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Desert hedgehog-primary cilia cross talk shapes mitral valve tissue by organizing smooth muscle actin.

Abstract：

:Non-syndromic mitral valve prolapse (MVP) is the most common heart valve disease affecting 2.4% of the population. Recent studies have identified genetic defects in primary cilia as causative to MVP, although the mechanism of their action is currently unknown. Using a series of gene inactivation approaches, we define a paracrine mechanism by which endocardially-expressed Desert Hedgehog (DHH) activates primary cilia signaling on neighboring valve interstitial cells. High-resolution imaging and functional assays show that DHH de-represses smoothened at the primary cilia, resulting in kinase activation of RAC1 through the RAC1-GEF, TIAM1. Activation of this non-canonical hedgehog pathway stimulates α-smooth actin organization and ECM remodeling. Genetic or pharmacological perturbation of this pathway results in enlarged valves that progress to a myxomatous phenotype, similar to valves seen in MVP patients. These data identify a potential molecular origin for MVP as well as establish a paracrine DHH-primary cilium cross-talk mechanism that is likely applicable across developmental tissue types.

journal_name

Dev Biol

journal_title

Developmental biology

authors

Fulmer D,Toomer KA,Glover J,Guo L,Moore K,Moore R,Stairley R,Gensemer C,Abrol S,Rumph MK,Emetu F,Lipschutz JH,McDowell C,Bian J,Wang C,Beck T,Wessels A,Renault MA,Norris RA

doi

10.1016/j.ydbio.2020.03.003

subject

Has Abstract

pub_date

2020-07-01 00:00:00

pages

26-38

issue

1

eissn

0012-1606

issn

1095-564X

pii

S0012-1606(20)30078-6

journal_volume

463

pub_type

杂志文章

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