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BIN1 knockdown rescues systolic dysfunction in aging male mouse hearts.
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- Author(s): Westhoff M;Westhoff M; Del Villar SG; Del Villar SG; Voelker TL; Voelker TL; Thai PN; Thai PN; Spooner HC; Spooner HC; Costa AD; Costa AD; Sirish P; Sirish P; Chiamvimonvat N; Chiamvimonvat N; Chiamvimonvat N; Chiamvimonvat N; Dickson EJ; Dickson EJ; Dixon RE; Dixon RE
- Source:
Nature communications [Nat Commun] 2024 Apr 25; Vol. 15 (1), pp. 3528. Date of Electronic Publication: 2024 Apr 25.- Publication Type:
Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural- Language:
English - Source:
- Additional Information
- Source: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
- Publication Information: Original Publication: [London] : Nature Pub. Group
- Subject Terms: Adaptor Proteins, Signal Transducing*/metabolism ; Adaptor Proteins, Signal Transducing*/genetics ; Aging*/metabolism ; Tumor Suppressor Proteins*/metabolism ; Tumor Suppressor Proteins*/genetics ; Myocardium*/metabolism ; Myocardium*/pathology ; Ryanodine Receptor Calcium Release Channel*/metabolism ; Ryanodine Receptor Calcium Release Channel*/genetics ; Nerve Tissue Proteins*; Animals ; Male ; Mice ; Gene Knockdown Techniques ; Endosomes/metabolism ; Calcium Channels, L-Type/metabolism ; Calcium Channels, L-Type/genetics ; Heart/physiopathology ; Mice, Inbred C57BL ; Humans ; Myocytes, Cardiac/metabolism ; Nuclear Proteins/metabolism ; Nuclear Proteins/genetics ; RNA, Small Interfering/metabolism ; RNA, Small Interfering/genetics ; Systole
- Abstract: Cardiac dysfunction is a hallmark of aging in humans and mice. Here we report that a two-week treatment to restore youthful Bridging Integrator 1 (BIN1) levels in the hearts of 24-month-old mice rejuvenates cardiac function and substantially reverses the aging phenotype. Our data indicate that age-associated overexpression of BIN1 occurs alongside dysregulated endosomal recycling and disrupted trafficking of cardiac Ca
V 1.2 and type 2 ryanodine receptors. These deficiencies affect channel function at rest and their upregulation during acute stress. In vivo echocardiography reveals reduced systolic function in old mice. BIN1 knockdown using an adeno-associated virus serotype 9 packaged shRNA-mBIN1 restores the nanoscale distribution and clustering plasticity of ryanodine receptors and recovers Ca 2+ transient amplitudes and cardiac systolic function toward youthful levels. Enhanced systolic function correlates with increased phosphorylation of the myofilament protein cardiac myosin binding protein-C. These results reveal BIN1 knockdown as a novel therapeutic strategy to rejuvenate the aging myocardium.
(© 2024. The Author(s).) - Comments: Erratum in: Nat Commun. 2024 May 23;15(1):4397. (PMID: 38782927)
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- Accession Number: 0 (Bin1 protein, mouse)
0 (Adaptor Proteins, Signal Transducing)
0 (Tumor Suppressor Proteins)
0 (Ryanodine Receptor Calcium Release Channel)
0 (Calcium Channels, L-Type)
0 (Nuclear Proteins)
0 (RNA, Small Interfering)
0 (Nerve Tissue Proteins) - Publication Date: Date Created: 20240425 Date Completed: 20240425 Latest Revision: 20240527
- Publication Date: 20240528
- Accession Number: PMC11045846
- Accession Number: 10.1038/s41467-024-47847-8
- Accession Number: 38664444
- Source:
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