@ARTICLE{Aleksandrovych_Veronika_Identification_2018, author={Aleksandrovych, Veronika and Białas, Magdalena and Pasternak, Artur and Bereza, Tomasz and Sajewicz, Marek and Walocha, Jerzy and Gil, Krzysztof}, volume={vol. 58}, number={No 3}, journal={Folia Medica Cracoviensia}, pages={89-102}, howpublished={online}, year={2018}, publisher={Oddział PAN w Krakowie; Uniwersytet Jagielloński – Collegium Medicum}, abstract={Introduction: Uterine leiomyoma is the most widespread benign tumor affecting women of childbearing age. There are still gaps in the understanding of its pathogenesiss. Telocytes are unique cells described in greater than 50 different locations inside the human body. The functional relationship of cells could clarify the pathogenesis of leiomyomata. In the current study, we focused on the identification of telocytes in all regions of the human uterus to explain their involvement in leiomyoma development. Materials and Methods: Tissue samples from a healthy and myomatous uterus were stained for c-kit, tryptase, CD34 and PDGFRα to identify telocytes. Routine histology was performed to analyze tissue morphology and collagen deposits. Results: Telocytes were detected in the cervix, corpus of the uterus and leiomyoma. The density of telocytes in fibroid foci was reduced compared with normal myometrium. Conclusions: Our results demonstrated the existence of telocytes in all parts of the human body affected and unaff ected by leiomyoma of the uterus. In addition, telocytes were also present in leiomyoma foci. Our results suggest that the reduced density of telocytes is important for the pathomechanisms of myometrial growth, demonstrating its value as a main component of the myomatous architecture.}, type={Artykuły / Articles}, title={Identification of uterine telocytes and their architecture in leiomyoma}, URL={http://journals.pan.pl/Content/109117/PDF/FMC%203-18%208-Aleksandrovych.pdf}, doi={10.24425/fmc.2018.125075}, keywords={telocytes, uterus, extracellular matrix (ECM), stem cells, collagen, CD34, PDGFRα}, }