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Impaired microRNA processing causes corpus luteum insufficiency and infertility in mice
Motoyuki Otsuka, Min Zheng, Masaaki Hayashi, Jing-Dwan Lee, Osamu Yoshino, Shengcai Lin, and Jiahuai Han
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Published June 2, 2008 - More info
J Clin Invest. 2008;118(6):2366–2366. https://doi.org/10.1172/JCI33680E1.
© 2008 The American Society for Clinical Investigation
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Abstract
The microRNA (miRNA) processing enzyme Dicer1 is required for zygotic and embryonic development, but the early embryonic lethality of Dicer1 null alleles in mice has limited our ability to address the role of Dicer1 in normal mouse growth and development. To address this question, we used a mouse mutant with a hypomorphic Dicer1 allele (Dicerd/d) and found that Dicer1 deficiency resulted in female infertility. This defect in female Dicerd/d mice was caused by corpus luteum (CL) insufficiency and resulted, at least in part, from the impaired growth of new capillary vessels in the ovary. We found that the impaired CL angiogenesis in Dicerd/d mice was associated with a lack of miR17-5p and let7b, 2 miRNAs that participate in angiogenesis by regulating the expression of the antiangiogenic factor tissue inhibitor of metalloproteinase 1. Furthermore, injection of miR17-5p and let7b into the ovaries of Dicerd/d mice partially normalized tissue inhibitor of metalloproteinase 1 expression and CL angiogenesis. Our data indicate that the development and function of the ovarian CL is a physiological process that appears to be regulated by miRNAs and requires Dicer1 function.
Authors
Motoyuki Otsuka, Min Zheng, Masaaki Hayashi, Jing-Dwan Lee, Osamu Yoshino, Shengcai Lin, Jiahuai Han
Original citation: J. Clin. Invest.118:1944–1954 (2008). doi:10.1172/JCI33680.
Citation for this erratum: J. Clin. Invest.118:2366 (2008). doi:10.1172/JCI33680E1.
During the preparation of the manuscript, panels D and E in Figure 5 were inadvertently mislabeled. The correctly labeled panels and their corresponding legends appear below.
Figure 5(D) miR17-5p and let7b had no effect on the proliferation of SVEC. Thirty-six hours after transfection of the indicated oligos into SVEC, 5 × 104 cells were seeded, and the number of cells was determined by cell counting at the indicated time points. Data are presented as mean ± SD (n = 4 per group, P = NS). (E) miR17-5p and let7b had no effect on the motility of SVEC. In vitro wound healing was quantified as the average length of the elongation of wound edges at 4 specific points over 24 hours. Data are presented as mean ± SD (n = 3 per group, P = NS).
The JCI regrets the error.
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