reduction of type iv collagen by upregulated mir-29 in normal elderly mouse and klotho-deficient, senescence-model mouseiv型胶原蛋白的减少调节正常老年老鼠和klotho-deficient mir-29,senescence-model鼠标.pdfVIP

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reduction of type iv collagen by upregulated mir-29 in normal elderly mouse and klotho-deficient, senescence-model mouseiv型胶原蛋白的减少调节正常老年老鼠和klotho-deficient mir-29,senescence-model鼠标.pdf

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reduction of type iv collagen by upregulated mir-29 in normal elderly mouse and klotho-deficient, senescence-model mouseiv型胶原蛋白的减少调节正常老年老鼠和klotho-deficient mir-29,senescence-model鼠标

Reduction of Type IV Collagen by Upregulated miR-29 in Normal Elderly Mouse and klotho-Deficient, Senescence- Model Mouse 1. 1. 2 1 Masaki Takahashi , Akiko Eda , Tatsunobu Fukushima , Hirohiko Hohjoh * 1 National Institute of Neuroscience, NCNP, Kodaira, Tokyo, Japan, 2 Yokohama Research Laboratories, Mitsubishi Rayon Co., LTD., Tsurumi-ku, Yokohama, Japan 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( 2/ 2)] 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( 2/ 2) 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. Citation: Takahashi M, Eda A, Fukushima T, Hohjoh H (2012) Reduction of Type IV Collagen by Upregulated miR-29 in Normal Elderly Mouse and klotho-Deficient, Senescence-Model Mouse. PLoS ONE 7(11): e48974. doi:10.1371/journal.pone.0048974 Editor: Bin Tian, UMDNJ-New Jersey Medical School, United States of America Received July 24, 2012; Accepted