A closer look into the cellular and molecular biology of myoepithelial cells across various exocrine glands

Mauduit, Olivier; Delcroix, Vanessa; Wong, Andrew; Ivanova, Anastasiia; Miles, Lindsey; Lee, Hyun Soo; Makarenkova, Helen

doi:10.1016/j.jtos.2023.12.003

Cited by 5 publications

References 117 publications

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Transgenic overexpression of the miR‐200b/200a/429 cluster prevents mammary tumor initiation in Neu/Erbb2 transgenic mice

Watson,

Moorehead

2024

Intl Journal of Cancer

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Although significant progress in the treatment of breast cancer has been achieved, toxic therapies would not be required if breast cancer could be prevented from developing in the first place. While breast cancer prevention is difficult to study in humans due to long disease latency and stochastic cancer development, transgenic mouse models with 100% incidence and defined mammary tumor onset, provide excellent models for tumor prevention studies. In this study, we used Neu/Erbb2 transgenic mice (MTB‐TAN) as a model of human HER2+ breast cancer to investigate whether a family of microRNAs, known as the miR‐200 family, can prevent mammary tumor development. Overexpression of Neu induced palpable mammary tumors in 100% of the mice within 38 days of Neu overexpression. When the miR‐200b/200a/429 cluster was co‐overexpressed with Neu in the same mammary epithelial cells (MTB‐TANba429 mice), the miR‐200b/200a/429 cluster prevented Neu from inducing mammary epithelial hyperplasia and mammary tumor development. RNA sequencing revealed alterations in the extracellular matrix of the mammary gland and a decrease in stromal cells including myoepithelial cells in Neu transgenic mice. Immunohistochemistry for smooth muscle actin confirmed that mammary epithelial cells in control and MTB‐TANba429 mice were surrounded by a layer of myoepithelial cells and these myoepithelial cells were lost in MTB‐TAN mice with hyperplasia. Thus, we have shown for the first time that elevated expression of miR‐200 family members in mammary epithelial cells can completely prevent mammary tumor development in Neu transgenic mice possibly through regulating myoepithelial cells.

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Transgenic overexpression of the miR‐200b/200a/429 cluster prevents mammary tumor initiation in Neu/Erbb2 transgenic mice

Watson,

Moorehead

2024

Intl Journal of Cancer

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Tempol mitigates inflammation, oxidative stress, and histopathological alterations of cadmium-induced parotid gland injury in rats

El-Fatah,

Nafea,

Yousef

et al. 2024

Life Sciences

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Unveiling a unique macrophage population in exocrine glands sustained by ILC2-derived GM-CSF

Westermann,

Tuzlak,

Kreiner

et al. 2024

Preprint

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Granulocyte-macrophage colony-stimulating factor (GM-CSF) has a non-redundant role in the emergence and maintenance of alveolar macrophages (AMs). However, its role in developmental and steady-state myelopoiesis outside the lung is largely unexplored. Scanning through developing tissues using a Fate-map and reporter of GM-CSF mouse strain, we discovered that GM-CSF was produced by type 2 innate lymphoid cells (ILC2s) in the submandibular and sublingual salivary gland (SG) during postnatal development. GM-CSF producing ILC2s foster the development of a hitherto undescribed phagocyte subset, which we named adenophages. Detailed analysis focusing on phenotypic and transcriptional profiling revealed that adenophages display shared aspects of both, macrophages and dendritic cells (DCs). We found them to be homogenously distributed across the SG, but always in close proximity to GM-CSF producing ILC2s and myoepithelial cells. Importantly, adenophages were present throughout all analyzed exocrine glands such as lacrimal glands and mammary glands, and were also identified in human SG sections, indicating a conserved role in exocrine glands across species.

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A closer look into the cellular and molecular biology of myoepithelial cells across various exocrine glands

Cited by 5 publications

References 117 publications

Transgenic overexpression of the miR‐200b/200a/429 cluster prevents mammary tumor initiation in Neu/Erbb2 transgenic mice

Transgenic overexpression of the miR‐200b/200a/429 cluster prevents mammary tumor initiation in Neu/Erbb2 transgenic mice

Tempol mitigates inflammation, oxidative stress, and histopathological alterations of cadmium-induced parotid gland injury in rats

Unveiling a unique macrophage population in exocrine glands sustained by ILC2-derived GM-CSF

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