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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03010naa a2200373 4500 | |
| 001 | oai:prod.swepub.kib.ki.se:129211402 | |
| 003 | SwePub | |
| 008 | 240701s2014 | |||||||||||000 ||eng| | |
| 024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1292114022 URI |
| 024 | 7 | a https://doi.org/10.2337/db13-07022 DOI |
| 040 | a (SwePub)ki | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Kulyte, Au Karolinska Institutet4 aut |
| 245 | 1 0 | a Additive effects of microRNAs and transcription factors on CCL2 production in human white adipose tissue |
| 264 | c 2014-03-13 | |
| 264 | 1 | b American Diabetes Association,c 2014 |
| 520 | a Adipose tissue inflammation is present in insulin-resistant conditions. We recently proposed a network of microRNAs (miRNAs) and transcription factors (TFs) regulating the production of the proinflammatory chemokine (C-C motif) ligand-2 (CCL2) in adipose tissue. We presently extended and further validated this network and investigated if the circuits controlling CCL2 can interact in human adipocytes and macrophages. The updated subnetwork predicted that miR-126/-193b/-92a control CCL2 production by several TFs, including v-ets erythroblastosis virus E26 oncogene homolog 1 (avian) (ETS1), MYC-associated factor X (MAX), and specificity protein 12 (SP1). This was confirmed in human adipocytes by the observation that gene silencing of ETS1, MAX, or SP1 attenuated CCL2 production. Combined gene silencing of ETS1 and MAX resulted in an additive reduction in CCL2 production. Moreover, overexpression of miR-126/-193b/-92a in different pairwise combinations reduced CCL2 secretion more efficiently than either miRNA alone. However, although effects on CCL2 secretion by co-overexpression of miR-92a/-193b and miR-92a/-126 were additive in adipocytes, the combination of miR-126/-193b was primarily additive in macrophages. Signals for miR-92a and -193b converged on the nuclear factor-κB pathway. In conclusion, TF and miRNA-mediated regulation of CCL2 production is additive and partly relayed by cell-specific networks in human adipose tissue that may be important for the development of insulin resistance/type 2 diabetes. | |
| 700 | 1 | a Belarbi, Y4 aut |
| 700 | 1 | a Lorente-Cebrian, S4 aut |
| 700 | 1 | a Bambace, C4 aut |
| 700 | 1 | a Arner, E4 aut |
| 700 | 1 | a Daub, COu Karolinska Institutet4 aut |
| 700 | 1 | a Heden, P4 aut |
| 700 | 1 | a Ryden, Mu Karolinska Institutet4 aut |
| 700 | 1 | a Mejhert, Nu Karolinska Institutet4 aut |
| 700 | 1 | a Arner, Pu Karolinska Institutet4 aut |
| 710 | 2 | a Karolinska Institutet4 org |
| 773 | 0 | t Diabetesd : American Diabetes Associationg 63:4, s. 1248-1258q 63:4<1248-1258x 1939-327Xx 0012-1797 |
| 856 | 4 | u https://diabetes.diabetesjournals.org/content/diabetes/63/4/1248.full.pdf |
| 856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:129211402 |
| 856 | 4 8 | u https://doi.org/10.2337/db13-0702 |
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- Kulyte, A
- Belarbi, Y
- Lorente-Cebrian, ...
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- Arner, E
- Daub, CO
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- Heden, P
- Ryden, M
- Mejhert, N
- Arner, P
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