Project description:The critical role of the endothelium in governing vascular, tissues homeostasis and pathological processes is increasingly recognized (Deanfield et al., 2007). Cellular senescence of endothelial cells has been proposed to be involved in endothelial dysfunction and atherogenesis (Minamino T et al., 2007), although the mechanisms underlying the aging induced attenuation of endothelium dependent functions are yet to be clarified. Recent evidences implicated overall miRNA levels and miRNA in regulating angiogenesis and endothelial function (Suarez et al., 2007; Kuehbacher et al., 2007; Harris et al., 2008; Fish et al. 2008; Wang et al., 2008).
Project description:The vacuole occupies a large portion of plant cell volume, it is especially true to fruit tissues. Berry flesh cell vacuole serves as storage organelle for water, sugars, acids, secondary metabolites and others, which largely determining berry quality (Fontes et al., 2011a, b; Shiratake and Martinoia, 2007, Conde et al., 2006). However, the molecular basis of these compartmentation processes is still poorly understood. As in many species, the major bottle neck to study these aspects in grapevine is to obtain highly purified vacuoles with a good yield (Fontes et al., 2010). Up to date, several vacuole or tonoplast proteome researches were applied on a few plants mainly on Arabidopsis thaliana, vacuoles or tonoplast were derived from mesophyll cells (Carter et al., 2004, Endler et al., 2006, Schulze, et al., 2012) or cell culture (Jaquinod et al 2006, Shimaoka et al 2004), cauliflower buds (Schmidt et al., 2007) and sugar beet taproots (Jung et al., 2015). Though the grape berry protoplasts and intact vacuoles were successfully isolated from Cabernet Sauvignon berry suspension-cultured cells (Fontes et al., 2010), the vacuoles isolated from grape berry or different development and ripening stages of grape berry mesocarp tissues were not achieved.
Project description:Progenitor cell death and dermal papilla relocation during the regression phase of the hair growth cycle are essential for stem cell activation and follicle regeneration. This drastic follicle remodeling is coordinated by dermal sheath (DS) smooth muscle contraction, but how DS-generated forces are regulated is unknown. Here, we identify endothelin signaling - a potent vasoconstriction-regulating pathway - as the key activating mechanism of DS contraction. Pharmacological blocking or genetic ablation of both endothelin receptors, ETA and ETB, impedes DS contraction and halts follicle regression. Progenitors at the epithelial strand bottleneck are the main source of endothelin ligand ET-1, which is required for follicle regression. ET signaling in DS cells and downstream contraction is dynamically regulated by cytoplasmic Ca2+ levels via cell membrane and sarcoplasmic reticulum calcium channels. Together, these findings illuminate an epithelial-mesenchymal-interaction paradigm in which progenitors - before undergoing programmed cell death - control the contraction of the surrounding sheath smooth muscle to orchestrate homeostatic tissue regression and follicle reorganization.
Project description:We combined glycopeptide enrichment by N-glyco-FASP (Zielinska et al., 2010), SPEG (Tian et al., 2007) with a hydrophobic segment-oriented hpTC method (Vít et al 2016) and a standard “detergent and trypsin” approach into a tree-pronged “Pitchfork” strategy for the analysis of membrane proteome in high-risk human paraganglioma.
Project description:Mechanical stress is a potent regulator of cell growth, contractility and gene regulation. Abnormal uterine distension during pregnancy increases the risk of preterm birth and likely activates crosstalk between multiple signaling networks with protein phosphorylation playing a critical role. Telomerized human uterine smooth muscle cells were exposed to 18% biaxial stretch for 5 min and the phosphoproteome was probed by mass spectrometry. We observed specific phospho-activation of mitogen activated protein kinase at threonine 183 and tyrosine 185, myosin regulatory light chain 9 at threonine 19, and heat shock protein 27 at serine 82. Our analysis revealed protein phosphorylation changes in signaling pathways related to actin cytoskeleton remodeling, activation of the focal adhesion kinase pathway, smooth muscle contraction and mechanistic target of rapamycin activation. These data point to potential mechanistic links between stretch-induced phosphorylation and development of the contractile phenotype in myometrial cells.
Project description:Fusarium oxysporum is an worldwide economically important plant fungi pathogen that can cause vascular wilt disease on a wide variety of hosts (Williamson et al., 2007). In recent years, extensive research has been conducted to interpret transcriptional regulation of virulence genes in FO. (Weiberg et al., 2013;Brandhoff et al., 2017;Wang et al., 2017;Wang et al., 2018;Porquier et al., 2019). However, gaps in the protein level studies limited deeper understanding of molecular basis of FO. pathogenesis. In this study, we conducted the first proteome-wide analysis in FO.
Project description:This series includes microarrays from 36 patient samples and 2 cell-culture controls, used to optimize and validate the pathogen detection microarray (Wong, et. al. 2007) Keywords: viral pathogen detection
Project description:Adult Neurogenesis and Gene Expression Changes in 5-HT7 Receptor Knockout Mice: In the adult, the formation of new nerve cells in the CNS is restricted to the subependymal layer and to the subgranular zone of the hippocampus (Duman et al., 2001). Clinically adult neurogenesis has received most attention for its possible role in major depression. Depressed patients have reduced hippocampal neurogenesis (Kasper & McEwen, 2008) and hippocampal volume (Colla et al., 2007). It has also been shown that chronic, but not acute, treatment with currently widely used antidepressants, most notably fluoxetine, results in increased hippocampal neurogenesis (Malberg et al., 2000; Miller et al., 2007). Pharmacologically antidepressants act by elevating the amount of synaptic serotonin (5-HT) and they do that within minutes of administration, but the clinical effect is often delayed, sometimes for weeks (Miller et al., 2007). This delay is believed to involve changes in plasticity and neurogenesis. With currently available treatment options for depression 20% or more of patients do not respond to the therapy. Thus, there is a need for an increased understanding of the mechanism behind plasticity and neurogenesis, and for the development of improved therapies for depression.
Project description:miR-142-3p is highly expressed in peripheral blood mononuclear cells (PBMCs) and has been described as a hematopoietic-restricted lineage, suggesting immune functions (Chen, Li et al. 2004; Landgraf, Rusu et al. 2007; Merkerova, Belickova et al. 2008). In order to determine the roles of miR-142-3p in B lymphocytes, we over-expressed this miRNA in the Raji B-cell line using a synthetic mimic of miR-142-3p and analyzed gene expression 24 hours after the transfection.