Reduction of type IV collagen by upregulated miR-29 in normal elderly mouse and klotho-deficient, senescence-model mouse.
PLoS One, 2012;7(11):e48974.
Takahashi M[1], Eda A, Fukushima T, Hohjoh H
Affiliations
PMID: 23139829DOI: 10.1371/journal.pone.0048974
Impact factor: 3.752
Abstract
MicroRNA (miRNA), a small non-coding RNA that functions as a mediator in gene silencing, plays important roles in gene regulation in various vital functions and activities. Here we show that the miR-29 members are upregulated in klotho-deficient [klotho(-/-)] mice, a senescence-model animal, and also in normal elderly ICR mice relative to wild-type littermates and young ICR mice. In addition, levels of type IV collagen, a major component of basement membranes and a putative target of miR-29, were lower in klotho(-/-) and elderly ICR mice than in wild-type littermates and young ICR mice. RNA degradation mediated by miR-29 may participate in the suppression of type IV collagen, both in vivo and in vitro. Taken together, our current findings suggest that the miR-29 upregulated in aging may be involved in the downregulation of type IV collagen, leading to a possible weakening of the basal membrane in senescent tissues, and miR-29 may be a useful molecular marker of senescence.
MeSH terms
8-Hydroxy-2'-Deoxyguanosine; Aging; Animals; Collagen Type IV; Creatinine; Deoxyguanosine; Gene Expression Profiling; Gene Knockdown Techniques; Gene Silencing; Genes, Reporter; Glucuronidase; HEK293 Cells; Humans; Klotho Proteins; Lysine; Male; Mice; Mice, Inbred ICR; MicroRNAs; Models, Biological; Up-Regulation
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