Expression of TASK-1 channel in mouse Leydig cells

• Published in: Journal of animal reproduction & biotechnology (Online) Vol. 38; no. 4; pp. 291 - 299
• Main Authors: Woo, Min Seok, Kim, Eun-Jin, Prayoga, Anjas Happy, Kim, Yangmi, Kang, Dawon
• Format: Journal Article
• Language: English
• Published: 한국동물생명공학회(구 한국수정란이식학회) 31.12.2023; 사단법인 한국동물생명공학회
• Subjects: 축산학; TASK-1; cell death; testosterone; mice; Leydig cells
• ISSN: 2671-4639; 2671-4663
• DOI: 10.12750/JARB.38.4.291

Background: Leydig cells, crucial for testosterone production, express ion channels like ANO1 that influence hormone secretion. This study investigates the expression and role of the Tandem of P domains in a weak inward rectifying K+ channel-related Acid-Sensitive K+-1 (TASK-1) channel in these cells, exploring its impact on testicular function and steroidogenesis. Methods: TASK-1 expression in Leydig cells was confirmed using immunostaining, while RT-PCR and Western Blot (WB) validated its expression in the TM3 Leydig cell line. The effect of a TASK-1 channel blocker on cell viability was assessed through live/dead staining and MTT assays. Additionally, the blocker’s effect on testosterone secretion was evaluated by measuring testosterone levels. Results: Immunohistochemical analysis revealed a predominant presence of TASK- 1, along with c-Kit and ANO-1, in Leydig cells adjacent to seminiferous tubules and also in Sertoli and spermatogenic cells. Expression levels of TASK-1 mRNA and protein were significantly higher in TM3 Leydig cells compared to TM4 Sertoli cells. In addition, blocking TASK-1 in TM3 cells with ML365 induced cell death but did not affect LHinduced testosterone secretion. Conclusions: These findings suggest that TASK-1 in Leydig cells is crucial for their viability and proliferation, highlighting its potential importance in testicular physiology.