Myoepithelial cell

Summary

Myoepithelial cells (sometimes referred to as myoepithelium) are cells usually found in glandular epithelium as a thin layer above the basement membrane but generally beneath the luminal cells. These may be positive for alpha smooth muscle actin and can contract and expel the secretions of exocrine glands. They are found in the sweat glands, mammary glands, lacrimal glands, and salivary glands. Myoepithelial cells in these cases constitute the basal cell layer of an epithelium that harbors the epithelial progenitor. In the case of wound healing, myoepithelial cells reactively proliferate. Presence of myoepithelial cells in a hyperplastic tissue proves the benignity of the gland and, when absent, indicates cancer. Only rare cancers like adenoid cystic carcinomas contains myoepithelial cells as one of the malignant components. It can be found in endoderm or ectoderm. Markers Myoepithelial cells are true epithelial cells positive for keratins, not to be confused with myofibrobl

Official source

https://en.wikipedia.org/wiki/Myoepithelial_cell

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Loss of organization is a principle feature of cancers; therefore it is important to understand how normal adult multilineage tissues, such as bilayered secretory epithelia, establish and maintain their architectures. The self-organization process that drives heterogeneous mixtures of cells to form organized tissues is well studied in embryology and with mammalian cell lines that were abnormal or engineered. Here we used a micropatterning approach that confined cells to a cylindrical geometry combined with an algorithm to quantify changes of cellular distribution over time to measure the ability of different cell types to self-organize relative to each other. Using normal human mammary epithelial cells enriched into pools of the two principal lineages, luminal and myoepithelial cells, we demonstrated that bilayered organization in mammary epithelium was driven mainly by lineage-specific differential E-cadherin expression, but that P-cadherin contributed specifically to organization of the myoepithelial layer. Disruption of the actomyosin network or of adherens junction proteins resulted in either prevention of bilayer formation or loss of preformed bilayers, consistent with continual sampling of the local microenvironment by cadherins. Together these data show that self-organization is an innate and reversible property of communities of normal adult human mammary epithelial cells.

2011

Probing the differential adhesion hypothesis in the mammary gland using different bioengineered cell culture substrata

Léa Chanson

During tissue development, cells are able to form different layers and to self organize. At the moment, there are two principal hypotheses that try to explain cell sorting. The so called differential adhesion hypothesis (DAH) posits that cells organize according to the level of expression of cell-cell adhesion proteins so as to reduce free-energy in the system. The second hypothesis explains the formation of different germ layers according to cortical tension among cells of distinct phenotypes. For this work, we wanted to study cell sorting in the mammary glands, which are bilayered branching structures composed of outer myoepithelial (MEP) and inner luminal epithelial cells (LEP). Both sorting hypotheses were tested using bioengineered cell culture substrata. Using arrays of micro-wells that were cast in polydimethylsiloxane (PDMS) coupled with quantitative image analysis, we observed that cell sorting occurred over time between LEP and MEP that were isolated by fluorescence-activated cell sorting from primary human mammary epithelial cells. Inhibitors of specific cadherins were able to prevent cell sorting in accordance with the DAH. However, chemical inhibitors of cytoskeletal proteins, which effectively prevented the cells from modulating their innate elasticity, also prevented cell sorting suggesting cortical tension also plays an important role. Thus, our data suggests a third hypothesis, which is essentially a unification of the original two, such that differences in cortical tension are essentially lineage-specific and are governed wholly or in-part by cell-cell adhesion molecules. Experimental resolution of this hypothesis is being actively pursued

2009

Adamts18 Function in Mammary Gland Development

Dalya Ataca

Ovarian hormones control mammary gland development and impinge on breast carcinogenesis acting via their cognate receptors in the luminal epithelium. The extracellular matrix has a key role in physiology and disease but how the two are linked is poorly understood. Here we show that deletion of the secreted protease Adamts18 delays mammary gland development. The proteaseâs role is mammary epithelial intrinsic and required for stem cell function and epithelial regeneration potential. Progesterone controls Adamts18 in the myoepithelium through upregulation of Wnt-4 expression with ensuing canonical Wnt signaling activation in basal cells. IP-Mass Spec shows that ADAMTS18 has binding partners located in the ECM and basement membrane. Consistent with Adamts18 being an important regulator of ECM function, deletion results in increased Collagen I and IV, Laminin, and Fibronectin deposition and synergizes genetically with the basal membrane proteoglycan Collagen18a1 in controlling mammary stem cell function. In vitro, Collagen18a1 and Fibronectin are cleaved by Adamts18. RNAseq analysis reveals that the stem cell regulatory hippo pathway is downstream of Adamts18 with consequent reduction of Fgfr2 expression. Our findings link hormonal signaling in luminal mammary epithelial cells to ECM remodeling via Adamts18, and demonstrate the importance of the ECM for stem cell function in the mammary gland.

EPFL2019