Rama Natarajan Lab

Research Lab Overview

We focus on the role of epigenetics and noncoding RNAs. We have interest in learning how prior hyperglycemia-associated epigenetic changes can impart metabolic memory and lead to gene malfunction and organ disease despite restoration of glucose balance.

Our group uses state-of-the art genomic approaches in cell culture and animal and clinical models to examine these mechanisms and develops innovative therapeutic interventions for diabetic complications.

Natarajan Lab Highlights

We have played a leading role in demonstrating how epigenetic chromatin histone post-translational modifications and DNA methylation regulate inflammatory and fibrotic genes in diabetes and participate in metabolic memory. Under diabetic conditions, our lab employs state-of-the-art Omics profiling and high-throughput sequencing approaches to map histone modifications, DNA methylation and binding of chromatin factors, chromatin accessibility and transcriptome changes genome-wide. Lab members are expert at powerful techniques such as Chromatin immunoprecipitation (ChIP)-linked to next generation sequencing (ChIP-seq), RNA-sequencing, ATAC-sequencing, single cell-RNA-seq, chromatin conformation capture and Hi-C genomic interactions, along with bioinformatics for sequencing data analyses.

We also study noncoding RNAs, including microRNAs and long non-coding RNAs (lncRNAs), and how they fine tune the actions of growth factors to control gene expression. We found novel roles for specific microRNAs and lncRNAs in diabetes-associated renal fibrosis, inflammation and vascular dysfunction. In ongoing studies, we are evaluating molecular mechanisms by which these non-coding RNAs exert their protective or pathologic effects in diabetes and obesity, and are using CRISPR-Cas9 technology to generate microRNA- and LncRNA-deficient mice to study the in vivo function of these moieties. Additionally, tests are ongoing of novel non-coding RNA inhibitors as possible treatments for diabetes-related complications, especially renal dysfunction.

The focus of our lab is to determine the molecular mechanisms that promote inflammation, and vascular and renal complications in diabetes. In this regard, we focus on the role of epigenetics and noncoding RNAs. We have an interest in learning how prior hyperglycemia-associated epigenetic changes can impart metabolic memory and lead to gene malfunction and organ disease despite restoration of glucose balance. Our group uses state-of-the-art genomic approaches in cell culture, animal and clinical models to examine these mechanisms, and develop innovative therapeutic interventions for diabetic complications.  

Research Highlights/Projects — We have played a leading role in demonstrating how epigenetic chromatin histone post-translational modifications and DNA methylation regulate inflammatory and fibrotic genes in diabetes and participate in metabolic memory.  Under diabetic conditions, our lab employs state-of-the-art Omics profiling and high-throughput sequencing approaches to map histone modifications, DNA methylation, and binding of chromatin factors, chromatin accessibility and transcriptome changes genome-wide. Lab members are experts at powerful techniques such as Chromatin immunoprecipitation (ChIP)-linked to next-generation sequencing (ChIP-seq), RNA-sequencing, ATAC-sequencing, single-cell RNA-seq, chromatin conformation capture, and Hi-C genomic interactions, along with sophisticated bioinformatics for integration of data from multiple high throughput sequencing datasets. We are also testing small molecule drugs as monotherapy for diabetes, its complications and metabolic memory.

In addition, we study noncoding RNAs, including microRNAs and long non-coding RNAs (lncRNAs), and how they fine-tune the actions of growth factors to control gene expression. We found novel roles for specific microRNAs and lncRNAs in diabetes-associated renal fibrosis, inflammation and vascular dysfunction. In ongoing studies, we are evaluating molecular mechanisms by which these noncoding RNAs exert their protective or pathologic effects in diabetes and obesity, and are using CRISPR-Cas9 technology to generate microRNA- and lncRNA-deficient mice to study the in vivo function of these moieties. Additionally, tests are ongoing on novel non-coding RNA inhibitors as possible treatments for diabetes-related complications, especially renal dysfunction.  

Partnerships

Who We Collaborate With

We collaborate with organizations in progressing the development of new treatments in our specialized areas of research.