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Expression of CD117 receptor in male gonads in traumatic brain injury

Genes & Cells: Vol XIII, №1, 2018, pp: 70-74 DOI: 10.23868/201805008

Authors

A.V. Fedotov, A.F. Astrakhantsev, M.P. Mazurova

Using the conventional histological methods (staining with hematoxylin and eosin), morphometric (counting the percentage of tubules with impaired spermatogenesis, measuring the crosssectional area of the tubules), as well as immunohistochemical methods of investigation (immunohistochemical staining with antibodies to C-kit (CD117), the gonads of 5 patients, who died from a craniocerebral trauma on the 15–35 day after the injury, and 6 patients who died from a craniocerebral injury at the scene. In both groups, a positive membranous staining of the spermatogonia of the basal section of the epithelio-spermatogenic layer is found, which is more pronounced in individuals who died in the long-term after traumatic brain injury, which may indicate activation of the proliferative activity of the spermatogonial population of regenerative nature. CD117 positive cell, similar to Cajal cells, are also detected in the walls of convoluted seminiferous tubules, located along the periphery of blood vessels, among interstitial endocrinocytes. The number of interstitial endocrinocytes, along with this, increases in the feces of the sex glands of individuals who died in the long-term after the craniocerebral trauma, which indicates their hyperplasia, as a compensatory adaptive response in response to atrophic changes in the epithelio-spermatogenic layer (so-called. “mixed atrophy of the testis”). CD117 positive cells, interacting with smooth muscle cells of the wall of convoluted seminiferous tubules, can participate both in the movement of spermatogenic cells from the basal membrane to the lumen of the tubule, and participate in the formation of the so-called. “Waves of spermatogenesis”, ensuring the movement of spermatogenic cells from the periphery to the middle zone.

Keywords: Traumatic brain injury, gonads, seminiferous epithelium, tyrozinkinase receptor, transient germinal cell aplasia.

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