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Article
Xiaoyan Qiu
Department of Immunology, School of Basic Medical Sciences, Peking University
Corresponding Author
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It is widely accepted that immunoglobulins (Igs) are produced only by B cells and function as antibodies. However, growing evidence has proven that almost all non-B cells also produce Igs with nonconventional roles, such as promotion of cell survival, proliferation and migration. In this study, we identified Ig light chain (κ chain) expression in mouse and human cardiomyocytes, especially on intercalated discs (ICDs). Unexpectedly, conditional knockout (cKO) of Igκ in adult cardiomyocytes in mice resulted in significant hypotension, a rapid decrease in cardiac contractility and conduction defects. Histologically, Igκ knockout in mouse cardiomyocytes led to structural disruption of intercalated discs (ICDs) and loss of localization of adhesion-related N-cadherin and CX43 on ICDs. Mechanistic investigation indicated that Igκ can bind with plectin/desmoplakin, a complex that connects desmin and desmosomes and enhances the protein stability of plectin. In conclusion, Our findings identify Igκ expressed by cardiomyocytes as a new ICD-related molecule that participates in cardiomyocyte contraction and conduction by stabilizing plectin.
Keywords
Arrhythmogenic cardiomyopathy, Immunoglobin(Ig), Intercalated disc(ICD), Myocardial contraction, Plectin
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supplymentary figure 3
- supplymentaryTable1.docx
Supplementary Table 1
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Supplementary Table 1
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Supplementary Table 2
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Supplementary Table 3
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This preprint is under consideration at a Nature Portfolio Journal. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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Article
Xiaoyan Qiu
Department of Immunology, School of Basic Medical Sciences, Peking University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 02 Dec, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
It is widely accepted that immunoglobulins (Igs) are produced only by B cells and function as antibodies. However, growing evidence has proven that almost all non-B cells also produce Igs with nonconventional roles, such as promotion of cell survival, proliferation and migration. In this study, we identified Ig light chain (κ chain) expression in mouse and human cardiomyocytes, especially on intercalated discs (ICDs). Unexpectedly, conditional knockout (cKO) of Igκ in adult cardiomyocytes in mice resulted in significant hypotension, a rapid decrease in cardiac contractility and conduction defects. Histologically, Igκ knockout in mouse cardiomyocytes led to structural disruption of intercalated discs (ICDs) and loss of localization of adhesion-related N-cadherin and CX43 on ICDs. Mechanistic investigation indicated that Igκ can bind with plectin/desmoplakin, a complex that connects desmin and desmosomes and enhances the protein stability of plectin. In conclusion, Our findings identify Igκ expressed by cardiomyocytes as a new ICD-related molecule that participates in cardiomyocyte contraction and conduction by stabilizing plectin.
Figure 1
Figure 1
Figure 2
Figure 2
Figure 3
Figure 3
Figure 4
Figure 4
Figure 5
Figure 5
Figure 6
Figure 6
There is NO Competing Interest.
This is a list of supplementary files associated with this preprint. Click to download.
- FigS1.tif
Supplementary Fig. 1
- FigS1.tif
Supplementary Fig. 1
- FigS2.tif
Supplementary Fig. 1
- FigS2.tif
Supplementary Fig. 1
- FigS3.tif
supplymentary figure 3
- FigS3.tif
supplymentary figure 3
- supplymentaryTable1.docx
Supplementary Table 1
- supplymentaryTable1.docx
Supplementary Table 1
- supplementarytable2.xlsx
Supplementary Table 2
- supplementarytable2.xlsx
Supplementary Table 2
- supplementaryTable3.docx
Supplementary Table 3
- supplementaryTable3.docx
Supplementary Table 3
- supplymentarytable4.xlsx
Supplementary Table 4
- supplymentarytable4.xlsx
Supplementary Table 4
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