TEAD1 Knockdown Ameliorates Diabetic Erectile Dysfunction in Rats and Is Associated With Modulation of Calcium Signaling-Mediated Contractile Machinery.

Authors

Tao Zhang, Chenxiao Wu, Youlong Lu, Weili Li, Huaru Zhang, Cheng Li

Published in

Drug development research. Volume 87. Issue 6. Pages e70365.

Abstract

Diabetes mellitus (DM) related erectile dysfunction (ED) is a common complication in males. We aim to explore the specific regulatory mechanisms of TEA domain family member 1 (TEAD1) in DMED rats. Diabetic ED in rats was induced by streptozotocin and evaluated by the intracavernosal pressure response to electrical stimulation and the apomorphine test. Corpus cavernosum smooth muscle cells (CCSMCs) were isolated to explore the role of TEAD1 in phenotypic transformation. TEAD1 knockdown was performed in DMED rats and CCSMCs using the CRISPR/Cas9 technology. Hematoxylin-Eosin and Masson staining were applied to observe the penile tissue pathology. The CCSMC function was evaluated by detecting viability and apoptosis. Protein and gene expression levels were examined by Western blot and real-time quantitative polymerase chain reaction. The TEAD1 gene knockdown ameliorated erectile function in DMED rats. Knockdown of TEAD1 in CCSMCs of DMED rats enhanced their viability and inhibited their apoptosis, promoting the transformation of CCSMCs from a synthetic to a contractile phenotype. Furthermore, bioinformatics analysis identified the calcium signaling pathway as a candidate pathway warranting further experimental investigation. TEAD1 knockdown was associated with altered expression of calcium-related proteins and elevated intracellular Ca²⁺ levels. The calcium channel blocker Nimodipine could reverse the improvement of erectile function in DMED rats and the transformation of CCSMC phenotype caused by TEAD1 knockdown. TEAD1 knockdown promotes the transformation of CCSMCs from a synthetic to a contractile phenotype and is associated with modulation of calcium signaling-mediated contractile machinery, contributing to the relief of DMED.

PMID:
42606539
Bibliographic data and abstract were imported from PubMed on 17 Aug 2026.

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