Modeling familial sinus node dysfunction with a large intergenic deletion between PITX2 and ANK2 using iPS cell-derived sinoatrial nodal-like cardiomyocytes Article Swipe
Takanori Aizawa
,
Takeru Makiyama
,
Hiroshige Murata
,
Takashi Takaki
,
Manon Baudic
,
Jingshan Gao
,
Tomoko Imamura
,
Seiko Ohno
,
Yoshinori Yoshida
,
Wataru Shimizu
,
Naomasa Makita
,
Julien Barc
,
Jean‐Jacques Schott
,
Minoru Horie
,
Takeshi Kimura
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1093/eurheartj/ehad655.268
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1093/eurheartj/ehad655.268
Background Pituitary homeobox 2 (PITX2) encoded by PITX2, is one of the transcription factors and plays an important role in establishing the left-right axis during development. In the heart, PITX2 inhibits the development of the sinoatrial node (SAN) in the left atrium, whereas the absence of PITX2 allows the development of SAN in the right atrium. In a multicenter study, we recently identified a sizeable intergenic deletion between PITX2 and ANK2 on chromosome 4q25 in familial sinus node dysfunction (SND). The deletion contains a CTCF-binding motif (19 bps) which forms a topologically associating domain (TAD) involved in PITX2, and putatively disrupts the TAD. In order to investigate how the intergenic deletion causes SND, we analyzed iPS cells (iPSCs) by specifically differentiating them into SAN cardiomyocytes. Methods and results We identified an intergenic heterozygous deletion of 30k bps in a Japanese family with SND by whole genome sequencing. In the SND family, all 11 genetically affected patients developed SND since childhood, and seven of them underwent pacemaker implantation (the mean age was 26). To elucidate the pathology, we utilized 3 iPSC lines: an iPSC line from a patient, a homozygous CTCF-binding motif knockout line by gene editing, and a control line from a healthy volunteer. We modified the previously reported SAN differentiation protocol1 and generated SAN-like iPSC-derived cardiomyocytes (SANLCMs). SANLCMs showed a higher beating rate than ventricular-like cardiomyocytes (VLCMs), and exhibited SAN-like action potential morphology recorded using a patch-clamp technique. SANLCMs contained lesser NKX2-5 positive cells than VLCMs by immunostaining analysis and their gene expression patterns were compatible with SAN cardiomyocytes: higher expression levels of SHOX2, TBX18, TBX3, and HCN4, and lower expression levels of PITX2, NKX2-5, and MYL2 compared with VLCMs. Then, we analyzed the gene expression profiles during the SAN differentiation. SANLCMs from CTCF-binding motif knockout iPSC lines showed lower beating rates than controls. We also found that the levels of PITX2 expression in SANLCMs from patient-derived and CTCF-binding motif knockout iPSC lines were significantly higher compared to those from the control. Conclusion Our findings suggest that the lack of CTCF-binding motif involved in a large intergenic deletion on chromosome 4q25 might be associated with a hypoplasia of SAN via PITX2 overexpression during cardiac development.
Related Topics
Concepts
PITX2
Homeobox
Sinoatrial node
Medicine
Genetics
CTCF
Haploinsufficiency
Induced pluripotent stem cell
Transcription factor
Gene
Biology
Molecular biology
Enhancer
Internal medicine
Phenotype
Embryonic stem cell
Blood pressure
Heart rate
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1093/eurheartj/ehad655.268
- https://academic.oup.com/eurheartj/article-pdf/44/Supplement_2/ehad655.268/53590016/ehad655.268.pdf
- OA Status
- bronze
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4388595651
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W4388595651Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1093/eurheartj/ehad655.268Digital Object Identifier
- Title
-
Modeling familial sinus node dysfunction with a large intergenic deletion between PITX2 and ANK2 using iPS cell-derived sinoatrial nodal-like cardiomyocytesWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-11-01Full publication date if available
- Authors
-
Takanori Aizawa, Takeru Makiyama, Hiroshige Murata, Takashi Takaki, Manon Baudic, Jingshan Gao, Tomoko Imamura, Seiko Ohno, Yoshinori Yoshida, Wataru Shimizu, Naomasa Makita, Julien Barc, Jean‐Jacques Schott, Minoru Horie, Takeshi KimuraList of authors in order
- Landing page
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https://doi.org/10.1093/eurheartj/ehad655.268Publisher landing page
- PDF URL
-
https://academic.oup.com/eurheartj/article-pdf/44/Supplement_2/ehad655.268/53590016/ehad655.268.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
bronzeOpen access status per OpenAlex
- OA URL
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https://academic.oup.com/eurheartj/article-pdf/44/Supplement_2/ehad655.268/53590016/ehad655.268.pdfDirect OA link when available
- Concepts
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PITX2, Homeobox, Sinoatrial node, Medicine, Genetics, CTCF, Haploinsufficiency, Induced pluripotent stem cell, Transcription factor, Gene, Biology, Molecular biology, Enhancer, Internal medicine, Phenotype, Embryonic stem cell, Blood pressure, Heart rateTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.cardiomyocytes. | 125 |
| abstract_inverted_index.cardiomyocytes: | 260 |
| abstract_inverted_index.differentiating | 121 |
| abstract_inverted_index.differentiation | 211 |
| abstract_inverted_index.patient-derived | 318 |
| abstract_inverted_index.differentiation. | 292 |
| abstract_inverted_index.ventricular-like | 226 |
| cited_by_percentile_year | |
| countries_distinct_count | 2 |
| institutions_distinct_count | 15 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.5899999737739563 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.32521612 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |