Obesity induces upregulation of genes involved in myocardial Ca2+ handling

Obesity is a complex multifactorial disorder that is often associated with cardiovascular diseases. Research on experimental models has suggested that cardiac dysfunction in obesity might be related to alterations in myocardial intracellular calcium (Ca2+) handling. However, information about the expression of Ca2+-related genes that lead to this abnormality is scarce. We evaluated the effects of obesity induced by a high-fat diet in the expression of Ca2+-related genes, focusing the L-type Ca2+ channel (Cacna1c), sarcolemmal Na+/Ca2+ exchanger (NCX), sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), ryanodine receptor (RyR2), and phospholamban (PLB) mRNA in rat myocardium. Male 30-day-old Wistar rats were fed a standard (control) or high-fat diet (obese) for 15 weeks. Obesity was defined as increased percent of body fat in carcass. The mRNA expression of Ca2+-related genes in the left ventricle was measured by RT-PCR. Compared with control rats, the obese rats had increased percent of body fat, area under the curve for glucose, and leptin and insulin plasma concentrations. Obesity also caused an increase in the levels of SERCA2a, RyR2 and PLB mRNA (P < 0.05) but did not modify the mRNA levels of Cacna1c and NCX. These findings show that obesity induced by high-fat diet causes cardiac upregulation of Ca2+ transport_related genes in the sarcoplasmic reticulum.

Detection of ATP2C1 gene mutation in familial benign chronic pemphigus / 华中科技大学学报（医学）（英德文版）

The ATP2C1 gene mutation in one case of familial benign chronic pemphigus was investigated. One patient was diagnosed as familial benign chronic pemphigus by pathology, ultrastructral examination and clinical features. Genomic DNA was extracted from blood samples. Mutation of ATP2C1 gene was detected by polymerase chain reaction (PCR) and DNA sequencing. The results showed that deletion mutation was detected in ATP2C1 gene in this patient, which was 2374delTTTG. No mutation was found in the family members and normal individuals. It was concluded that the 2374delTTTG mutation in ATP2C1 gene was the specific mutation for the clinical phenotype for this patient and was a de novo mutation.

Partial sequence analysis of a Plasmodium vivax cation transporting ATPase gene homologue & a putative pseudohomologue.

Molecular characterization of P. vivax is essential to develop suitable antimalarial drugs and vaccines. We describe here isolation and sequence analysis of a partial cDNA of a calcium ATPase as well as a putative pseudogene from this parasite. The immunoscreening of lambda gtll- P. vivax DNA library with patients serum has earlier resulted in the isolation of several seroreactive clones including Pv14. This clone contains a 299 bp insert having 18 amino acids (aa) reading frame fused with beta galactosidase. A larger fragment of approximately 15 kb was isolated from the EMBL3 library for Pv14 but it had only 2 extra aa in its reading frame. The far upstream region of Pv14 revealed a 101aa long putative open reading frame (ORF) showing homology to a variety of calcium ATPases in the M8 and M9 transmembrane region. But in the absence of a transcript in the parasite could indicate that it represents a pseudogene. However, the real gene for calcium ATPase in P. vivax was detected by RT-PCR using degenerate primers, designed from the conserved sequences of energy transduction and phosphorylation domains. The amplified cDNA-PCR product of 550 bp was cloned and sequenced which showed a significant aa homology to the calcium ATPase4 of P. falciparum. The present study, therefore, establishes the existence of calcium ion pumps in P. vivax which will be useful in drug development.