Biomedical subjects

Simran Kaur

Publications and source records attributed to Simran Kaur.

5 recordsLinked to original sources

PubMed2006

MicroRNA expression during chick embryo development.

MicroRNAs (miRNAs) are small, abundant, noncoding RNAs that modulate protein abundance by interfering with target mRNA translation or stability. miRNAs are detected in organisms from all domains and may regulate 30% of transcripts in vertebrates. Understanding miRNA function requires a detailed determination of expression, yet this has not been reported in an amniote species. High-throughput whole mount in situ hybridization was performed on chicken embryos to map expression of 135 miRNA genes including five miRNAs that had not been previously reported in chicken. Eighty-four miRNAs were detected before day 5 of embryogenesis, and 75 miRNAs showed differential expression. Whereas few miRNAs were expressed during formation of the primary germ layers, the number of miRNAs detected increased rapidly during organogenesis. Patterns highlighted cell-type, organ or structure-specific expression, localization within germ layers and their derivatives, and expression in multiple cell and tissue types and within sub-regions of structures and tissues. A novel group of miRNAs was highly expressed in most tissues but much reduced in one or a few organs, including the heart. This study presents the first comprehensive overview of miRNA expression in an amniote organism and provides an important foundation for investigations of miRNA gene regulation and function.

Animals↗

PubMed2004

Acidic duodenal pH alters gene expression in the cystic fibrosis mouse pancreas.

The duodenum is abnormally acidic in cystic fibrosis (CF) due to decreased bicarbonate ion secretion that is dependent on the CF gene product CFTR. In the CFTR null mouse, the acidic duodenum results in increased signaling from the intestine to the exocrine pancreas in an attempt to stimulate pancreatic bicarbonate ion secretion. Excess stimulation is proposed to add to the stress/inflammation of the pancreas in CF. DNA microarray analysis of the CF mouse revealed altered pancreatic gene expression characteristic of stress/inflammation. When the duodenal pH was corrected genetically (crossing CFTR null with gastrin null mice) or pharmacologically (use of the proton pump inhibitor omeprazole), expression levels of genes measured by quantitative RT-PCR were significantly normalized. It is concluded that the acidic duodenal pH in CF contributes to the stress on the exocrine pancreas and that normalizing duodenal pH reduces this stress.

Acids↗

PubMed2004

Inflammation of the cystic fibrosis mouse small intestine.

The CFTR null mouse [cystic fibrosis (CF) mouse] has a severe intestinal phenotype that serves as a model for CF-related growth deficiency, meconium ileus, and distal intestinal obstructive syndrome. DNA microarray analysis was used to investigate gene expression in the CF mouse small intestine. Sixty-one genes exhibited a statistically significant twofold or greater increase in expression, and 98 genes were downregulated twofold or greater. Of the upregulated genes, most were associated with inflammation and included markers for cells of the innate immune system (mast cells and neutrophils) and for acute-phase genes (serum amyloid A and complement factors). The downregulated genes include 10 cytochrome P-450 genes; several are involved in lipid metabolism, and several are involved in various transport processes. Confirmation by quantitative RT-PCR showed gene expression was significantly increased for mast cell protease 2 (27-fold), hematopoietic cell transcript 1 (17-fold), serum amyloid A3 (2.9-fold), suppressor of cytokine signaling 3 (2.0-fold), leucine-rich alpha(2)-glycoprotein (21-fold), resistin-like molecule-beta (49-fold), and Muclin (2.5-fold) and was significantly decreased for cytochrome P-450 4a10 (28-fold) and cubilin (114-fold). Immune cell infiltration was confirmed histologically by staining for mast cells and neutrophils. These data demonstrate that the CF intestine exhibits an inflammatory state with upregulation of components of the innate immune system.

Animals↗

PubMed2003

Decreased gastric bacterial killing and up-regulation of protective genes in small intestine in gastrin-deficient mouse.

Gastrin regulates gastric acid secretion, believed to be primarily responsible for killing ingested microbes. We examined gastric killing of gavaged E. coli in gastrin-deficient mice, which have decreased gastric acid production. Additionally, the expression of intestinal genes involved in epithelial protection were analyzed: the mucus layer glycoprotein muclin, the polymeric Ig receptor, trefoil factor 3, and small proline-rich protein 2a (sprr2a). Gastric pH was 2.5 pH units greater in gastrin-deficient mice, and E. coli survival was increased greater than 20-fold at 10 min after gavage compared to control. Muclin and sprr2a gene expression were significantly increased (2.0- and 2.6-fold) in the intestine, and antibiotic treatment reversed these effects. In conclusion, reduced gastric acid secretion results in increased survival of ingested microorganisms in gastrin-deficient mice. Bacterial survival is associated with increased expression of muclin and sprr2a in the intestine, indicating that these genes play protective roles in the intestine.

Animals↗

PubMed2002

Surfactant protein-A in lung lavage fluid obtained from patients with idiopathic pulmonary fibrosis.

BACKGROUND: Alterations in surface-active material may contribute to the pathogenesis of idiopathic pulmonary fibrosis both by increasing the elastic recoil due to surface forces and by promoting alveolar collapse. This study intends to evaluate the surfactant protein-A levels in bronchoalveolar lavage in patients of idiopathic pulmonary fibrosis. MATERIAL AND METHODS: Ten patients of idiopathic pulmonary fibrosis (IPF) of either sex were taken up for estimation of surfactant protein-A (SP-A) levels in bronchoalveolar lavage. The final diagnosis of IPF was based on histopathology and high resolution CT. Ten controls were taken out of which five patients were histopathologically proven cases of sarcoidosis and five patients with normal chest X-ray and CT scan. History, physical examination and routine investigations were done to rule out any concomitant illness. RESULTS: Age range of patients varied from 37-65 years (mean +/- SD of 50.65 +/- 9.05) and controls 30-62 years (42.50 +/- 9.95). Fiberoptic bronchoscopy and bronchoalveolar lavage was carried out and fluid aspirated was studied for surfactant protein-A. The level of surfactant protein-A recovered was lower in patients with idiopathic pulmonary fibrosis in comparison to control group p < 0.01 (1.86 +/- 1.26 and 5.76 +/- 2.0 microg/ml respectively). The levels of surfactant protein-A also revealed that the level decreased with derangement of pulmonary function. CONCLUSIONS: The study thus showed that the level of surfactant protein A is reduced in patients with idiopathic pulmonary fibrosis. It is likely that they have a significant role in pathogenesis of idiopathic pulmonary fibrosis and its progression. Surfactant-A may have important therapeutic implications. Further studies are required for a definite answer.

Adult↗