Publications by authors named "Anindhya Sundar Das"

Background: Recent Na-MRI reports show higher salt deposition in malignant breast tissue than in surrounding normal tissue. The effect of high salt on cancer progression remains controversial. Here, we investigated the direct effect of high salt on breast cancer progression in vitro.

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Ribosomal proteins (RPs) are constituents of macromolecular machinery, ribosome that translates genetic information into proteins. Besides ribosomal functions, RPs are now getting appreciated for their 'moonlighting'/extra-ribosomal functions modulating many cellular processes. Accumulating evidence suggests that a number of RPs are involved in inflammation.

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The YTH-domain family (YTHDF) of RNA binding proteins can control gene expression at the post-transcriptional level by regulating mRNAs with N-methyladenosine (mA) modifications. Despite the established importance of mA in the heart, the cardiac role of specific mA-binding proteins remains unclear. Here, we characterized the function of YTHDF1 in cardiomyocytes using a newly generated cardiac-restricted mouse model.

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How post-transcriptional regulation of gene expression, such as through -methyladenosine (mA) messenger RNA methylation, impacts heart function is not well understood. We found that loss of the mA binding protein YTHDF2 in cardiomyocytes of adult mice drove cardiac dysfunction. By proteomics, we found myocardial zonula adherens protein (MYZAP) within the top up-regulated proteins in knockout cardiomyocytes.

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Naturally occurring post-transcriptional chemical modifications serve critical roles in impacting RNA structure and function. More directly, modifications may affect RNA stability, intracellular transport, translational efficiency, and fidelity. The combination of effects caused by modifications are ultimately linked to gene expression regulation at a genome-wide scale.

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Objective: IL-6-induced STAT3 activation is associated with various chronic inflammatory diseases. In this study, we investigated the anti-STAT3 mechanism of the dietary polyphenol, biochanin A (BCA), in IL-6-treated macrophages.

Methods: The effect of BCA on STAT3 and p38 MAPK was analyzed by immunoblot.

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Nanogels have potential for encapsulating cancer therapeutics, yet their susceptibility to physiological degradation and lack of cellular specificity hinder their use as effective oral delivery vehicles. Herein, we engineered novel albumin-core with folic acid functionalized hyperbranched amylopectin shell-type nanogels, prepared through a two-step reaction and loaded with curcumin while the proteinaceous core was undergoing thermal gelation. The nanogels had a mean hydrodynamic diameter of ca.

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Monocyte infiltration to the site of pathogenic invasion is critical for inflammatory response and host defence. However, this process demands precise regulation as uncontrolled migration of monocytes to the site delays resolution of inflammation and ultimately promotes chronic inflammation. C-C motif chemokine ligand 2 (CCL2) plays a key role in monocyte migration, and hence, its expression should be tightly regulated.

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Saturated free fatty acid-induced adipocyte inflammation plays a pivotal role in implementing insulin resistance and type 2 diabetes. Recent reports suggest A adenosine receptor (AAR) could be an attractive choice to counteract adipocyte inflammation and insulin resistance. Thus, an effective AAR agonist devoid of any toxicity is highly appealing.

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The transformation of macrophages into lipid-loaded foam cells is a critical and early event in the pathogenesis of atherosclerosis. Several recent reports highlighted that induction of TLR4 signaling promotes macrophage foam cell formation; however, the underlying molecular mechanisms have not been clearly elucidated. Here, we found that the TLR4 mediated inflammatory signaling communicated with mTORC2-Akt-mTORC1 metabolic cascade in macrophage and thereby promoting lipid uptake and foam cell formation.

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Cycloxygenase-2 (COX-2) is the inducible isoform of cycloxygenase enzyme family that catalyzes synthesis of inflammatory mediators, prostanoids and prostaglandins, and therefore, can be targeted by anti-inflammatory drugs. Here, we showed a plant polyphenol, kaempferol, attenuated IL-6-induced COX-2 expression in human monocytic THP-1 cells suggesting its beneficial role in chronic inflammation. Kaempferol deactivated and prevented nuclear localization of two major transcription factors STAT3 and NF-κB, mutually responsible for COX-2 induction in response to IL-6.

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