Mitochondrial function controls intestinal epithelial stemness and proliferation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-10-27

AUTHORS

Emanuel Berger, Eva Rath, Detian Yuan, Nadine Waldschmitt, Sevana Khaloian, Michael Allgäuer, Ori Staszewski, Elena M. Lobner, Theresa Schöttl, Pieter Giesbertz, Olivia I. Coleman, Marco Prinz, Achim Weber, Markus Gerhard, Martin Klingenspor, Klaus-Peter Janssen, Mathias Heikenwalder, Dirk Haller

ABSTRACT

Control of intestinal epithelial stemness is crucial for tissue homeostasis. Disturbances in epithelial function are implicated in inflammatory and neoplastic diseases of the gastrointestinal tract. Here we report that mitochondrial function plays a critical role in maintaining intestinal stemness and homeostasis. Using intestinal epithelial cell (IEC)-specific mouse models, we show that loss of HSP60, a mitochondrial chaperone, activates the mitochondrial unfolded protein response (MT-UPR) and results in mitochondrial dysfunction. HSP60-deficient crypts display loss of stemness and cell proliferation, accompanied by epithelial release of WNT10A and RSPO1. Sporadic failure of Cre-mediated Hsp60 deletion gives rise to hyperproliferative crypt foci originating from OLFM4+ stem cells. These effects are independent of the MT-UPR-associated transcription factor CHOP. In conclusion, compensatory hyperproliferation of HSP60+ escaper stem cells suggests paracrine release of WNT-related factors from HSP60-deficient, functionally impaired IEC to be pivotal in the control of the proliferative capacity of the stem cell niche. More... »

PAGES

13171

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ncomms13171

    DOI

    http://dx.doi.org/10.1038/ncomms13171

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1045622063

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27786175


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