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Uncovering mutation-specific morphogenic phenotypes and paracrine-mediated vessel dysfunction in a biomimetic vascularized mammary duct platform.

Abstract：

:The mammary gland is a highly vascularized tissue capable of expansion and regression during development and disease. To enable mechanistic insight into the coordinated morphogenic crosstalk between the epithelium and vasculature, we introduce a 3D microfluidic platform that juxtaposes a human mammary duct in proximity to a perfused endothelial vessel. Both compartments recapitulate stable architectural features of native tissue and the ability to undergo distinct forms of branching morphogenesis. Modeling HER2/ERBB2 amplification or activating PIK3CA(H1047R) mutation each produces ductal changes observed in invasive progression, yet with striking morphogenic and behavioral differences. Interestingly, PI3KαH1047R ducts also elicit increased permeability and structural disorganization of the endothelium, and we identify the distinct secretion of IL-6 as the paracrine cause of PI3KαH1047R-associated vascular dysfunction. These results demonstrate the functionality of a model system that facilitates the dissection of 3D morphogenic behaviors and bidirectional signaling between mammary epithelium and endothelium during homeostasis and pathogenesis.

journal_name

Nat Commun

journal_title

Nature communications

authors

Kutys ML,Polacheck WJ,Welch MK,Gagnon KA,Koorman T,Kim S,Li L,McClatchey AI,Chen CS

doi

10.1038/s41467-020-17102-x

subject

Has Abstract

pub_date

2020-07-06 00:00:00

pages

3377

issue

1

issn

2041-1723

pii

10.1038/s41467-020-17102-x

journal_volume

11

pub_type

杂志文章

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