Autophagy is a vital process that maintains cellular homeostasis by joining lysosomes and providing energy production substrates. In testicular tissue, Sertoli cells play functional roles in spermatogenesis and steroidogenesis. It is well known that autophagy physiologically occurs in the Sertoli cells. Under pathological conditions, such as testicular torsion, autophagy can be activated under high-stress stimuli. It is worth noting that Sertoli cells receive autophagy-induced signals through some extracellular matrix proteins, e.g. laminin and fibronectin. The present study aims to evaluate Sertoli cells' autophagy-associated extracellular matrix proteins' alteration following testicular torsion in rat model. The animals were divided into two groups as sham and testicular torsion/detorsion groups. In the testicular torsion/detorsion group, testicular torsion was maintained for 6 hr, followed by detorsion for 14 days. The obtained results revealed that testicular torsion-induced oxidative stress leads to increased autophagy in Sertoli cells as well as the whole testicular tissue. Moreover, extracellular matrix proteins including laminin and fibronectin act as autophagy-regulating proteins, in which their expression levels are reduced and increased respectively. In addition, the level of caspase-3, as an autophagy inhibitory protein, did not increase significantly in the cytoplasm of Sertoli cells as opposed to whole testicular tissue, indicating that autophagy is active after testicular torsion in these cells.
Keywords: autophagy; caspase-3; fibronectin; sertoli cell; testicular torsion.
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