Anti-PVALB (native) polyclonal antibody

The contraction and relaxation events of the muscle is mediated by the coordination of many important calcium cycling proteins of ryanodine receptor (RYR), troponin C (TNNC), parvalbumin (PVALB), sarcoendoplasmic reticulum calcium transport ATPase (SERCA) and calsequestrin (CASQ). In higher vertebrates, the expression level of calcium cycling proteins are positively correlated to the muscle contraction/relaxation ability of the cell. In this study, we used RNAseq to explore the expression profile of calcium cycling genes between two marine fish of Bombay duck (Harpadon nehereus) and beltfish (Trichiurus lepturus) with poor and robust swimming activities, respectively. We have studied the hypothesis whether the expression level of calcium cycling proteins are also positive correlated to swimming ability in fish. We used Illumina sequencing technology (NextSeq500) to sequence, assemble and annotate the muscle transcriptome of Bombay duck for the first time. A total of 47,752,240 cleaned reads (deposited in NCBI SRA database with accession number of SRX1706379) were obtained from RNA sequencing and 26,288 unigenes (with N50 of 486 bp) were obtained after de novo assembling with Trinity software. BLASTX against NR, GO, KEGG and eggNOG databases show 100%, 65%, 26%, 94% and 88% annotation rate, respectively. Comparison of the dominantly expressed unigenes in fish muscle shows calcium cycling gene expression in beltfish (SRX1674471) is 1.4-to 51.6-fold higher than Bombay duck. Among five calcium cycling genes, the fold change results are very significant in CASQ (51.6 fold) and PVALB (9.1 fold) and both of them are responsive for calcium binding to reduce free calcium concentration in the sarcoendoplasmic reticulum and cytoplasm. In conclusion, we confirmed that the high abundant expression rate of calcium cycling genes in robust swimming fish species. The current muscle transcriptome and identified calcium cycling gene data can provide more insights into the muscle physiology of fish. (C) 2017 Published by Elsevier Inc.

Hypertension can originate from pre- and post-natal insults. High-fat (HF) diet and prenatal dexamethasone (DEX) exposure are both involved in hypertension of developmental origins We examined whether postnatal HF diet sex-specifically increases the vulnerability to prenatal DEX exposure-induced programmed hypertension in adult offspring. Additionally, we sought to identify candidate proteins involved in programmed hypertension through a mass spectrometry-based quantitative proteomic approach. Male and female offspring were studied separately: control, DEX, HF, and DEX + HF (n=8/group). Pregnant Sprague-Dawley rats received dexamethasone (0.1 mg/kg body weight) or vesicle from gestational day 16-22. Offspring received high-fat diet (D12331, Research Diets) or regular diet from weaning to 4 months of age. Rats were sacrificed at 4 months of age. We found that postnatal HF diet increased vulnerability of prenatal DEX-induced hypertension in male but not in female adult offspring Additionally, HF and DEX elicited renal programming in a sex-specific fashion. In males, DEX + HF increased renal parvalbumin (PVALB) and carbonic anhydrase III (CA III) protein levels. While prenatal DEX down-regulated PVALB and CA III protein abundance in female offspring kidneys. Moreover, DEX + HF increased renal protein level of type 3 sodium hydrogen exchanger (NHE3) in males but not in females. In conclusion, postnatal HF diet and prenatal DEX exposure synergistically induced programmed hypertension in male-only offspring. DEX + HF induced sex-specific alterations of protein profiles in offspring kidneys. By identifying candidate proteins underlying sex-specific mechanisms, our results could lead to novel offspring sex-specific interventions to prevent hypertension induced by antenatal corticosteroids and postnatal HF intake in both sexes. (C) 2018 Elsevier Inc. All rights reserved.