My Team

Team Members

Dr. Mahesh S Krishna

Mahesh S Krishna, PhD
Post-doctoral Fellow

Modulation of upstream/downstream regulators of PPAR gamma using miRNA as molecular switches to reduce adipocyte hypertrophy and hyperplasia
We are focussed on the regulation of adipogenesis using micro RNA (miRNA) as a tool. Adipogenesis is a complicated process involving activation and interaction of various transcription factors and associated genes. PPAR gamma is considered as master regulator of adipogenesis. The differentiation of pre-adipocytes to adipocyte happens with the activation of C/EBPs, PPARs and other steroid responsive nuclear factors. Of these, activation of PPAR gamma leads to expression of most of the genes responsible for fatty acid metabolism, transport, glucose homeostasis and associated enzymes. PPAR gamma is a versatile protein with varied functions in body including inflammatory response, cell growth and is linked to diseases like diabetes, obesity, cancer, arthritis etc. Here, we are trying to modulate the functional roles of PPAR gamma by regulating the binding or expressional pattern of co-factors associated with this, using the translational repressor potential of micro RNA.

Dr. Kalaivani V

Kalaivani V, PhD
Post-doctoral Fellow

Effects of O-glycans of Apo(a) on Angiogenesis and its Implications in Pre-eclampsia
Pre-eclampsia (PE), a medical condition in which hypertension arises in pregnancy, is the 3rd leading cause of maternal mortality and the 7th leading cause of the perinatal mortality. The pathogenesis of PE is caused by poor placentation with impaired angiogenesis of maternal spiral arteries leading to intra-uterine growth restriction. Lipoprotein (a) [Lp(a)] deposits were found on the placenta that had undergone acute-atherosis, another characteristic event of PE. Moreover, an increased plasma Lp(a) level was observed in PE subjects. Presence of apolipoprotein (a) [apo(a)], a unique glycoprotein subunit of Lp(a), on diseased placenta along with its emerging role as an anti-angiogenic agent suggests its involvement in PE pathogenesis. However, the exact domain of apo(a) behind this effect is poorly understood. The extended O-glycan structure of apo(a) is a strong ligand for galectin-1, a pro-angiogenic, O-glycan specific lectin abundant in placenta. In vivo studies have shown that the inhibition of galectin-1-mediated angiogenesis leads to poor placentation and provokes PE-like symptoms. There are very few studies which addressed physiologic or pathologic functions of apo(a) O-glycans. In this context, the present project aims to identify the role of the extended O-glycan structure of apo(a) in the modulation of galectin-1-mediated angiogenesis associated with pre-eclampsia.

Aneesh Kumar Asokan

Aneesh Kumar Asokan
PhD Student

Identification of Altered Metabolism in Individuals at risk for Type 2 Diabetes Mellitus through Mass Spectrometry-based Metabolomics.

Gopika Satheesh

Gopika Satheesh
Research Fellow

Metabolomics profiling of Normal Healthy People in Kerala: Impact of family history of diabetes.

Akhila Suresh S S

Akhila Suresh S S
Project Assistant

Laboratory management assistance.