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research overview The focus in the lab is to understand the why and the how behind neonates developing diseases, with the goal of preventing/curing them. The lab starts with disease phenotypes and study the pathogenic mechanisms underlying disease evolution to guide the development of novel future therapies. The phenotypes of interest are necrotizing enterocolitis (NEC), bronchopulmonary dysplasia (BPD), and rare infectious diseases such as herpes simplex virus (HSV) and Group B Streptococcus (GBS). The major challenge is that diseases in neonates and premature infants occupy a unique niche, wherein, injury to the host caused by noxious stimuli such as oxygen toxicity and bacteria occur during critical ontogenic windows. Therefore, disease pathogenesis needs to be examined in the context of developmental processes to decipher mechanism and test potential therapy. The lab uses human genomic studies, rodent pre-clinical models, cell culture studies, and bioinformatics to investigate the mechanisms and sub-phenotype neonatal diseases. The long-term goal is to build an internationally renowned program in neonatal research by integrating the skill sets of a diverse team of motivated scientists and collaborators. The lab uses knowledge obtained through the investigations to develop precision tools for identifying infants at risk of disease and develop novel treatment strategies to prevent or cure disease. The three major areas of research interest are: I. Lung and BPD Research: Bronchopulmonary dysplasia (BPD) is a debilitating chronic lung disease in premature infants. An area of emphasis is understanding the role of lung endothelial cell (EC) injury/reprogramming in impaired lung and vascular development in BPD. To address this issue, the lab has developed new pre-clinical models of disease, and several transgenic lines to identify the key molecular players that regulate normal and abnormal vascular development. A second challenge is the inability to discern BPD sub-phenotypes, at a genomic and functional level. The lab is addressing this challenge by performing genetic and deep phenotypic characterization in BPD infants. II. Necrotizing Enterocolitis Research: Necrotizing enterocolitis is a major cause of mortality in premature infants, and represents phenotypes for deviant host-microbiome interactions in the gut. The lab uses forward- and reverse genetics, microbiota studies, and host-bacteria interaction studies to investigate NEC. The immediate focus of this research is the gene, Single Immunoglobulin Interleukin-1 Related Receptor (SIGIRR), which the lab identified as a putative locus for NEC susceptibility. Using novel transgenic mice that encode a NEC-associated genetic mutation the lab discovered and the lab investigated the pathogenesis of NEC. They are also testing several therapies in the pre-clinical and in vivo models. III. Genetic Basis of Neonatal Disease Susceptibility: The team is one of the leaders in the field of neonatal genomics. The team used low throughput-based single gene or pathway approaches, and are initiating high throughput genome-wide approaches. Apart from complex phenotypes such as BPD and NEC, they are vested in unraveling the genetic basis of rare infectious disease phenotypes such as herpes simplex virus (HSV) and Group B Streptococcus (GBS). They are also initiating deep phenotyping and transcriptome analysis for complex phenotypes, which in combination with genetics, will help sub-classify complex phenotypes. These combined approaches can spur discovery approaches based on mechanism, as well as outcomes research based on interventions.

One or more keywords matched the following items that are connected to Sampath, Venkatesh

Item TypeName
Concept Mice, Inbred C3H
Concept Mice, Inbred C57BL
Concept Mice, Mutant Strains
Concept Mice, Transgenic
Concept Mice, Knockout
Concept Mice
Academic Article Altered postnatal lung development in C3H/HeJ mice.
Academic Article Lipopolysaccharide (LPS)-mediated angiopoietin-2-dependent autocrine angiogenesis is regulated by NADPH oxidase 2 (Nox2) in human pulmonary microvascular endothelial cells.
Academic Article Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 Regulates LPS-Induced Inflammation and Alveolar Remodeling in the Developing Lung.
Academic Article Single-Immunoglobulin Interleukin-1-Related Receptor regulates vulnerability to TLR4-mediated necrotizing enterocolitis in a mouse model.
Academic Article Lung epithelial-specific TRIP-1 overexpression maintains epithelial integrity during hyperoxia exposure.
Academic Article Endothelial immune activation programmes cell-fate decisions and angiogenesis by inducing angiogenesis regulator DLL4 through TLR4-ERK-FOXC2 signalling.
Academic Article Up-regulation of SFTPB expression and attenuation of acute lung injury by pulmonary epithelial cell-specific NAMPT knockdown.
Academic Article DNMT and HDAC inhibitors together abrogate endotoxemia mediated macrophage death by STAT3-JMJD3 signaling.
Academic Article Enteric infection coupled with chronic Notch pathway inhibition alters colonic mucus composition leading to dysbiosis, barrier disruption and colitis.
Academic Article Histone deacetylase 6 regulates endothelial MyD88-dependent canonical TLR signaling, lung inflammation, and alveolar remodeling in the developing lung.
Grant Single Immunoglobulin Interleukin-1 Related Receptor and necrotizing enterocolitis in premature infants
Grant Inflammatory Angiogenesis in the Lung
Academic Article NEC-like intestinal injury is ameliorated by Lactobacillus rhamnosus GG in parallel with SIGIRR and A20 induction in neonatal mice.
Academic Article FOSL1 is a novel mediator of endotoxin/lipopolysaccharide-induced pulmonary angiogenic signaling.
Academic Article Delta-like 4 is required for pulmonary vascular arborization and alveolarization in the developing lung.
Academic Article Angiopoietin-1 protects against endotoxin-induced neonatal lung injury and alveolar simplification in mice.
Academic Article Ciclesonide activates glucocorticoid signaling in neonatal rat lung but does not trigger adverse effects in the cortex and cerebellum.
Academic Article SIGIRR Mutation in Human Necrotizing Enterocolitis (NEC) Disrupts STAT3-Dependent microRNA Expression in Neonatal Gut.
Academic Article Dietary Interventions Ameliorate Infectious Colitis by Restoring the Microbiome and Promoting Stem Cell Proliferation in Mice.
Grant A Safer Glucocorticoid to Treat Neonatal Lung Injury with Limited Adverse Neurologic Effects
Academic Article Effect of Various Preterm Infant Milk Formulas on NEC-Like Gut Injury in Mice.

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