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Abies Spectabilis (D. Don) G. Don (Syn. A. Webbiana Lindl.) Family: Coniferae
Published in L.D. Kapoor, Handbook of Ayurvedic Medicinal Plants, 2017
Chemical constituents — Nutmegs yield 5 to 15% of a volatile oil and also 30 to 40% of fat, photosterin, starch, amylodextrin, coloring matter, and a saponin.69 They yield about 3% of total ash and about 0.2% of acid-insoluble ash. Essential oil of mace is of a yellowish color with the odor of mace, and consists of macene. Mace (arillus) contains a volatile oil (8 to 17%), a fixed oil, resin, fat, sugar, destrin, and mucilage.
Chondrocyte protein co-synthesis network analysis links ECM mechanosensing to metabolic adaptation in osteoarthritis
Published in Expert Review of Proteomics, 2021
Aspasia Destouni, Konstantinos C. Tsolis, Anastassios Economou, Ioanna Papathanasiou, Charalampos Balis, Evanthia Mourmoura, Aspasia Tsezou
Indentation-type atomic force microscopy in biopsies from OA patients has revealed that the nano-stiffness of damaged cartilage is lower than the healthy non-degraded cartilage and that OA cartilage becomes softer due to progressive disintegration of the collagen meshwork [68]. The observed depletion of ECM and PCM structural components and the concurrent upregulation of CD44, a sensor of ECM integrity indicate a shift toward a low ECM adhesion microenvironment in OA [69]. In low ECM adhesion conditions, integrin signaling has been shown to be dampened and integrin-anchored actin filaments become shorter and fragmented [70]. We observed that key structural components of integrin activation and cytoskeleton remodeling such as, TLN, vinculin (VCL), Rho family GTPases RhoA and Rac1, as well as structural components of F-actin stress fibers and focal adhesions, actinin-α isoform 1 (ACTN1) cluster in the core chondrocyte network (Figure 3a). ACTN1 was found abundant in healthy and depleted in hypertrophic OA chondrocytes, whereas F-actin depolymerizing destrin (DSTN) was abundant in OA chondrocytes (Figure 3a) indicating increased actin remodeling in OA. Although the integrin activator and linker to actin filaments TLN1 is more abundant in OA, VCL which stabilizes the interaction between TLN and the actin cytoskeleton under high tension conditions was depleted in OA chondrocytes. These interactions indicate an adaptation of the ECM-focal adhesion interface to low ECM forces.
Quantitative proteomic analysis of trypsin-treated extracellular vesicles to identify the real-vesicular proteins
Published in Journal of Extracellular Vesicles, 2020
Dongsic Choi, Gyeongyun Go, Dae-Kyum Kim, Jaewook Lee, Seon-Min Park, Dolores Di Vizio, Yong Song Gho
Most of the candidate real-vesicular proteins were closely related in EV structure and biogenesis. For example, cytoskeletal proteins such as ACTG1 (Actin, cytoplasmic 2), ACTN4 (Alpha-actinin-4), PFN1 (Profilin-1), CFL1 (Cofilin-1), MSN (Moesin), KRT1 (Keratin, type II cytoskeletal 1), KRT9 (Keratin, type I cytoskeletal 9), KRT10 (Keratin, type I cytoskeletal 10), FLNA (Filamin-A), WDR1 (WD repeat-containing protein 1), COTL1 (Coactosin-like protein) and DSTN (Destrin) are involved in the actin cytoskeleton regulation. For example, cofilin-1 stimulates the generation of EVs via the regulation of actin cytoskeleton depolymerization activated by RhoA signalling [28]. Interestingly, our protein–protein interaction network analyses showed the intravesicular proteins derived from the cytosol are possibly inter-connected with other cytosolic proteins. Among them, 14-3-3 proteins (YWHAB, YWHAE, YWHAH, YWHAQ, YWHAZ and SFN), heat shock proteins (HSPA4, HSPA5, HSPA8 and HSP90AA1), GAPDH and CALM1 (Calmodulin-1) have lots of the interaction partners in EV proteome. It is known that these proteins play a role in intracellular protein trafficking responding to intracellular signalling [29–32], implying their involvement in the protein sorting into EVs. Besides cytoskeletal and cytosolic proteins, there were relatively small number of intravesicular proteins derived from the nucleus, endoplasmic reticulum and Golgi apparatus. However, ARF3 (ADP-ribosylation factor 3), ARF6 (ADP-ribosylation factor 6) and RAB proteins of Golgi apparatus are well known to contribute in intravesicular trafficking and the biogenesis processes of EVs [33,34].
Activated human astrocyte-derived extracellular vesicles modulate neuronal uptake, differentiation and firing
Published in Journal of Extracellular Vesicles, 2020
Yang You, Kathleen Borgmann, Venkata Viswanadh Edara, Satomi Stacy, Anuja Ghorpade, Tsuneya Ikezu
Recent evidence shows ADEVs shed in response to acute cellular stressors (e.g. IL-1β, TNF-α, LPS) impaired neurite development and weakened neuronal activity [9]. Notably, our examination of ADEVs on neuronal differentiation also found that IL-1β-ADEVs exerted detrimental effects on neurite development and neural activity. The small GTPases cluster enriched in IL-1β-ADEVs, which play an important role in cytoskeletal reorganization, signal transduction, cell invasion, cellular interaction and inflammation, may explain how ADEVs could modulate neuritogenesis and synaptogenesis [39]. For example, profilin 1 (PFN1), fascin actin-bundling protein 1 (FSCN1) and destrin (DSTN), which were highly expressed in IL-1β-ADEVs, regulate actin dynamics; disruption of which might lead to abnormal neuronal development [40–42]. The Ras homolog family member A (RhoA), which showed significant upregulation in IL-1β-ADEVs, inhibited axonal outgrowth following CNS injury and counteracted regeneration [43]. A recent study reported an increased RhoA activity, which caused altered cell migration and impaired neuritogenesis in human induced pluripotent stem cell-derived neural cells with PARK2 mutation [44]. RhoA is also known to inhibit the formation, growth, and maintenance of synaptic spines [45]. Another explanation is the enrichment of MHC proteins in IL-1β-ADEVs compared to CTL-ADEVs. Indeed, emerging evidence suggests an important non-immune role of MHC proteins in brain. Soluble forms of MHC-I (HLA-A, B, C) negatively regulated neurite outgrowth in the embryonic mouse retina [46]. MHC-I also disrupted the establishment of neuronal connections and reduced synapse density [47]. Thus, our findings from functional validations were consistent with interpretations of proteomic analyses. Further studies to identify the critical proteins in IL-1β-ADEV-mediated effects are warranted to identify novel targets to control ADEV functions particularly under pathophysiological conditions.