Tags

Type your tag names separated by a space and hit enter

MicroRNA-29a regulates lipopolysaccharide (LPS)-induced inflammatory responses in murine macrophages through the Akt1/ NF-κB pathway.
Exp Cell Res. 2017 11 15; 360(2):74-80.EC

Abstract

Akt activation in macrophages enhances lipopolysaccharide (LPS)-induced inflammatory responses through upregulation of the NF-κB signal pathway. Akt phosphorylation via microRNA (miR) caused the downregulation of Akt1. Here, we evaluated the role of miR-29a in LPS-triggered inflammatory responses. LPS stimulation of primary macrophages and RAW264.7 cells gradually increased the levels of miR-29a and was dependent on the LPS concentration. Overexpression of miR-29a in macrophages enhanced the expression of proinflammatory cytokines including IL-1β and IL-6, but not TNF-α. Conversely, knockdown of miR-29a diminished cytokine expression. Bioinformatics analyses indicated that Akt1 was a potential target of miR-29a through its interaction with the CDS region of Akt1. The miR-29a also enhanced LPS-induced NF-κB signaling through increased NF-κB transcriptional activity and phosphorylation of p65, and through binding to Akt1. Moreover, Akt1 silencing promoted the LPS-induced expression of IL-1β and IL-6, and upregulated the NF-κB pathway. Taken together, our results suggested that miR-29a participates in the regulation of inflammatory responses in LPS-stimulated macrophages by promoting NF-κB activation through targeting Akt1.

Authors+Show Affiliations

First Affiliated Hosp Dalian Med Univ, Dept Oncol, Dalian 116011, PR China.Chinese Academy of Medical Sciences, Peking Union Medical College, PR China.First Affiliated Hosp Dalian Med Univ, Dept Oncol, Dalian 116011, PR China.First Affiliated Hosp Dalian Med Univ, Dept Oncol, Dalian 116011, PR China.First Affiliated Hosp Dalian Med Univ, Dept Oncol, Dalian 116011, PR China.First Affiliated Hosp Dalian Med Univ, Dept Oncol, Dalian 116011, PR China.First Affiliated Hosp Dalian Med Univ, Dept Oncol, Dalian 116011, PR China.Department of Molecular Biological,Shanxi Cancer Hospital/InstituteAffiliated Cancer Hospital of Shanxi Medical University, No. 3 Zhigongxinjie Xinghualing District, Taiyuan, 030013 Shanxi Province, PR China. Electronic address: lifenglover@sina.com.First Affiliated Hosp Dalian Med Univ, Dept Oncol, Dalian 116011, PR China. Electronic address: 516245530@qq.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28811129

Citation

Tang, Bufu, et al. "MicroRNA-29a Regulates Lipopolysaccharide (LPS)-induced Inflammatory Responses in Murine Macrophages Through the Akt1/ NF-κB Pathway." Experimental Cell Research, vol. 360, no. 2, 2017, pp. 74-80.
Tang B, Li X, Ren Y, et al. MicroRNA-29a regulates lipopolysaccharide (LPS)-induced inflammatory responses in murine macrophages through the Akt1/ NF-κB pathway. Exp Cell Res. 2017;360(2):74-80.
Tang, B., Li, X., Ren, Y., Wang, J., Xu, D., Hang, Y., Zhou, T., Li, F., & Wang, L. (2017). MicroRNA-29a regulates lipopolysaccharide (LPS)-induced inflammatory responses in murine macrophages through the Akt1/ NF-κB pathway. Experimental Cell Research, 360(2), 74-80. https://doi.org/10.1016/j.yexcr.2017.08.013
Tang B, et al. MicroRNA-29a Regulates Lipopolysaccharide (LPS)-induced Inflammatory Responses in Murine Macrophages Through the Akt1/ NF-κB Pathway. Exp Cell Res. 2017 11 15;360(2):74-80. PubMed PMID: 28811129.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MicroRNA-29a regulates lipopolysaccharide (LPS)-induced inflammatory responses in murine macrophages through the Akt1/ NF-κB pathway. AU - Tang,Bufu, AU - Li,Xingchen, AU - Ren,Yanling, AU - Wang,Jing, AU - Xu,Di, AU - Hang,Yiru, AU - Zhou,Tingting, AU - Li,Feng, AU - Wang,Ling, Y1 - 2017/08/12/ PY - 2017/07/10/received PY - 2017/08/03/revised PY - 2017/08/05/accepted PY - 2017/8/16/pubmed PY - 2017/11/4/medline PY - 2017/8/17/entrez KW - Akt1 KW - Inflammatory KW - Macrophage KW - MiR-29a KW - NF-κB SP - 74 EP - 80 JF - Experimental cell research JO - Exp Cell Res VL - 360 IS - 2 N2 - Akt activation in macrophages enhances lipopolysaccharide (LPS)-induced inflammatory responses through upregulation of the NF-κB signal pathway. Akt phosphorylation via microRNA (miR) caused the downregulation of Akt1. Here, we evaluated the role of miR-29a in LPS-triggered inflammatory responses. LPS stimulation of primary macrophages and RAW264.7 cells gradually increased the levels of miR-29a and was dependent on the LPS concentration. Overexpression of miR-29a in macrophages enhanced the expression of proinflammatory cytokines including IL-1β and IL-6, but not TNF-α. Conversely, knockdown of miR-29a diminished cytokine expression. Bioinformatics analyses indicated that Akt1 was a potential target of miR-29a through its interaction with the CDS region of Akt1. The miR-29a also enhanced LPS-induced NF-κB signaling through increased NF-κB transcriptional activity and phosphorylation of p65, and through binding to Akt1. Moreover, Akt1 silencing promoted the LPS-induced expression of IL-1β and IL-6, and upregulated the NF-κB pathway. Taken together, our results suggested that miR-29a participates in the regulation of inflammatory responses in LPS-stimulated macrophages by promoting NF-κB activation through targeting Akt1. SN - 1090-2422 UR - https://www.unboundmedicine.com/medline/citation/28811129/MicroRNA_29a_regulates_lipopolysaccharide__LPS__induced_inflammatory_responses_in_murine_macrophages_through_the_Akt1/_NF_κB_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4827(17)30421-4 DB - PRIME DP - Unbound Medicine ER -