress. Stabilization of membrane microdomains may be a pathway for future therapeutic development.
Identifiants
pubmed: 32613144
doi: 10.1016/j.jacbts.2020.03.006
pii: S2452-302X(20)30121-2
pmc: PMC7315191
doi:
Types de publication
Journal Article
Langues
eng
Pagination
561-578Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL133286
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL138577
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL152691
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2020 The Authors.
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