new insight into the role of mmp14 in metabolic balance

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ID: 140206
2016
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Abstract
Membrane-anchored matrix metalloproteinase 14 (MMP14) is involved broadly in organ development through both its proteolytic and signal-transducing functions. Knockout of Mmp14 (KO) in mice results in a dramatic reduction of body size and wasting followed by premature death, the mechanism of which is poorly understood. Since the mammary gland develops after birth and is thus dependent for its functional progression on systemic and local cues, we chose it as an organ model for understanding why KO mice fail to thrive. A global analysis of the mammary glands’ proteome in the wild type (WT) and KO mice provided insight into an unexpected role of MMP14 in maintaining metabolism and homeostasis. We performed mass spectrometry and quantitative proteomics to determine the protein signatures of mammary glands from 7 to 11 days old WT and KO mice and found that KO rudiments had a significantly higher level of rate-limiting enzymes involved in catabolic pathways. Glycogen and lipid levels in KO rudiments were reduced, and the circulating levels of triglycerides and glucose were lower. Analysis of the ultrastructure of mammary glands imaged by electron microscopy revealed a significant increase in autophagy signatures in KO mice. Finally, Mmp14 silenced mammary epithelial cells displayed enhanced autophagy. Applied to a systemic level, these findings indicate that MMP14 is a crucial regulator of tissue homeostasis. If operative on a systemic level, these findings could explain how Mmp14KO litter fail to thrive due to disorder in metabolism.
Reference Key
mori2016peerjnew Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Hidetoshi Mori;Ramray Bhat;Alexandre Bruni-Cardoso;Emily I. Chen;Danielle M. Jorgens;Kester Coutinho;Katherine Louie;Benjamin Ben Bowen;Jamie L. Inman;Victoria Tecca;Sarah J. Lee;Sabine Becker-Weimann;Trent Northen;Motoharu Seiki;Alexander D. Borowsky;Manfred Auer;Mina J. Bissell
Journal pediatrics
Year 2016
DOI
10.7717/peerj.2142
URL
https://peerj.com/articles/2142/
Keywords
autophagy homeostasis glycogen

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