Candidate odorant-binding protein and chemosensory protein genes in the turnip aphid Lipaphis erysimi.

The turnip aphid, Lipaphis erysimi Kaltenbach, inflicts heavy damage on cruciferous crops worldwide. In these insects, olfactory perception is crucial for mating, host location, and oviposition. Both odorant-binding proteins (OBPs) and chemosensory proteins (CSPs) are responsible for the delivery of host odorants and pheromones during initial molecular interactions. In this study, antennal and body transcriptomes of L. erysimi were generated through the deep sequencing of RNA libraries. A dataset of 11 LeryOBP and four LeryCSP transcripts was identified among assembled unigenes and subjected to sequence analysis. Phylogenetic analysis found a one-to-one orthologous relationship between LeryOBP/LeryCSP and its corresponding homologs from other aphid species. Further quantitative real-time PCR analyses across developmental stages and tissues showed that five LeryOBP genes (i.e., LeryGOBP, LeryOBP6, LeryOBP7, LeryOBP9, and LeryOBP13) and LeryCSP10 were specifically or significantly elevated in the antennae compared with other tissues. Moreover, two transcripts (i.e., LeryGOBP and LeryOBP6) exhibited remarkably higher expression levels in alate aphids, implying their potentially functional role in the perception of new host plant locations. These results present the identification and expression of OBP/CSP genes in L. erysimi, providing valuable insights into their putative role in olfactory signal transduction.

Mogroside IIIE attenuates gestational diabetes mellitus through activating of AMPK signaling pathway in mice.

As one kind of complications of pregnancy, gestational diabetes mellitus (GDM) can influence the health of maternal-child in clinical practice. The C57 BL/KsJdb/+(db/+) mice, genetic GDM model, and C57 BL/KsJ+/+ (wild-type) mice were purchased and classified into three groups: normal pregnancy (C57 BL/KsJ+/+), GDM (C57 BL/KsJdb/+), and GDM plus Mogroside IIIE (20.0 mg/kg) group. GDM symptoms (maternal body weight, serum glucose, and insulin levels), glucose and insulin tolerance, and reproductive outcome (body weight at birth and litter size of offspring) were investigated. The inflammatory factors such as IL-1ß, IL-6, and TNF-α in the serum and the pancreas were detected by ELISA and qRT-PCR, while the expression of pAMPK, AMPK, pHDAC4, HDAC4, and G6Pase in the livers were analyzed by Western Blot. Mogroside IIIE greatly improved glucose metabolism, insulin tolerance, and reproductive outcome of the GDM mice. Moreover, Mogroside IIIE treatment significantly decreased inflammatory factors expression and relieved GDM symptoms through enhanced AMPK activation, inhibited HDAC4 expression, and reduced production of G6Pase. The alleviation of GDM by Mogroside IIIE was mediated by elevated AMPK activation, which in turn inhibited HDAC4 phosphorylation, and eventually down-regulated G6Pase expression and activity.

Deletion of GIT1 Impacts eNOS Activity To Aggravate sFlt-1-Induced Preeclampsia Phenotype in Mice.

Preeclampsia, a serious multisystem disorder specific to human pregnancy, remains a considerable burden of disease worldwide. Reduced nitric oxide bioavailability is proved to be crucial in the maternal and fetal pathophysiology of preeclampsia. G-protein-coupled Receptor Kinase Interactor-1 (GIT1) is a novel endothelial nitric oxide synthases (eNOS) interactor mediator. The aim of this paper is to investigate the effect of GIT1 on preeclampsia. Blood pressure (BP) was measured using a carotid catheter-calibrated eight-chamber tail-cuff system (CODA) at the same time daily. Urinary albumin excretion (UAE) was determined using Albuwell-M kits (Exocell Inc) and creatinine clearance (CCr) was determined by measuring urinary creatinine concentration with tandem liquid chromatography-mass spectrometry. The release of nitrite was analyzed to detect nitric oxide (NO) production using a Sievers Chemiluminescence NO Analyzer. NOS activity was examined by measuring the conversion of 3H-labeled l-arginine to 3H-labeled l-citrulline. BP was significantly increased in GIT1-/- mice with or without sFIT-1 treatment. In addition, GIT1-/- mice possessed higher UAE and lower CCr. Depletion of GIT1 impedes the NO production and placenta eNOS activity. Additional GIT1 attenuates sFlt-1-induced preeclampsia phenotypes. Our findings suggest that GIT1 significantly extenuates the sFlt-1-induced preeclampsia phenotypes by inhibiting eNOS activity, indicating a crucial role of GIT1 in the progression of preeclampsia.