Telocytes (TCs), also known as CD34+ stromal/interstitial cells, have recently been identified within the connective tissue of a variety of organs including the normal human testis. Testicular TCs appear to constitute a widespread reticular network distributed either in the peritubular or in the intertubular stromal spaces where they have been suggested to play different roles, such as participation to testis morphogenesis, postnatal preservation of the normal tissue/organ three-dimensional structure, and regulation of spermatogenesis and androgen hormone secretion and release. Although increasing evidence indicates that TCs may be involved in the pathophysiology of various diseases, no study has yet reported possible changes in these cells within the stromal compartment of seminoma, one of the most frequent malignant testicular cancers in humans. Therefore, here we carried out the first investigation of the presence and tissue distribution of TCs/CD34+ stromal cells in human testicular seminoma in comparison with normal human testis using either CD34 immunohistochemistry or CD34/CD31 and CD34/α-smooth muscle actin (α-SMA) double immunofluorescence analyses. In seminoma tissue sections, we observed an overall loss of TCs (CD34+/CD31− stromal cells) accompanying a severe degeneration of the normal architecture of seminiferous tubules and stromal tissue associated with dense cellularity increase and presence of interstitial fibrosis. Noteworthy, in the seminoma tissue the disappearance of TCs was paralleled by an expansion of α-SMA+ myoid cells. Moreover, the CD34+/CD31+ blood vessel network was greatly expanded, while steroidogenic Leydig cells were undetectable in seminoma specimens. Since TCs are emerging as important regulators of tissue and organ homeostasis, collectively the present findings indicate that the possible pathophysiologic implications of the loss of TCs in human testicular seminoma should not be further overlooked.

Changes in the telocyte/CD34+ stromal cell and α-SMA+ myoid cell networks in human testicular seminoma

Eleonora Sgambati;
2019-01-01

Abstract

Telocytes (TCs), also known as CD34+ stromal/interstitial cells, have recently been identified within the connective tissue of a variety of organs including the normal human testis. Testicular TCs appear to constitute a widespread reticular network distributed either in the peritubular or in the intertubular stromal spaces where they have been suggested to play different roles, such as participation to testis morphogenesis, postnatal preservation of the normal tissue/organ three-dimensional structure, and regulation of spermatogenesis and androgen hormone secretion and release. Although increasing evidence indicates that TCs may be involved in the pathophysiology of various diseases, no study has yet reported possible changes in these cells within the stromal compartment of seminoma, one of the most frequent malignant testicular cancers in humans. Therefore, here we carried out the first investigation of the presence and tissue distribution of TCs/CD34+ stromal cells in human testicular seminoma in comparison with normal human testis using either CD34 immunohistochemistry or CD34/CD31 and CD34/α-smooth muscle actin (α-SMA) double immunofluorescence analyses. In seminoma tissue sections, we observed an overall loss of TCs (CD34+/CD31− stromal cells) accompanying a severe degeneration of the normal architecture of seminiferous tubules and stromal tissue associated with dense cellularity increase and presence of interstitial fibrosis. Noteworthy, in the seminoma tissue the disappearance of TCs was paralleled by an expansion of α-SMA+ myoid cells. Moreover, the CD34+/CD31+ blood vessel network was greatly expanded, while steroidogenic Leydig cells were undetectable in seminoma specimens. Since TCs are emerging as important regulators of tissue and organ homeostasis, collectively the present findings indicate that the possible pathophysiologic implications of the loss of TCs in human testicular seminoma should not be further overlooked.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11695/90746
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