Nanoscale coupling of junctophilin-2 and ryanodine receptors regulates vascular smooth muscle cell contractility.
Animals
Cerebral Arteries
/ cytology
Gene Knockdown Techniques
Male
Membrane Proteins
/ genetics
Mice, Inbred C57BL
Mice, Transgenic
Muscle Contraction
/ physiology
Muscle, Smooth, Vascular
/ physiology
Nanoparticles
Potassium Channels, Calcium-Activated
/ physiology
Ryanodine Receptor Calcium Release Channel
/ physiology
Signal Transduction
Ca2+ signaling
cerebral arteries
electrophysiology
ion channels
super-resolution microscopy
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
22 10 2019
22 10 2019
Historique:
pubmed:
9
10
2019
medline:
3
4
2020
entrez:
9
10
2019
Statut:
ppublish
Résumé
Junctophilin proteins maintain close contacts between the endoplasmic/sarcoplasmic reticulum (ER/SR) and the plasma membrane in many types of cells, as typified by junctophilin-2 (JPH2), which is necessary for the formation of the cardiac dyad. Here, we report that JPH2 is the most abundant junctophilin isotype in native smooth muscle cells (SMCs) isolated from cerebral arteries and that acute knockdown diminishes the area of sites of interaction between the SR and plasma membrane. Superresolution microscopy revealed nanometer-scale colocalization of JPH2 clusters with type 2 ryanodine receptor (RyR2) clusters near the cell surface. Knockdown of JPH2 had no effect on the frequency, amplitude, or kinetics of spontaneous Ca
Identifiants
pubmed: 31591206
pii: 1911304116
doi: 10.1073/pnas.1911304116
pmc: PMC6815135
doi:
Substances chimiques
Membrane Proteins
0
Potassium Channels, Calcium-Activated
0
Ryanodine Receptor Calcium Release Channel
0
junctophilin
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
21874-21881Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM130459
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL146054
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL091905
Pays : United States
Organisme : NIGMS NIH HHS
ID : P20 GM103440
Pays : United States
Organisme : NIGMS NIH HHS
ID : P30 GM110767
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL137852
Pays : United States
Organisme : British Heart Foundation
ID : PG/18/7/33535
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : NHLBI NIH HHS
ID : R01 HL139585
Pays : United States
Organisme : NIDDK NIH HHS
ID : P01 DK041315
Pays : United States
Organisme : British Heart Foundation
ID : FS/12/81/29882
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/18/7/33535
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 203128/Z/16/Z
Pays : United Kingdom
Informations de copyright
Copyright © 2019 the Author(s). Published by PNAS.
Déclaration de conflit d'intérêts
The authors declare no competing interest.
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