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Bhavani S. Sahu

Bio: Bhavani S. Sahu is an academic researcher from Indian Institute of Technology Madras. The author has contributed to research in topics: Receptor & Chromogranin A. The author has an hindex of 11, co-authored 16 publications receiving 273 citations. Previous affiliations of Bhavani S. Sahu include University of Cambridge & University of California, San Diego.

Papers
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Journal ArticleDOI
TL;DR: TiO(2) nanoparticle-assisted PCR may be useful for profound reduction of the overall PCR reaction period and for enhanced amplification of DNA amplicons from a variety of samples, including GC-rich templates that are often observed to yield unsatisfactory results.
Abstract: Improvement of the specificity and efficiency of the polymerase chain reaction (PCR) by nanoparticles is an emerging area of research. We observed that TiO2 nanoparticles of ∼25 nm diameter caused significant enhancement of PCR efficiency for various types of templates (namely plasmid DNA, genomic DNA and complementary DNA). By a series of experiments, the optimal TiO2 concentration was determined to be 0.4 nM, which resulted in up to a seven-fold increase in the amount of PCR product. As much as 50% reduction in overall reaction time (by reduction of the number of cycles and the time periods of cycles) was also achieved by utilizing TiO2 nanoparticles without compromising the PCR yield. Investigations of the mechanism of such PCR enhancement by simulations using the ‘Fluent K epsilon turbulent model’ provided evidence of faster heat transfer in the presence of TiO2 nanoparticles. Consistent with these findings, TiO2 nanoparticles were observed to augment the denaturation of genomic DNA, indicating more efficient thermal conductivity through the reaction buffer. TiO2 nanoparticle-assisted PCR may be useful for profound reduction of the overall PCR reaction period and for enhanced amplification of DNA amplicons from a variety of samples, including GC-rich templates that are often observed to yield unsatisfactory results. (Some figures in this article are in colour only in the electronic version)

59 citations

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TL;DR: Previously unknown roles for NF-κB and CREB to regulate Hspa1a expression and a coordinated action by several transcription factors for HspA1a transactivation under heat-shock/ischemia-like conditions are discovered and thereby provided new insights into the mechanism of Hsp a1a regulation.

48 citations

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TL;DR: Interestingly, renalase promoter activity was augmented by nicotine and catecholamines; while Sp1 and STAT3 synergistically activated the nicotine-induced effect, Sp1 appeared to enhance epinephrine-evoked renalase transcription.
Abstract: Renalase, a novel monoamine oxidase, is emerging as an important regulator of cardiovascular, metabolic, and renal diseases. However, the mechanism of transcriptional regulation of this enzyme rema...

34 citations

Journal ArticleDOI
TL;DR: Accumulated evidence establishes CHGA as a novel susceptibility gene for EH, which acts as a prohormone giving rise to bioactive peptides such as vasostatin-I and catestatin that exhibit several cardiovascular regulatory functions.
Abstract: Chromogranin A (CHGA) is ubiquitously expressed in secretory cells of the endocrine, neuroendocrine, and neuronal tissues. Although this protein has long been known as a marker for neuroendocrine tumors, its role in cardiovascular disease states including essential hypertension (EH) has only recently been recognized. It acts as a prohormone giving rise to bioactive peptides such as vasostatin-I (human CHGA1–76) and catestatin (human CHGA352–372) that exhibit several cardiovascular regulatory functions. CHGA is over-expressed but catestatin is diminished in EH. Moreover, genetic variants in the promoter, catestatin, and 3′-untranslated regions of the human CHGA gene alter autonomic activity and blood pressure. Consistent with these findings, targeted ablation of this gene causes severe arterial hypertension and ventricular hypertrophy in mice. Transgenic expression of the human CHGA gene or exogenous administration of catestatin restores blood pressure in these mice. Thus, the accumulated evidence establishes CHGA as a novel susceptibility gene for EH.

30 citations

Journal ArticleDOI
TL;DR: TLQP-21 does not possess lipolytic properties per se, but it enhances β-AR activation-induced lipolysis by a mechanism requiring Ca2+ mobilization and ERK activation of Hormone Sensitive Lipase (HSL).
Abstract: Objectives Obesity is characterized by excessive fat mass and is associated with serious diseases such as type 2 diabetes Targeting excess fat mass by sustained lipolysis has been a major challenge for anti-obesity therapies due to unwanted side effects TLQP-21, a neuropeptide encoded by the pro-peptide VGF (non-acronymic), that binds the complement 3a receptor 1 (C3aR1) on the adipocyte membrane, is emerging as a novel modulator of adipocyte functions and a potential target for obesity-associated diseases The molecular mechanism is still largely uncharacterized Methods We used a combination of pharmacological and genetic gain and loss of function approaches 3T3-L1 and mature murine adipocytes were used for in vitro experiments Chronic in vivo experiments were conducted on diet-induced obese wild type, β 1 , β 2 , β 3 -adrenergic receptor (AR) deficient and C3aR1 knockout mice Acute in vivo lipolysis experiments were conducted on Sprague Dawley rats Results We demonstrated that TLQP-21 does not possess lipolytic properties per se Rather, it enhances β-AR activation-induced lipolysis by a mechanism requiring Ca 2+ mobilization and ERK activation of Hormone Sensitive Lipase (HSL) TLQP-21 acutely potentiated isoproterenol-induced lipolysis in vivo Finally, chronic peripheral TLQP-21 treatment decreases body weight and fat mass in diet induced obese mice by a mechanism involving β-adrenergic and C3a receptor activation without associated adverse metabolic effects Conclusions In conclusion, our data identify an alternative pathway modulating lipolysis that could be targeted to diminish fat mass in obesity without the side effects typically observed when using potent pro-lipolytic molecules

30 citations


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TL;DR: How ASCVD risk factors affect the South Asian population is focused on in order to make recommendations for clinical strategies to reduce disease and for directions for future research to reduce ASCVD in this population.
Abstract: South Asians (from Bangladesh, Bhutan, India, the Maldives, Nepal, Pakistan, and Sri Lanka) make up one quarter of the world's population and are one of the fastest-growing ethnic groups in the United States. Although native South Asians share genetic and cultural risk factors with South Asians abroad, South Asians in the United States can differ in socioeconomic status, education, healthcare behaviors, attitudes, and health insurance, which can affect their risk and the treatment and outcomes of atherosclerotic cardiovascular disease (ASCVD). South Asians have higher proportional mortality rates from ASCVD compared with other Asian groups and non-Hispanic whites, in contrast to the finding that Asian Americans (Asian Indian, Chinese, Filipino, Japanese, Korean, and Vietnamese) aggregated as a group are at lower risk of ASCVD, largely because of the lower risk observed in East Asian populations. Literature relevant to South Asian populations regarding demographics and risk factors, health behaviors, and interventions, including physical activity, diet, medications, and community strategies, is summarized. The evidence to date is that the biology of ASCVD is complex but is no different in South Asians than in any other racial/ethnic group. A majority of the risk in South Asians can be explained by the increased prevalence of known risk factors, especially those related to insulin resistance, and no unique risk factors in this population have been found. This scientific statement focuses on how ASCVD risk factors affect the South Asian population in order to make recommendations for clinical strategies to reduce disease and for directions for future research to reduce ASCVD in this population.

306 citations

Journal ArticleDOI
TL;DR: The structure and function of granins and granin-derived peptides and expansive new genetic evidence are reviewed, including recent single-nucleotide polymorphism mapping, genomic sequence comparisons, and analysis of transgenic and knockout mice, which together support an important and evolutionarily conserved role for these proteins in large dense-core vesicle biogenesis and regulated secretion.
Abstract: The chromogranins (chromogranin A and chromogranin B), secretogranins (secretogranin II and secretogranin III), and additional related proteins (7B2, NESP55, proSAAS, and VGF) that together comprise the granin family subserve essential roles in the regulated secretory pathway that is responsible for controlled delivery of peptides, hormones, neurotransmitters, and growth factors. Here we review the structure and function of granins and granin-derived peptides and expansive new genetic evidence, including recent single-nucleotide polymorphism mapping, genomic sequence comparisons, and analysis of transgenic and knockout mice, which together support an important and evolutionarily conserved role for these proteins in large dense-core vesicle biogenesis and regulated secretion. Recent data further indicate that their processed peptides function prominently in metabolic and glucose homeostasis, emotional behavior, pain pathways, and blood pressure modulation, suggesting future utility of granins and granin-derived peptides as novel disease biomarkers.

289 citations

Journal ArticleDOI
TL;DR: A review of anatomical, genetic and pharmacological studies on the neural regulation of adipose function, including lipolysis, non-shivering thermogenesis, browning and leptin secretion, can be found in this article.
Abstract: Interactions between the brain and distinct adipose depots have a key role in maintaining energy balance, thereby promoting survival in response to metabolic challenges such as cold exposure and starvation. Recently, there has been renewed interest in the specific central neuronal circuits that regulate adipose depots. Here, we review anatomical, genetic and pharmacological studies on the neural regulation of adipose function, including lipolysis, non-shivering thermogenesis, browning and leptin secretion. In particular, we emphasize the role of leptin-sensitive neurons and the sympathetic nervous system in modulating the activity of brown, white and beige adipose tissues. We provide an overview of advances in the understanding of the heterogeneity of the brain regulation of adipose tissues and offer a perspective on the challenges and paradoxes that the community is facing regarding the actions of leptin on this system.

163 citations

Journal ArticleDOI
TL;DR: Results suggest that DPB3-1 could form a transcriptional complex with NF-YA and NF-YB subunits and that the identified trimer enhances heat stress-inducible gene expression during heat stress responses in cooperation with DREB2A.
Abstract: DEHYDRATION-RESPONSIVE ELEMENT BINDING PROTEIN2A (DREB2A) is a key transcription factor for drought and heat stress tolerance in Arabidopsis thaliana. DREB2A induces the expression of dehydration- and heat stress-inducible genes under the corresponding stress conditions. Target gene selectivity is assumed to require stress-specific posttranslational regulation, but the mechanisms of this process are not yet understood. Here, we identified DNA POLYMERASE II SUBUNIT B3-1 (DPB3-1), which was previously annotated as NUCLEAR FACTOR Y, SUBUNIT C10 (NF-YC10), as a DREB2A interactor, through a yeast two-hybrid screen. The overexpression of DPB3-1 in Arabidopsis enhanced the expression of a subset of heat stress-inducible DREB2A target genes but did not affect dehydration-inducible genes. Similarly, the depletion of DPB3-1 expression resulted in reduced expression of heat stress-inducible genes. Interaction and expression pattern analyses suggested the existence of a trimer comprising NF-YA2, NF-YB3, and DPB3-1 that could synergistically activate a promoter of the heat stress-inducible gene with DREB2A in protoplasts. These results suggest that DPB3-1 could form a transcriptional complex with NF-YA and NF-YB subunits and that the identified trimer enhances heat stress-inducible gene expression during heat stress responses in cooperation with DREB2A. We propose that the identified trimer contributes to the target gene selectivity of DREB2A under heat stress conditions.

129 citations

Journal ArticleDOI
TL;DR: The mechanistic importance of miRs in modulating endothelial cell (EC) function in physiology and in disease is addressed and Drawbacks of currently available therapeutic options are discussed, pointing at the challenges and clinical opportunities provided by miR‐based treatments.
Abstract: Accumulating evidence indicates that microRNAs (miRs)-non-coding RNAs that can regulate gene expression via translational repression and/or post-transcriptional degradation-are becoming one of the most fascinating areas of physiology, given their fundamental roles in countless pathophysiological processes. The relative roles of different miRs in vascular biology as direct or indirect post-transcriptional regulators of fundamental genes implied in vascular remodeling designate miRs as potential biomarkers and/or promising drug targets. The mechanistic importance of miRs in modulating endothelial cell (EC) function in physiology and in disease is addressed here. Drawbacks of currently available therapeutic options are also discussed, pointing at the challenges and clinical opportunities provided by miR-based treatments. J. Cell. Physiol. 231: 1638-1644, 2016. © 2015 Wiley Periodicals, Inc.

114 citations