Afsar Naqvi, PhD
Building & Room:
UIC College of Dentistry 801 S. Paulina St., IL 60612
Fordham JB, Naqvi AR, Nares S. 2016. MiR-142-3p is a RANKL-dependent inducer of cell death in osteoclasts. Sci Rep. In press.
Naqvi AR, Zhong S, Dang H, Fordham JB, Nares S, Khan A. 2016. Expression Profiling of Lipopolysaccharide Responsive miRNA in Primary Human Macrophages. J Microb Biochem Technol. In press.
Kulkarni V*, Naqvi AR*, Uttamani JR, Nares S. 2016. MiRNA-Target Interaction Reveals Cell-Specific Post-Transcriptional Regulation in Mammalian Cell Lines. Int J Mol Sci. (* Equal contribution).
Fordham JB, Naqvi AR, Nares S. 2015. MiR-24 Regulates Macrophage Plasticity and Polarisation. J Clin Cell Immunol.
Fordham JB, Naqvi AR, Nares S. 2015. Regulation of miR-24, miR-30b and miR-142-3p Expression During Macrophage and Dendritic Cell Differentiation Potentiates Innate Immunity. J Leukoc Biol.
Naqvi AR, Fordham JB, Nares S. 2014. MiR-24, miR-30b and miR-142-3p Regulate Phagocytosis in Myeloid Inflammatory Cells. J Immunol.
Galicia JC, Naqvi AR, Ko CC, Nares S, Khan AA. 2014. MiRNA-181a regulates Toll-like receptor agonist-induced inflammatory response in human fibroblasts. Genes Immun.
Fordham JB, Naqvi AR, Nares S. 2014. Leukocyte Production of Inflammatory Mediators is Inhibited by the Anti-oxidants Phloretin, Silymarin, Hesperetin and Resveratrol. Mediators Inflamm.
Aqil M, Naqvi AR, Mallik S, Bandyopadhyay S, Maulik U, Jameel S. 2014. The HIV Nef protein modulates cellular and exosomal miRNA profiles in human monocytic cells. J Extracell Vesicles.
Naqvi AR, Fordham JB, Khan A, Nares S. 2013. MicroRNAs Responsive to A. actinomycetemcomitans and P. gingivalis LPS Modulate Expression of Genes Regulating Innate Immunity in Human Macrophages. Innate Immun.
Aqil M, Naqvi AR, Bano AS, Jameel S. 2013. The HIV-1 Nef protein binds argonaute-2 and functions as a viral suppressor of RNA interference. PLoS One.
Fordham JB, Naqvi AR, Nares S. 2012. Identifying miRNA Function in Innate Immunity. MiRNA and Non-coding RNA: Technology, Developments and Applications.
- Postdoctoral Associate, UIC
- Postdoctoral Fellow, University of Chapel Hill at North Carolina
- Post-Doctoral Scientist, Virology Group, International Center for Genetic Engineering and Biotechnology, India
- PhD Molecular Biology/Virology, Jamia Millia Islamia and International Center for Genetic Engineering and Biotechnology, India
- MSc Biotechnology, Jamia Millia Islamia, India
Research Currently in Progress
Macrophages, monocytes and dendritic cells (DCs) are members of Mononuclear Phagocyte System (MPS) that regulate innate immune responses and shape adaptive immunity. Depending on the inflammatory environment, these cells exhibit unique functional properties to counter immediate threat. MiRNAs are noncoding RNA molecules that post-transcriptionally regulate expression of target mRNAs thus regulating a plethora of fundamental biological processes including cell differentiation, signaling, and pathogen response. Our laboratory characterizes the role of miRNAs in differentiation and function of myeloid cells. We have catalogued hundreds of differentiation associated miRNAs in macrophages and DCs which are screened for their regulatory role in differentiation, phagocytosis, antigen processing and presentation. The levels of these miRNAs are also examined in inflammation related oral diseases with an aim to identify miRNAs as diagnostic markers.
Concurrently, my laboratory also focuses on studying the role of virus encoded miRNAs. Members of the human herpesvirus (HHV) families cause the most common primary or recurrent viral infections of the oral cavity. Depending on the virus in context, the seroprevalence ranges from 50-90% of the U.S. population. Interestingly, HHV are the predominant class of viruses that encode miRNAs (vmiRs). Epithelial cells are primary sites of productive infection, allowing virus to disseminate and establish latency in target cells (generally hematopoietic or neuronal cells). Dynamic interaction of myeloid cells with surrounding oral keratinocytes is required to amplify innate responses for a favorable outcome. Long term latency in HHV requires efficient immune subversion. This is further exacerbated by the secretion of vmiRs in exosomes, key mediators of information exchange across cells, causing functional dysregulation in multiple target cells. In recent years, our laboratory has identified several vmiRs associated with oral diseases. Our lab focuses on identifying the mechanistic aspect of vmiRs in modulating target cell (myeloid cells and oral keratinocytes) function including alterations in immune cell responses. We systematically investigate the impact of vmiRs on host miRnome and transcriptome expression to identify key pathways targeted by vmiRs in order to identify potential therapeutic targets.
What can the herpesvirus teach us about oral inflammation?
Dr. Naqvi's lab is using a $2 million grant from the National Institutes of Health to study how herpesviruses, and their underlying molecular mechanisms, contribute to increased inflammation in oral diseases, like periodontitis, commonly referred to as gum disease.