Peritubular myoid cell

PTM cells are endothelial cells which are understood to have derived from mesonephric cells.[4] The structure and organization between PTM cells have been observed to be distinctly different between mammalian species. In humans, PTM cells are spindle shaped and form several thin elongated layers, approximately 5-7 cell layers, and surround Sertoli cells.

These are detected in the lamina propria of the seminiferous tubule and immunohistochemical studies have shown functional distinctions between these layers. The inner layers have been shown to express desmin, a smooth muscle phenotype, whereas the outer layers express vimentin, a connective tissue phenotype.[2]

In rodents, PTM cells are one layer thick. Both human and rodent PTM cells are joined by junctional complexes.[2]

PTMs become recognisable at 12 weeks gestation in humans, and 13.5 days post conception in mice.[8] However, where they arise from is currently unclear. Previous studies suggested that PTMs originate from a group of cells called mesonephric cells, which migrate into the developing gonad from an adjacent area called the mesonephric primordia.[3] It was thought that the mesonephric cells would then have one of three fates: becoming Leydig cells, vascular tissue or myoid cells. Those becoming myoid cells would sit on a basement membrane surrounding the developing seminiferous tubules.[3]

However, more recent evidence has found that mesonephric cells do not give rise to PTMs but instead have only a vascular fate,[8] leaving more uncertainty over where PTMs come from. The main difficulty in studying the development of PTMs is the lack of a molecular marker specific to them that is visible during early differentiation of the testis.[8]

Current knowledge suggests that PTMs arise from cells within the developing gonad itself, or alternatively from a layer of cells surrounding the outside of the gonad, called coelomic epithelium, by a process named epithelial-mesenchymal transition.[8]

PTMs acquire androgen receptors during their development, enabling them to respond to androgens which help them to maintain seminiferous tubule function.[3]

PTMs were first observed in 1901, when Claudius Regaud made a detailed study of the histology and physiology of the seminiferous tubules in rats.[9] He described the PTMs as a single layer of flattened cells, which enclose the seminiferous tubules, and called them ‘’modified connective tissue cells’’.

In 1958, Yves Clermont made a further investigation of the cells by electron microscopy. He found that these cells have a cytological resemblance to smooth muscle cells – they contain actin filaments, have invaginations at the cell surface and their organelles are located in the centre of the cell. He also suggested that these cells are responsible for the tubular contraction and referred to them as ‘’interlamellar cells’’.[2]

Subsequently, in 1967, Michael Ross studied the fine structure of these cells in mice and proved that the smooth muscle-like cells are contractile. He called them ‘’peritubular contractile cells’’. In 1969, Don Wayne Fawcett et al. termed these cells ‘’peritubular myoid cells’’, because of their similarities to smooth muscle cells.[2]

As PTMs became better characterized, the associated nomenclature underwent a series of changes.

In very early literature these cells may be referred to as ‘modified connective tissue cells’ or ‘interlamellar cells’. Subsequent experiments resulted in renaming these cells to better reflect their contractile nature. The term ‘peritubular contractile cells’ was first used in 1967.[2]

In 1969, Don Fawcett labelled these cells as ‘peritubular myoid cells’. ‘Peritubular’ refers to their anatomical location: adjacent to the seminiferous tubule. ‘Myoid’ stems from the Greek ‘myo’ (/ˈmʌɪəʊ/), which means relating to muscle. (PTMs resemble smooth muscle cells under an electron microscope).[2]

• Media related to Peritubular myoid cell at Wikimedia Commons