Apoptosis-mediated vasa down-regulation controls developmental transformation in Japanese Copidosoma floridanum female soldiers.

Copidosoma floridanum is a polyembryonic, caste-forming, wasp species. The ratio of investment in different castes changes with environmental stressors (e.g. multi-parasitism with competitors). The vasa gene was first identified in Drosophila melanogaster as a germ-cell-determining factor, and C. floridanum vasa (Cf-vas) gene positive cells have been known to develop into reproductive larvae. Cf-vas seems to control the ratio of investment in C. floridanum larval castes. In this study, we identified environmental factors that control Cf-vas mRNA expression in Japanese C. floridanum by examining Cf-vas mRNA expression under competitor (Meteorus pulchricornis) venom stress; we treated the male and female morulae with M. pulchricornis venom. We also assessed the effects of multi-parasitism of Japanese C. floridanum with M. pulchricornis and found an increasing number of female soldier larvae. The results showed that several amino acid sequences differ between the Japanese and US Cf-vas. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) showed that Japanese Cf-vas mRNA is expressed in both male and female larvae and pupae, but mRNA expression decreases in adults. Cf-vas mRNA expression significantly decreased, while C. floridanum dronc (Cf-dronc) mRNA expression increased, in female morulae after M. pulchricornis venom treatment at 20 h and 0 h of the culture period, respectively. Females and males showed different Cf-vas or Cf-dronc mRNA expression after M. pulchricornis venom treatment. Therefore, M. pulchricornis venom could affect the ratio of investment in different female castes of Japanese C. floridanum by decreasing Cf-vas mRNA expression via apoptosis.

Dietary capsaicin-mediated attenuation of hypertension in a rat model of renovascular hypertension.

Background: Capsaicin, a pungent component of chili pepper, has been reported to decrease blood pressure (BP) and to cause vasorelaxation via nitric oxide (NO) production. However, it is still unclear how dietary capsaicin effects on renovascular hypertension. To examine this, we observed the effects of dietary capsaicin on BP in 2-kidney, 1-clip renovascular hypertension (2K1C) rats, and investigated the participation of NO in the mechanism.Methods: Rats with 2K1C or sham-operated rats (SHAM) were treated with 0.006% capsaicin diet (CAP) or control diet (CTL) for 6 weeks. Systolic BP (SBP) was measured by tail-cuff method once a week. In the end, mean arterial BP (MAP) was measured in the rats under anesthesia. These observations were performed also in the rats taking a NO synthase (NOS) inhibitor (LN). After rats were euthanized, thoracic aortas were collected and used for western blot analyses to evaluate the phosphorylated ratio of endothelial NOS (eNOS), protein kinase A (PKA) and B (Akt), in order to explore a mechanism of the effects on BP by dietary capsaicin.Results: SBP and MAP in 2K1C rats were significantly higher than in SHAM rats when fed CTL, but not when fed CAP. Those in 2K1C-CAP rats were significantly lower than in 2K1C-CTL rats. LN suppressed the effect of dietary capsaicin. The ratios of phosphorylated (p-) eNOS/eNOS and p-Akt/Akt, but not p-PKA/PKA, were significantly increased in rats fed CAP compared with rats fed CTL.Conclusion: Dietary capsaicin may alleviate 2K1C renovascular hypertension, probably via enhancing phosphorylation of Akt and eNOS.Abbreviations: 2K1C: 2-kidney, 1-clip hypertension model; Akt: protein kinase B; Ang II: angiotensin II; ANOVA: measures analysis of variance; BP: blood pressure; EC: endothelial cell; eNOS: endothelial nitric oxide synthase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; L-NAME, LN: Nω-Nitro-L-arginine methyl ester hydrochloride; MA: mesenteric arteries; MAP: mean arterial blood pressure; NO: nitric oxide; PKA: protein kinase A; PVDF: polyvinylidene difluoride; SBP: Systolic blood pressure; SHR: spontaneously hypertensive rats; SN: sympathetic nervous; TRPV1: transient receptor potential vanilloid type 1; WKY: Wistar Kyoto rats.