Dysregulation of TMEM16A impairs oviductal transport of embryos

Author:

Ning Nannan12ORCID,Luo Dan3,Xia Wei45,Mou Guangjing6,Zhao Jiangli6,Zhang Jian4,Li Cheng7,Wang Hongchun12,Li Jingxin6ORCID

Affiliation:

1. Department of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, People’s Republic of China

2. Shandong Engineering Research Center of Biomarker and Artificial Intelligence Application, Jinan, People’s Republic of China

3. Department of Breast Surgery, Qilu Hospital of Shandong University, Jinan, People’s Republic of China

4. Department of Obstetrics and Gynecology, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, People’s Republic of China

5. Shanghai Key Laboratory Embryo Original Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China

6. Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, People’s Republic of China

7. Obstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, People’s Republic of China

Abstract

The ion channel protein TMEM16A is expressed in the epithelium and smooth muscle of the human fallopian tube and is upregulated in patients with tubal pregnancy. TMEM16A is involved in regulating the smooth muscle contraction and the cilia beating. Dysregulated TMEM16A may result in embryo retention in the oviduct and delayed early embryo development. Our study reveals a new regulatory point for embryo transport and development.

Funder

Young Elite Scientists Sponsorship Program by CAST

Science and Technology Program of Jinan

MOST | National Natural Science Foundation of China

Natural Science Foundation of Shandong Province

Publisher

American Physiological Society

Subject

Cell Biology,Physiology

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