isolation-culture-adipogenic-induction-neural-crest-original-adipose

Isolation, Culture, and Adipogenic Induction of Neural Crest Original Adipose-Derived Stem Cells from Periaortic Adipose Tissue

An excessive amount of adipose tissue surrounding the blood vessels (perivascular adipose tissue, also known as PVAT) is associated with a high risk of ...

Chinese Academy of Sciences

In order to investigate the defect effect on photocatalytic performance of the visible light photocatalyst, Zn-Cd-S solid solution with surface defects is prepared in the hydrazine hydrate. X-ray photoelectron spectra and photoluminescence results confirm the existence of defects, such as sulfur vacancies, interstitial metal, and Zn and Cd in the low valence state on the top surface of solid solutions. The surface defects can be effectively removed by treating with sulfur vapor. The solid solution with surface defect exhibits a narrower band gap, wider light absorption range, and better photocatalytic perfomance. The optimized solid solution with defects exhibits 571 μmol h(-1) for 50 mg photocatalyst without loading Pt as cocatalyst under visible light irradiation, which is fourfold better than that of sulfur vapor treated samples. The wavelength dependence of photocatalytic activity discloses that the enhancement happens at each wavelength within the whole absorption range. The theoretical calculation shows that the surface defects induce the conduction band minimum and valence band maximum shift downward and upward, respectively. This constructs a type I junction between bulk and surface of solid solution, which promotes the migration of photogenerated charges toward the surface of nanostructure and leads to enhanced photocatalytic activity. Thus a new method to construct highly efficient visible light photocatalysts is opened. 

Surface Defects Enhanced Visible Light Photocatalytic H2 Production for Zn-Cd-S Solid Solution.

It is highly desirable and a great challenge for red light emission of carbon dots under long wavelength excitation. Here, we developed a facile route to synthesize carbon dots with red emission due to the doping effect of S and N elements, borrowing from the concept of the semiconductor. The maximum emission locates at 594 nm under 560 nm excitation. The absolute photoluminescence (PL) quantum yield (QY) is as high as 29% and 22% in ethanol and water, respectively. XPS and FTIR spectra illustrated that there exist -SCN and -COOH groups on the surface of the carbon dots. They endow the carbon dots with high sensitivity for ion detection of Fe. The quenched PL emission of Fe-S,N-CDs can be recovered by adding ascorbic acid to release the -COOH and -SCN group due to Fe formation in the presence of ascorbic acid. High PL QY of red emission is beneficial to application in bioimaging. Doxorubicin was loaded onto carbon dots through π-π stacking to form a theranostic agent. When the CD-Dox was injected into the tumor site, a strong PL emission was observed. The PL intensity indicates the concentration of the theranostic agent. After 7 times injection, both the tumor size and weight clearly decrease. The results demonstrate that the S,N-CDs are a potentially excellent bioimaging component in the theranostic field.

Red Emissive Sulfur, Nitrogen Codoped Carbon Dots and Their Application in Ion Detection and Theraonostics.

The mechanisms that promote the generation of new coronary vasculature during cardiac homeostasis and after injury remain a fundamental and clinically important area of study in the cardiovascular field. Recently, it was reported that mesenchymal-to-endothelial transition (MEndoT) contributes to substantial numbers of coronary endothelial cells after myocardial infarction. Therefore, the MEndoT has been proposed as a paradigm mediating neovascularization and is considered a promising therapeutic target in cardiac regeneration. Here, we show that preexisting endothelial cells mainly beget new coronary vessels in the adult mouse heart, with essentially no contribution from other cell sources through cell-lineage transdifferentiation. Genetic-lineage tracing revealed that cardiac fibroblasts expand substantially after injury, but do not contribute to the formation of new coronary blood vessels, indicating no contribution of MEndoT to neovascularization. Moreover, genetic-lineage tracing with a pulse-chase labeling strategy also showed that essentially all new coronary vessels in the injured heart are derived from preexisting endothelial cells, but not from other cell lineages. These data indicate that therapeutic strategies for inducing neovascularization should not be based on targeting presumptive lineage transdifferentiation such as MEndoT. Instead, preexisting endothelial cells appear more likely to be the therapeutic target for promoting neovascularization and driving heart regeneration after injury.

Preexisting endothelial cells mediate cardiac neovascularization after injury.

Correction to Red Emissive Sulfur, Nitrogen Codoped Carbon Dots and Their Application in Ion Detection and Theranostics.

Myasthenia gravis is an autoimmune disorder of the neuromuscular junction manifested as fatigable muscle weakness, which is typically caused by pathogenic autoantibodies against postsynaptic CHRN/AChR (cholinergic receptor nicotinic) in the endplate of skeletal muscle. Our previous studies have identified CA3 (carbonic anhydrase 3) as a specific protein insufficient in skeletal muscle from myasthenia gravis patients. In this study, we investigated the underlying mechanism of how CA3 insufficiency might contribute to myasthenia gravis. Using an experimental autoimmune myasthenia gravis animal model and the skeletal muscle cell C2C12, we find that inhibition of CAR3 (the mouse homolog of CA3) promotes CHRN internalization via a lipid raft-mediated pathway, leading to accelerated degradation of postsynaptic CHRN. Activation of CAR3 reduces CHRN degradation by suppressing receptor endocytosis. CAR3 exerts this effect by suppressing chaperone-assisted selective autophagy via interaction with BAG3 (BCL2-associated athanogene 3) and by dampening endoplasmic reticulum stress. Collectively, our study illustrates that skeletal muscle cell CAR3 is critical for CHRN homeostasis in the neuromuscular junction, and its deficiency leads to accelerated degradation of CHRN and development of myasthenia gravis, potentially revealing a novel therapeutic approach for this disorder.

Suppression of CHRN endocytosis by carbonic anhydrase CAR3 in the pathogenesis of myasthenia gravis.

Multiple-color-emissive carbon dots (CDots) have potential applications in various fields such as bioimaging, light-emitting devices, and photocatalysis. The majority of the current CDots to date exhibit excitation-wavelength-dependent emissions with their maximum emission limited at the blue-light region. Here, a synthesis of multiple-color-emission CDots by controlled graphitization and surface function is reported. The CDots are synthesized through controlled thermal pyrolysis of citric acid and urea. By regulating the thermal-pyrolysis temperature and ratio of reactants, the maximum emission of the resulting CDots gradually shifts from blue to red light, covering the entire light spectrum. Specifically, the emission position of the CDots can be tuned from 430 to 630 nm through controlling the extent of graphitization and the amount of surface functional groups, COOH. The relative photoluminescence quantum yields of the CDots with blue, green, and red emission reach up to 52.6%, 35.1%, and 12.9%, respectively. Furthermore, it is demonstrated that the CDots can be uniformly dispersed into epoxy resins and be fabricated as transparent CDots/epoxy composites for multiple-color- and white-light-emitting devices. This research opens a door for developing low-cost CDots as alternative phosphors for light-emitting devices.

Synthesis of Carbon Dots with Multiple Color Emission by Controlled Graphitization and Surface Functionalization.

Noncanonical NF-κB pathway is essential for the B cell activation and antibody production, which centralize the critical role of B cells in regulating the pathogenesis of systemic lupus erythematosus (SLE). We have previously demonstrated that Pellino1 (Peli1) negatively regulates noncanonical NF-κB activation and lupus autoimmunity. Here, we showed that poly IC is a potent inducer of Peli1 protein in mouse splenic B cells in dose- and time-dependent manners, and poly IC-induced Peli1 protein dramatically suppressed the activation of noncanonical NF-κB pathway. In addition, poly IC-pretreated B cells failed to induce lupus-like disease in BM12 CD4+ T cell-immunized mice. Accordingly, the induction of antibody-producing plasma cells and germinal center B cells, as well as the production of autoantibodies were significantly impaired in immunized μMT mice that were transferred with poly IC-pretreated B cells. Our findings demonstrate that poly IC-induced Peli1 negatively regulates the noncanonical NF-κB pathway in the context of restraining the pathogenesis of lupus-like disease.

Article	Year
Surface Defects Enhanced Visible Light Photocatalytic H2 Production for Zn-Cd-S Solid Solution. Small (Weinheim an der Bergstrasse, Germany)\| PubMed ID: 26691211	2016
Red Emissive Sulfur, Nitrogen Codoped Carbon Dots and Their Application in Ion Detection and Theraonostics. ACS applied materials & interfaces\| PubMed ID: 28508626	2017
Preexisting endothelial cells mediate cardiac neovascularization after injury. The Journal of clinical investigation\| PubMed ID: 28650345	2017
Correction to Red Emissive Sulfur, Nitrogen Codoped Carbon Dots and Their Application in Ion Detection and Theranostics. ACS applied materials & interfaces\| PubMed ID: 28714665	2017
Suppression of CHRN endocytosis by carbonic anhydrase CAR3 in the pathogenesis of myasthenia gravis. Autophagy\| PubMed ID: 28933591	2017
Synthesis of Carbon Dots with Multiple Color Emission by Controlled Graphitization and Surface Functionalization. Advanced materials (Deerfield Beach, Fla.)\| PubMed ID: 29178388	2018
Poly IC pretreatment suppresses B cell-mediated lupus-like autoimmunity through induction of Peli1. Acta biochimica et biophysica Sinica\| PubMed ID: 30032173	2018

Xiang Miao

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