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SUMMARY:Discovering Mitokine Networks in Mammalian Models
DTSTART:20160519T150000
DTEND:20160519T160000
DTSTAMP:20260406T032310Z
UID:ad25820668d9ffe3b119bc4ec89a1c746fe73ff52e072ce397343992
CATEGORIES:Conferences - Seminars
DESCRIPTION:Prof. Minho SHONG\, M.D.\, Ph.D. Chungnam National University\
 , South Korea\nSEMINAR of the LAUSANNE INTEGRATIVE METABOLISM and NUTRITIO
 N ALLIANCE (LIMNA)Abstract:\nRecent in vivo studies in C. elegans and Dros
 ophila revealed that UPRmt activation by inhibition of mitochondrial elect
 ron transport chain (ETC) functions increases lifespan (Houtkooper RH et a
 l.\, Nature 2013\; Durieux J et al.\, Cell 2011). This effect of ETC inhib
 ition on longevity is modulated by cell-autonomous and cell-non-autonomous
  factors\, known as mitokines\, which may promote metabolic homeostasis. H
 owever\, extrapolation of these studies into mammalian systems is extremel
 y difficult because generalized impairment of ETC function in mice uniform
 ly results in progressive deterioration of organ functions and premature d
 eath. To investigate whether the role of cell-non-autonomous mitokine netw
 orks is conserved in mammalian systems\, we designed a spatio-temporal app
 roach for gene expression and secretome analysis in mice with tissue-speci
 fic UPRmt activation.  \nRecently\, we successfully generated and demonst
 rated relevant mouse models of tissue-specific UPRmt activation and ETC de
 ficiency that are reminiscent of complex human disorders\, e.g.\, neurodeg
 eneration (Kim et al.\, Cell Metab\, 2012)\, Parkinson’s disease\, insul
 in resistance (Ryu et al.\, PLOS Genetics\, 2013)\, and type 1 diabetes (K
 im et al.\, Diabetologia\, 2015). These models are based on tissue-specifi
 c knockout (KO) of Crif1\, which encodes a factor required for biogenesis 
 of ETC subunits. Loss of Crif1 resulted in abnormal proteostasis in the mi
 tochondrial matrix and triggered the mitochondrial unfolded protein respon
 se (UPRmt).\nPreliminary observations on phenotypes of tissue-specific Cri
 f1-deficient mice revealed that Crif1-deficient cells and tissues express 
 unique UPRmt activation e.g.\, adaptive transcriptomic changes and secreto
 me responses (mitokines)\, which can be considered to be part of the pheno
 menon of “mitohormesis” (Yun J and Finkel T\, Cell Metab\, 2014). Base
 d on these observations\, we postulated that tissue-specific UPRmt and mit
 okine responses are critical cell-non-autonomous modifiers in disease prog
 ression\, and that individual mitokines may act as disease markers and pot
 ential therapeutic targets in complex human disorders.Bio:\nDr. Minho Song
  was born in Seoul\, South Korea. He earned his B. S. degree in Applied An
 imal Science from Korea University in Seoul in 2003. He then migrated to t
 he U. S. and earned his MS degree in swine nutrition under the guidance of
  Dr. Samuel Baidoo at the University of Minnesota in 2007. His Master's th
 esis was on the effects of distillers dried grains with soluble on perform
 ance\, energy and nitrogen digestibility\, and milk composition of lactati
 ng sows. After completion of his Master's degree\, he joined the Animal Sc
 iences Department at the University of Illinois and earned his Ph. D. degr
 ee in swine nutritional immunology and microbiology under the guidance of 
 Dr. James Pettigrew in 2011. Dr. Song's Ph. D. and postdoctoral research f
 ocused on evaluations of feed ingredients as well as of dietary effects on
  pig health and productive performance\, using nutritional\, microbiologic
 al\, and immunological approaches. From 2011 to 2012\, he was a postdoctor
 al research associate in swine nutrition and physiology under the guidance
  of Dr. Hans Stein. In 2012\, Dr. Song took a position as an assistant pro
 fessor of nonruminant nutrition at Chungnam National University in Daejeon
 \, South Korea.
LOCATION:AI 1153 https://plan.epfl.ch/?room==AI%201153
STATUS:CONFIRMED
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