Mouse Pla2g2a(Phospholipase A2, membrane associated) ELISA Kit

Obesity, type 2 diabetes, and cardiovascular disease correlate with infiltration to adipose tissue of different immune cells, with uncertain influences on metabolism. Rats were fed a diet high in carbohydrates and saturated fats to develop diet-induced obesity over 16 weeks. This nutritional overload caused overexpression and secretion of phospholipase A(2) group IIA (pla2g2a) from immune cells in adipose tissue rather than adipocytes, whereas expression of adipose-specific phospholipase A(2) (pla2g16) was unchanged. These immune cells produce prostaglandin E-2 (PGE(2)), which influences adipocyte signaling. We found that a selective inhibitor of human pla2g2a (5-(4-benzyloxyphenyl)-(4S)-(phenyl-heptanoylamino)pentanoic acid [KH064]) attenuated secretion of PGE(2) from human immune cells stimulated with the fatty acid, palmitic acid, or with lipopolysaccharide. Oral administration of KH064 (5 mg/kg/day) to rats fed the high-carbohydrate, high-fat diet prevented the overexpression of pla2g2a and the increased macrophage infiltration and elevated PGE(2) concentrations in adipose tissue. The treatment also attenuated visceral adiposity and reversed most characteristics of metabolic syndrome, producing marked improvements in insulin sensitivity, glucose intolerance, and cardiovascular abnormalities. We suggest that pla2g2a may have a causal relationship with chronic adiposity and metabolic syndrome and that its inhibition in vivo may be a valuable new approach to treat obesity, type 2 diabetes, and metabolic dysfunction in humans. Diabetes 61:2320-2329, 2012

Introduction: Small-cell variant of RO is a rare subtype of renal tumor that can be easily misdiagnosed. To date, only 20 cases had been reported, with its genetic alterations largely unknown due to insufficient information. Materials and methods: We report a case of the tumor with genetic characterization using exome sequencing chip. We also reviewed literature on this lesion to summarize clinicopathological presentation and differential diagnosis of the tumor. Discussion: Grossly, the tumor is yellow to grayish brown, with clear boundary, central scar, or cystic degeneration. Microscopically, small-cell variant RO show scant eosinophilic cytoplasm with small-round nuclei, arranged in small acini and tubules. Nucleoli and necrosis are rarely observed. Immunohistochemically, the tumor is positive for EMA, cytokeratin 18, CD117 and E-cadherin. Genetically, 4745 differentially expressed genes in this tumor, which encode tricarboxylic acid cycle enzymes and are involved in mitochondria] respiratory chain. This result strongly supports the diagnosis of small cell variant of RO. Findings from the molecular genetic analysis of our case suggests that metabolic pathway-related genes (PIK3R5, PI3KCB, PLA2G4E, PLA2G2A, PLA2G6, PLCB4, PLCG2) may be exploited as potential targets for diagnosis and treatment when necessary. These genes may provide new clues for future research. Conclusion: Small-cell variant of RO is considered benign renal neoplasms with good prognosis. A histochemical and immunohistochemical stains assist in diagnosis of this tumor. Definitive diagnosis can help avoid unnecessary total renal nephrectomy. The exact mechanism of Small-cell variant of RO remains to be further investigated.