Research Papers: Pathology:

TSH inhibits SERCA2a and the PKA/PLN pathway in rat cardiomyocytes

Jiajia Dong, Cuixia Gao, Jing Liu, Yunshan Cao and Limin Tian _

PDF  |  HTML  |  How to cite

Oncotarget. 2016; 7:39207-39215. https://doi.org/10.18632/oncotarget.9393

Metrics: PDF 2157 views  |   HTML 2427 views  |   ?  


Jiajia Dong1, Cuixia Gao2, Jing Liu1, Yunshan Cao3 and Limin Tian1

1 Department of Endocrinology, Gansu Provincial Hospital, Lanzhou, Gansu, China

2 Department of Ultrasonic Diagnosis, Gansu Provincial Hospital, Lanzhou, Gansu, China

3 Department of Cardiology, Gansu Provincial Hospital, Lanzhou, Gansu, China

Correspondence to:

Limin Tian, email:

Keywords: TSH, SERCA2a, cardiomyocyte, PLN, PKA, Pathology Section

Received: November 10, 2015 Accepted: April 16, 2016 Published: May 16, 2016


Elevated thyroid-stimulating hormone (TSH) levels often accompany impaired LV diastolic function and subtle systolic dysfunction in subclinical hypothyroidism (sHT). These cardiac dysfunctions are characterized by increases in mean aortic acceleration and pre-ejection/ejection time ratios. To explore the mechanism underlying these pathologies, we investigated the effects of TSH on sarcoplasmic reticulum calcium ATPase (SERCA2a) activity and expression in neonatal rat cardiomyocytes. TSH inhibited SERCA2a activity and expression by binding to TSH receptors in cardiomyocyte membranes and inhibiting the protein kinase A/phoshpolamban (PKA/PLN) signaling pathway. These results suggest that increases in serum TSH levels contribute to the development of cardiac diastolic and systolic dysfunction.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 9393