Highly fluorescent and bioresorbable polymeric nanoparticles with enhanced photostability for cell imaging

Nanoscale ◽  
2015 ◽  
Vol 7 (3) ◽  
pp. 889-895 ◽  
Author(s):  
Shuo Huang ◽  
Shiying Liu ◽  
Kai Wang ◽  
Cangjie Yang ◽  
Yimin Luo ◽  
...  

Highly fluorescent and bioresorbable nanoparticles formed by well-defined synthetic polycaprolactones with di(thiophene-2-yl)-diketopyrrolopyrroles exhibited enhanced photostability in cell imaging and long-term tracing.

Author(s):  
Parisa Dehghani ◽  
Monireh Esameili Rad ◽  
Atefeh Zarepour ◽  
Ponnurengam Malliappan Sivakumar ◽  
Ali Zarrabi

: Diabetes mellitus (DM) is a type of chronic metabolic disease that has affected millions of people worldwide and is known with a defect in the amount of insulin secretion, insulin functions, or both. This deficiency leads to an increase in the amounts of glucose, which could be accompanied by long-term damages to other organs such as eyes, kidneys, heart, and nervous system. Thus, introducing an appropriate approach for diagnosis and treatment of different types of DM is the aim of several researches. By the emergence of nanotechnology and its application in medicine, new approaches were presented for these purposes. The object of this review article is to introduce different types of polymeric nanoparticles (PNPs), as one of the most important classes of nanoparticles, for diabetic management. To achieve this goal, at first, some of the conventional therapeutic and diagnostic methods of DM will be reviewed. Then, different types of PNPs, in two forms of natural and synthetic polymers with different properties, as a new method for DM treatment and diagnosis will be introduced. In the next section, the transport mechanisms of these types of nano-carriers across the epithelium, via paracellular and transcellular pathways will be explained. Finally, the clinical use of PNPs in the treatment and diagnosis of DM will be summarized. Based on the results of this literature review, PNPs could be considered one of the most promising methods for DM management.


2020 ◽  
Vol 3 (8) ◽  
pp. 5438-5445 ◽  
Author(s):  
Min Wang ◽  
Zilong Guo ◽  
Shiyong Teng ◽  
Zhenzhen Huang ◽  
Peng Zhang ◽  
...  

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 892-892
Author(s):  
Lucie Leveque ◽  
Therese Vu ◽  
Rachel D Kuns ◽  
Bianca E Teal ◽  
Mary Lor ◽  
...  

Abstract Hematopoiesis originates from a rare pool of hematopoietic stem cells (HSC) that are uniquely capable of both self-renewal and terminal differentiation into lineage-committed progenitor cells. Autophagy is a process of cytoplasmic protein recycling which maintains cellular homeostasis and protects the cell during periods of metabolic stress and nutrient deprivation and has an established role in the survival and function of immunological cells. Recent publications have linked autophagy with preservation of normal long term HSCs (LT-HSCs) during aging (Nature; 2013: 494:323-7). We therefore sought to determine the role of autophagy in LT-HSC function at homeostasis and during the clinically relevant stress of G-CSF-induced HSC mobilization. Using single cell imaging flow cytometry to monitor autophagosome formation in LC3-GFP transgenic mice (LC3-GFP punctae formation is a reporter of autophagy activity) we demonstrated autophagic activity in HSC populations but not in committed myeloid progenitors. In line with this, inhibition of autophagy degradation by chloroquine administration resulted in the accumulation of autophagy related protein p62 in purified HSCs compared to myeloid progenitors. To determine the contribution of autophagy to HSC development and function, we analyzed mice deficient in Atg5, a protein essential for autophagosome formation. Autophagy was not required for fetal liver (FL) HSC development, however, Atg5-/- FL HSCs showed mildly reduced long-term repopulating function in bone marrow (BM) transplantation assays (16 weeks peripheral blood (PB) engraftment Atg5-/- 83.45% vs. WT 93.10%, n=12, p<0.001). Importantly, Atg5-/- LT-HSCs (Lin-Sca-1+c-kit+Flk2-CD150+CD48-) were markedly reduced in congenic recipients compared to WT FL LT-HSCs (Atg5-/- 0.02% vs. WT 0.04%, n=11, p<0.001). Secondary competitive transplantation was used to determine the effect of autophagy loss on LT-HSC function in vivo. Atg5-/- LT-HSCs exhibited a profound impairment in the repopulation of secondary congenic recipients (Atg5-/-4.65% vs. WT 32.3%, n=5, p<0.01). Mechanistically, microarray analysis of purified LT-HSCs from Atg5-/- vs. WT FL chimeras demonstrated clear differences in gene expression by unsupervised hierarchical clustering. Differentially expressed genes included Cxcl12, Sdc2 and Apex1, regulators of HSC fate. Gene Ontology enrichment analysis demonstrated that autophagy deficient LT-HSCs had impaired metabolism, enhanced cellular differentiation, enforced proliferation and increased apoptosis. Validating these findings, there was a loss of quiescence in the Atg5-/- compared to WT LT-HSC (quiescent Atg5-/- 30% vs. WT 39%, n=16 p<0.05) and Atg5-/- FL HSCs exhibited enhanced apoptosis after culture in cytokine enriched media (Atg5-/-21.2% vs. WT 14.2%, n=5, p<0.01). Given the requirement for autophagy in homeostasis of LT-HSC and its role in proliferation and metabolic stress, we next investigated whether autophagy participated in the HSC response to G-CSF. G-CSF is commonly used to ameliorate neutropenia in patients treated with chemotherapy and is also used to mobilize HSCs for patients undergoing HSC transplantation. Using single cell imaging flow cytometry, autophagosome formation was enhanced in HSCs after 6 days of G-CSF mobilization (10mcg/day). G-CSF treatment efficiently mobilized PB neutrophils and colony forming units (CFU) in WT chimeras, however Atg5-/- chimeras showed a striking reduction in G-CSF-induced neutrophil (Atg5-/- 4.95 x106/mL vs. WT 10.46 x106/mL, n=20, p<0.0001) and PB CFU mobilization post-G-CSF (Atg5-/- 47/100µL vs. WT 126/100µL, n=5, p<0.01). BM CFU numbers were similar in Atg5-/- and WT FL chimeras both pre- and post-G-CSF mobilization. Atg5-/-neutrophils demonstrated increased apoptosis after G-CSF treatment suggesting that autophagy limits PB neutrophil survival, but not BM neutrophil development during G-CSF mobilization. These data demonstrate that autophagy is an active process in LT-HSCs and that genetic deletion of Atg5 results in the failure of adult LT-HSC maintenance and function. Autophagic activity is augmented by G-CSF-induced HSC stress and is required for G-CSF-induced HSC mobilization. These findings are particularly relevant to HSC transplantation and hematopoietic function in the context of a rapid rise in the clinical use of agents that have modulatory effects on autophagy. Disclosures: No relevant conflicts of interest to declare.


2017 ◽  
Author(s):  
Sarah Mues ◽  
Inga Lilge ◽  
Holger Schönherr ◽  
Björn Kemper ◽  
Jürgen Schnekenburger

Polymer ◽  
2017 ◽  
Vol 118 ◽  
pp. 75-84 ◽  
Author(s):  
Xing Wang ◽  
Yanyu Yang ◽  
Fei Yang ◽  
Hong Shen ◽  
Decheng Wu

2011 ◽  
Vol 17 (3) ◽  
pp. 440-445 ◽  
Author(s):  
Steffen Lorenz ◽  
Stephanie Tomcin ◽  
Volker Mailänder

AbstractLabeling of organelles for microscopy is achieved generally by specific dyes that either accumulate in a cellular compartment such as cyanine dyes in mitochondria or are only fluorescent under specific conditions such as the low pH in the lysosome. Here we demonstrate that Cy5—a fluorescent molecule that does not enter cells by itself—can be loaded into cells by attaching a short oligonucleotide. This very inexpensive labeling procedure can be done in the presence of serum. Therefore, very sensitive cell types should also be amenable to this procedure, and longer observations can be achieved compared to other commercially available dyes as the labeling reagent does not need to be washed out. This also points to the pitfall of using fluorescently labeled oligonucleotides for live cell imaging where the oligonucleotide is supposed to detect a specific target sequence in its subcellular distribution.


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