title: High glucose-induced human cellular immune response is governed by miR-2909 RNomics.
abstract: Regulation of NFkB family member RelA translocation by tumour suppressor genes encoding p53 and KLF4, has been widely recognized as the critical for human peripheral blood mononuclear cells (PBMCs) to meet their energy requirement for tailoring their immune response against any perceived threat. Our study was addressed to understand as to how human PBMCs respond to high glucose threat in terms of their genomics-directed immune response. The results of such a study revealed for the first time that NFkB induced miR-2909 RNomics is crucial for the regulation of RelA translocation within human PBMCs exposed to high glucose thereby enabling these epigenetically programmed cells to tailor immune response involving genes coding for CCL5; IFN-γ and IL-17. Based upon these results an attempt was also made to propose a mechanistic pathway that links high glucose induced cellular miR-2909 RNomics with the genes involved in energy metabolism and immune response.
authors.affiliation: Department of Experimental Medicine, Post-graduate Institute of Medical Education & Research, Chandigarh 160012, India; Department of Biotechnology, Post-graduate Institute of Medical Education & Research, Chandigarh 160012, India. Electronic address: dkaul_24@hotmail.com.
authors.forename: Deepak
authors.initials: D
authors.lastname: Kaul
authors.affiliation: Department of Experimental Medicine, Post-graduate Institute of Medical Education & Research, Chandigarh 160012, India; Department of Biotechnology, Post-graduate Institute of Medical Education & Research, Chandigarh 160012, India.
authors.forename: Sugandha
authors.initials: S
authors.lastname: Sharma
mesh_terms: D018946:Chemokine CCL5 / Q000235:genetics / Q000276:immunology; D004734:Energy Metabolism / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D044127:Epigenesis, Genetic; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects* / Q000235:genetics; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology; D000090062:Kruppel-Like Factor 4; D051741:Kruppel-Like Transcription Factors / Q000235:genetics / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D035683:MicroRNAs / Q000235:genetics / Q000276:immunology*; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology; D061251:Primary Cell Culture; D021381:Protein Transport; D015398:Signal Transduction; D051996:Transcription Factor RelA / Q000235:genetics / Q000276:immunology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000276:immunology
chemical_list: C483024:CCL5 protein, human; D018946:Chemokine CCL5; D020381:Interleukin-17; C000715467:KLF4 protein, human; D000090062:Kruppel-Like Factor 4; D051741:Kruppel-Like Transcription Factors; C000589020:MIRN2909 microRNA, human; D035683:MicroRNAs; D016328:NF-kappa B; C498143:RELA protein, human; D051996:Transcription Factor RelA; D016159:Tumor Suppressor Protein p53; D007371:Interferon-gamma; D005947:Glucose
keywords: Aerobic-glycolysis; CCL5; IFN-γ; IL-17; miR-2909 RNomics