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Research in practice: More than skin deep –aging of subcutaneous fat tissue
Author(s) -
Berneburg Mark
Publication year - 2010
Publication title -
jddg: journal der deutschen dermatologischen gesellschaft
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.463
H-Index - 60
eISSN - 1610-0387
pISSN - 1610-0379
DOI - 10.1111/j.1610-0387.2010.07480.x
Subject(s) - cockayne syndrome , mitochondrial dna , dermis , premature aging , oxidative stress , mitochondrion , dna repair , nucleotide excision repair , biology , dna damage , deoxyguanosine , mutation , adipose tissue , microbiology and biotechnology , dna , genetics , gene , biochemistry , anatomy
Summary Mitochondria, responsible for the generation of energy in our cells, contain their own genome, mitochondrial (mt)DNA. It is known that mutations of mtDNA accumulate during normal aging and that this can be accelerated by oxidative stress, i.e. induced by ultraviolet radiation. These mutations are functionally relevant and they play a causative role in normal aging as well as premature aging induced by ultraviolet radiation. While the focus of scientific research was more on epidermis and dermis within the last years, alterations of subcutaneous fat tissue were not investigated thus far. Cockayne syndrome (CS) A and B are two proteins known to repair oxidatively induced DNA damage via nucleotide excision repair (NER) in the nucleus. We could show that these two proteins enrich in mitochondria upon oxidative stress, directly interact with mtDNA and the two repair‐associated proteins mtSSBP‐1 and mtOGG‐1 and protect from deletions of mtDNA. If CSA or CSB are lacking, mtDNA mutations accumulate particularly in the cells of subcutaneous fat tissue which appears to mediate loss of adipocytes via apoptosis. Therefore, the two NER‐associated proteins CSA and CSB appear to play a direct role in protection from mutations which in turn are causative in aging‐associated loss of subcutaneous fat tissue.