{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yu J"],"funding":["National Institute of Arthritis and Musculoskeletal and Skin Diseases","NEI NIH HHS","Dermatology Foundation","National Institutes of Health","NIAMS NIH HHS"],"pagination":["3950-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2996908"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(10)"],"pubmed_abstract":["microRNA-205 (miR-205) and miR-184 coordinately regulate the lipid phosphatase SHIP2 for Akt survival signaling in keratinocytes. As the PI3K-Akt pathway has also been implicated in regulating the actin cytoskeleton and cell motility, we investigated the role that these 2 miRNAs play in keratinocyte migration. We used antagomirs (antago) to reduce the levels of miR-205 and miR-184 in primary human epidermal keratinocytes (HEKs) and corneal epithelial keratinocytes (HCEKs) as well as direct SHIP2 silencing using siRNA oligos. Treatment of HEKs and HCEKs with antago-205 increased SHIP2 levels and impaired the ability of these cells to seal linear scratch wounds compared with untreated or irrelevant-antago treatments. In contrast, AKT signaling was enhanced and wounds sealed faster in HCEKs where miR-184 was suppressed, enabling miR-205 to inhibit SHIP2. Similar increases in migration were observed following direct SHIP2 silencing in HEKs. Furthermore, down-regulation of miR-205 resulted in an increase in Rho-ROCKI activity, phosphorylation of the actin severing protein cofilin, and a corresponding diminution of filamentous actin. The connection among miR-205, RhoA-ROCKI-cofilin inactivation, and the actin cytoskeleton represents a novel post-translational mechanism for the regulation of normal human keratinocyte migration."],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["MicroRNA-205 promotes keratinocyte migration via the lipid phosphatase SHIP2."],"pmcid":["PMC2996908"],"funding_grant_id":["P30AR057216","EY017536","P30 AR057216","R21 EY017536","EY019463","R01 EY019463"],"pubmed_authors":["Peng H","Lavker RM","Ruan Q","Yu J","Fatima A","Getsios S"],"additional_accession":[]},"is_claimable":false,"name":"MicroRNA-205 promotes keratinocyte migration via the lipid phosphatase SHIP2.","description":"microRNA-205 (miR-205) and miR-184 coordinately regulate the lipid phosphatase SHIP2 for Akt survival signaling in keratinocytes. As the PI3K-Akt pathway has also been implicated in regulating the actin cytoskeleton and cell motility, we investigated the role that these 2 miRNAs play in keratinocyte migration. We used antagomirs (antago) to reduce the levels of miR-205 and miR-184 in primary human epidermal keratinocytes (HEKs) and corneal epithelial keratinocytes (HCEKs) as well as direct SHIP2 silencing using siRNA oligos. Treatment of HEKs and HCEKs with antago-205 increased SHIP2 levels and impaired the ability of these cells to seal linear scratch wounds compared with untreated or irrelevant-antago treatments. In contrast, AKT signaling was enhanced and wounds sealed faster in HCEKs where miR-184 was suppressed, enabling miR-205 to inhibit SHIP2. Similar increases in migration were observed following direct SHIP2 silencing in HEKs. Furthermore, down-regulation of miR-205 resulted in an increase in Rho-ROCKI activity, phosphorylation of the actin severing protein cofilin, and a corresponding diminution of filamentous actin. The connection among miR-205, RhoA-ROCKI-cofilin inactivation, and the actin cytoskeleton represents a novel post-translational mechanism for the regulation of normal human keratinocyte migration.","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Oct","modification":"2025-04-05T15:53:11.508Z","creation":"2019-03-27T00:01:28Z"},"accession":"S-EPMC2996908","cross_references":{"pubmed":["20530248"],"doi":["10.1096/fj.10-157404"]}}