Testicular Migration: Remodeling of Connective Tissue and Muscle Cells in Human Gubernaculum Testis

Background/Aim. Myomas of the uterus, the most common benign tumors, have been studied for decades from the aspects of different basic and clinical disciplines. Despite this fact, their pathogenesis is still poorly understood. The aim of this study was to determine immunocytochemical characteristics of smooth muscle cells and connective tissue components of submucosal myomas of the uterus. Method. During the course of this study, 25 samples of submucosal myomas of the uterus were analyzed, all of them obtained during the surgery, after abdominal histerctomy by Aldridge. The samples were fixed in 4% formalin and embedded in paraffin. Sections of 5 ?m thickness were stained immunocytochemically using the DAKO LSAB+/HRP technique to identify ?- smooth muscle actin (?-SMA), vimentin, desmin, CD34, CD45, CD68 and PCNA (DAKO specification). Results. Our results suggest that submucosal myomas of the uterus are build-up of smooth muscle cells which are immunoreactive to ?-SMA and desmin, but also to a certain number of smooth muscle cells which are immunoreactive to ?-SMA and vimentin. Some of vimentin-immunoreactive cells also show an immunoreactivity of PCNA. In the build-up of connective stroma CD34-immunoreactive fibroblasts and neovascular formations are also present. By examining the distribution of CD45 antigen, at all the analyzed samples we observed a weak reaction. Conclusion. Submucosal myomas of the uterus are made-up of smooth muscle cells of the highly differentiated contractile phenotype (?-SMA- and desminimmunoreactivity), as well as smooth muscle cell of the synthetic phenotype which proliferate (?-SMA-, vimentin- and PCNA-immunoreactivity). In submucosal myoma of the uterus there is a significant presence of connective tissue as a result of synthetic activity of fibroblasts, which clearly differ in their immunocytochemical characteristics from smooth muscle cells of the synthetic phenotype.

Download Full-text

Uterine Leiomyoma or Sarcoma?

Handbook of Research on Oncological and Endoscopical Dilemmas in Modern Gynecological Clinical Practice - Advances in Medical Diagnosis, Treatment, and Care ◽

10.4018/978-1-7998-4213-2.ch020 ◽

2021 ◽

pp. 289-304

Author(s):

Theodoros Theodoridis ◽

Dimitra Aivazi ◽

Leonidas Zepiridis ◽

Nikolaos Vlachos

Keyword(s):

Differential Diagnosis ◽

Smooth Muscle ◽

Connective Tissue ◽

Muscle Cells ◽

Uterine Sarcoma ◽

Current Evidence ◽

Optimal Management ◽

Benign Neoplasms ◽

Uterine Sarcomas ◽

Epithelial Neoplasms

Uterine leiomyomas are benign neoplasms derived from the smooth muscle cells of the myometrium. In contrast, uterine sarcomas are rare tumors, with a prevalence of 3-7 per 100,000 women, originating from myometrial cells or endometrial connective tissue. Uterine sarcomas and especially leiomyosarcomas are more aggressive than uterine epithelial neoplasms. The differential diagnosis between leiomyoma and uterine sarcoma preoperatively remains challenging for the clinical practitioner in order to determine optimal treatment. The chapter aims to summarize current evidence regarding differential diagnosis and optimal management of these two challenging clinical entities.

Download Full-text

The Role of Endothelial Cell Injury and Platelet Response in Atherogenesis

10.1055/s-0039-1680472 ◽

1977 ◽

Author(s):

L. A. Harker ◽

R. Ross ◽

J. Glomset

Keyword(s):

Smooth Muscle ◽

Endothelial Cell ◽

Connective Tissue ◽

Smooth Muscle Cells ◽

Lipid Accumulation ◽

Blood Platelets ◽

Muscle Cells ◽

Endothelial Injury ◽

Intimal Proliferation ◽

Flowing Blood

Endothelium forms a resistant barrier between flowing blood and vessel wall structures. Endothelial thromboresistance is maintained in part by the synthesis of prostacyclin, a potent prostaglandin inhibitor of platelet function. Loss of endothelial cells, mediated by physical, chemical, infectious or immune mechanisms, exposes the sub endothelium to flowing blood. Platelets react to the subendothelial connective tissue structures, undergoing adhesion and release of intracellular constituents, including a factor that is mitogenic to smooth muscle cells. This growth factor is a heat stable, basic protein (IP 7.4–9.4) of 20,000 Daltons and appears to be responsible for the intimal proliferation of smooth muscle cells that follows endothelial cell desquamation. After a single injury event the intimal lesion regresses over several months. Repeated or continuous endothelial cell loss results in progressive intimal proliferation of smooth muscle cells, their secretion of connective tissue matrix components (collagen, elastin and proteoglycans) and accumulation of lipid when animals are on a hypercholesterolemic diet to form early atherosclerotic intimal lesions. Discontinuance of endothelial injury and restoration of the endothelium appear to be followed by lesion regression except when lipid accumulation is extensive. Possible approaches to atherosclerosis prevention include: 1) protection of the endothelium by interruption or avoidance of endothelial injury factors, and perhaps by pharmacologic protection; 2) inhibition of platelet reactivity; 3) modification of SMC proliferation, secretion or lipid accumulation.

Download Full-text