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Sökning: onr:"swepub:oai:DiVA.org:uu-386443" > WAKMAR2, a Long Non...

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FältnamnIndikatorerMetadata
00004501naa a2200505 4500
001oai:DiVA.org:uu-386443
003SwePub
008190625s2019 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:140987850
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3864432 URI
0247 a https://doi.org/10.1016/j.jid.2018.11.0332 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1409878502 URI
040 a (SwePub)uud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Herter, Eva K.u Karolinska Inst, Dermatol & Venereol Sect, Dept Med Solna, SE-17176 Stockholm, Sweden4 aut
2451 0a WAKMAR2, a Long Noncoding RNA Downregulated in Human Chronic Wounds, Modulates Keratinocyte Motility and Production of Inflammatory Chemokines
264 1b ELSEVIER SCIENCE INC,c 2019
338 a electronic2 rdacarrier
520 a Chronic wounds represent a major and growing health and economic burden worldwide. A better understanding of molecular mechanisms of normal as well as impaired wound healing is needed to develop effective treatment. Herein we studied the potential role of long noncoding RNA LOC100130476 in skin wound repair. LOC100130476 is an RNA polymerase IIeencoded polyadenylated transcript present in both cytoplasm and nucleus. We found that its expression was lower in wound-edge keratinocytes of human chronic wounds compared to normal wounds of healthy donors and intact skin. In cultured keratinocytes, LOC100130476 expression was induced by TGF-beta signaling. By reducing LOC100130476 expression with antisense oligos or activating its transcription with CRISPR/Cas9 Synergistic Activation Mediator system, we showed that LOC100130476 restricted the production of inflammatory chemokines by keratinocytes, while enhancing cell migration. In line with this, knockdown of LOC100130476 impaired re-epithelization of human ex vivo wounds. Based on these results, we named LOC100130476 wound and keratinocyte migration-associated long noncoding RNA 2 (WAKMAR2). Moreover, we identified a molecular network that may mediate the biological function of WAKMAR2 in keratinocytes using microarray. In summary, our data suggest that WAKMAR2 is an important regulator of skin wound healing and its deficiency may contribute to the pathogenesis of chronic wounds.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Dermatologi och venereologi0 (SwePub)302042 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Dermatology and Venereal Diseases0 (SwePub)302042 hsv//eng
7001 a Li, Dongqingu Karolinska Institutet4 aut
7001 a Toma, Maria A.u Karolinska Institutet4 aut
7001 a Vij, Manikau Karolinska Inst, Dermatol & Venereol Sect, Dept Med Solna, SE-17176 Stockholm, Sweden4 aut
7001 a Li, Xiu Karolinska Inst, Dermatol & Venereol Sect, Dept Med Solna, SE-17176 Stockholm, Sweden4 aut
7001 a Visscher, Daniu Karolinska Inst, Dermatol & Venereol Sect, Dept Med Solna, SE-17176 Stockholm, Sweden4 aut
7001 a Wang, Aoxueu Dalian Med Univ, Dept Dermatol, Hosp 2, Dalian, Peoples R China4 aut
7001 a Chu, Tongbinu Dalian Med Univ, Hosp 2, Dept Wound Regenerat, Dalian, Peoples R China4 aut
7001 a Sommar, Pehru Karolinska Institutet4 aut
7001 a Blomqvist, Lennartu Karolinska Inst, Dept Med Huddinge, Stockholm, Sweden4 aut
7001 a Berglund, David,d 1984-u Uppsala universitet,Klinisk immunologi4 aut0 (Swepub:uu)davbe892
7001 a Stahle, Monau Karolinska Institutet4 aut
7001 a Wikstrom, Jakob D.u Karolinska Institutet4 aut
7001 a Landen, Ning Xuu Karolinska Institutet4 aut
7102 a Karolinska Institutetb Karolinska Inst, Dermatol & Venereol Sect, Dept Med Solna, SE-17176 Stockholm, Sweden4 org
7730 t Journal of Investigative Dermatologyd : ELSEVIER SCIENCE INCg 139:6, s. 1373-1384q 139:6<1373-1384x 0022-202Xx 1523-1747
8564 u https://doi.org/10.1016/j.jid.2018.11.033y Fulltext
8564 u https://uu.diva-portal.org/smash/get/diva2:1330456/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
8564 u http://www.jidonline.org/article/S0022202X18013015/pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-386443
8564 8u https://doi.org/10.1016/j.jid.2018.11.033
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:140987850

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