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The mechanisms underlying reactive astrocyte proliferation upon injury remain partially understood. MicroRNAs (miRNAs) function as a major class of post\u2010transcriptional gene expression regulators that participate in many biological processes. However, miRNA function during reactive astrogliosis, particularly in injury\u2010induced astrocyte proliferation, has not been carefully examined. In this study, we conditionally deleted <jats:italic>Dicer1<\/jats:italic> gene encoding an enzyme that is required for mature miRNA generation, and examined the proliferative behavior of <jats:italic>Dicer1<\/jats:italic>\u2010null reactive astrocytes in the transected mouse spinal cord. We found that injury\u2010induced proliferation is blocked in <jats:italic>Dicer1<\/jats:italic>\u2010null astrocytes. Previous reports indicate that miR\u201017\u20105p family members are upregulated during SCI. We therefore tested functional contribution of miR\u201017\u20105p to the proliferation of reactive astrocytes <jats:italic>in vitro<\/jats:italic>. Our results showed that a synthetic miR\u201017\u20105p mimic is able to rescue the proliferation defect of <jats:italic>Dicer1<\/jats:italic>\u2010null astrocytes, while an antisense inhibitor of miR\u201017\u20105p blocked lipopolysaccharide\u2010induced astrocytic proliferation. Similar results are also observed in leukemia inhibitory factor (LIF)\u2010treated astroglial cultures suggesting that miR\u201017\u20105p particularly modulates reactive astrocyte proliferation initiated by LIF presumably via the JAK\/STAT3 pathway. Furthermore, overexpression of miR\u201017\u20105p leads to decrease of several cell cycle regulators in cultured astroglia and astrocytoma cell line C6. Our conclusion is that miRNAs are indispensable to the injury\u2010induced reactive astrocyte proliferation, and that miR\u201017\u20105p may be a major player regulating this pathological process by affecting cell cycle machinery. 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