A novel variant in the SLCO2A1 gene in a Chinese patient with chronic gastroenteropathy and primary hypertrophic osteoarthropathy.


Journal

Orphanet journal of rare diseases
ISSN: 1750-1172
Titre abrégé: Orphanet J Rare Dis
Pays: England
ID NLM: 101266602

Informations de publication

Date de publication:
11 Jun 2024
Historique:
received: 21 08 2023
accepted: 19 05 2024
medline: 12 6 2024
pubmed: 12 6 2024
entrez: 11 6 2024
Statut: epublish

Résumé

Chronic enteropathy associated with SLCO2A1 gene (CEAS) results from loss-of-function variants in SLCO2A1, which encodes the prostaglandin transporter (PGT). CEAS follows an autosomal recessive inheritance pattern. To date, approximate 30 pathogenic variants have been reported in CEAS. We performed whole exome sequencing (WES) to screen for potential pathogenic variants in a patient suspected of having CEAS, and confirmed a variant in SLCO2A1 using Sanger sequencing. We established an in vitro minigene model to compare splicing between wild type (WT) and mutant transcripts. Quantitative polymerase chain reaction (qPCR) was used to evaluate SLCO2A1 transcription in the stomach and colon tissues from the patient and a healthy control (HC). The transcripts were further cloned and sequenced. The patient had a novel, homozygous, recessive c.929A > G variant in exon 7 of SLCO2A1, which has not been previously reported in CEAS or PHO. This variant altered splicing, resulting in an exon 7-truncated transcript lacking 16 bases. No normal transcript was detected in the patient's stomach or colon tissue. qPCR also showed significantly decreased SLCO2A1 transcription compared to HC. A previously unreported variant caused defective SLCO2A1 splicing and reduced mRNA levels in a patient with CEAS and PHO. This research enhances understanding of CEAS and PHO pathophysiology and aids genetic counseling and diagnosis.

Sections du résumé

BACKGROUND BACKGROUND
Chronic enteropathy associated with SLCO2A1 gene (CEAS) results from loss-of-function variants in SLCO2A1, which encodes the prostaglandin transporter (PGT). CEAS follows an autosomal recessive inheritance pattern. To date, approximate 30 pathogenic variants have been reported in CEAS.
METHODS METHODS
We performed whole exome sequencing (WES) to screen for potential pathogenic variants in a patient suspected of having CEAS, and confirmed a variant in SLCO2A1 using Sanger sequencing. We established an in vitro minigene model to compare splicing between wild type (WT) and mutant transcripts. Quantitative polymerase chain reaction (qPCR) was used to evaluate SLCO2A1 transcription in the stomach and colon tissues from the patient and a healthy control (HC). The transcripts were further cloned and sequenced.
RESULTS RESULTS
The patient had a novel, homozygous, recessive c.929A > G variant in exon 7 of SLCO2A1, which has not been previously reported in CEAS or PHO. This variant altered splicing, resulting in an exon 7-truncated transcript lacking 16 bases. No normal transcript was detected in the patient's stomach or colon tissue. qPCR also showed significantly decreased SLCO2A1 transcription compared to HC.
CONCLUSION CONCLUSIONS
A previously unreported variant caused defective SLCO2A1 splicing and reduced mRNA levels in a patient with CEAS and PHO. This research enhances understanding of CEAS and PHO pathophysiology and aids genetic counseling and diagnosis.

Identifiants

pubmed: 38862970
doi: 10.1186/s13023-024-03221-x
pii: 10.1186/s13023-024-03221-x
doi:

Substances chimiques

SLCO2A1 protein, human 0
Organic Anion Transporters 0

Types de publication

Journal Article Case Reports

Langues

eng

Sous-ensembles de citation

IM

Pagination

229

Subventions

Organisme : Natural Science Foundation of Beijing Municipality
ID : 7212078
Organisme : CAMS Innovation Fund for Medical Sciences (CIFMS) from Chinese Academy of Medical Sciences
ID : 2021-I2M-1-062

Informations de copyright

© 2024. The Author(s).

Références

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Auteurs

Yimin Dai (Y)

Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 1, Shuaifuyuan, Beijing, 100730, China.

Miao He (M)

McKusick-Zhang Center for Genetic Medicine, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Bei Tan (B)

Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 1, Shuaifuyuan, Beijing, 100730, China.

Weixun Zhou (W)

Department of Pathology, Peking Union Medical College Hospital, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.

Wei Liu (W)

Department of Radiology, Peking Union Medical College Hospital, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, No. 1, Shuaifuyuan, Beijing, 100730, China.

Qiang Wang (Q)

Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 1, Shuaifuyuan, Beijing, 100730, China.

Jingyi Huang (J)

Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 1, Shuaifuyuan, Beijing, 100730, China.

Qing Shang (Q)

Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 1, Shuaifuyuan, Beijing, 100730, China.

Yaping Liu (Y)

The State Key Laboratory for Complex, Severe, and Rare Diseases, The State Key Sci-tech Infrastructure for Translational Medicine, Peking Union Medical College Hospital, Beijing, 100730, China. ypliu_pumc@163.com.

Yue Li (Y)

Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 1, Shuaifuyuan, Beijing, 100730, China. liyue@pumch.ac.cn.

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