scholarly journals Gd loading by hypotonic swelling: an efficient and safe route for cellular labeling

2013 ◽  
Vol 8 (6) ◽  
pp. 475-486 ◽  
Author(s):  
Enza Di Gregorio ◽  
Giuseppe Ferrauto ◽  
Eliana Gianolio ◽  
Silvio Aime
Keyword(s):  
Cellular Labeling ◽  
Hypotonic Swelling

scholarly journals Mesenchymal Stem Cells Do Not Lose Direct Labels Including Iron Oxide Nanoparticles and DFO-89Zr Chelates through Secretion of Extracellular Vesicles

Membranes ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 484
Author(s):  
Yue Gao ◽  
Anna Jablonska ◽  
Chengyan Chu ◽  
Piotr Walczak ◽  
Miroslaw Janowski
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Iron Oxide ◽  
Iron Oxide Nanoparticles ◽  
Extracellular Vesicles ◽  
Superparamagnetic Iron Oxide ◽  
Cell Labeling ◽  
Oxide Nanoparticles ◽  
Stem Cell Delivery ◽  
Cellular Labeling

Rapidly ageing populations are beset by tissue wear and damage. Stem cell-based regenerative medicine is considered a solution. Years of research point to two important aspects: (1) the use of cellular imaging to achieve sufficient precision of therapeutic intervention, and the fact that (2) many therapeutic actions are executed through extracellular vesicles (EV), released by stem cells. Therefore, there is an urgent need to interrogate cellular labels in the context of EV release. We studied clinically applicable cellular labels: superparamagnetic iron oxide nanoparticles (SPION), and radionuclide detectable by two main imaging modalities: MRI and PET. We have demonstrated effective stem cell labeling using both labels. Then, we obtained EVs from cell cultures and tested for the presence of cellular labels. We did not find either magnetic or radioactive labels in EVs. Therefore, we report that stem cells do not lose labels in released EVs, which indicates the reliability of stem cell magnetic and radioactive labeling, and that there is no interference of labels with EV content. In conclusion, we observed that direct cellular labeling seems to be an attractive approach to monitoring stem cell delivery, and that, importantly, labels neither locate in EVs nor affect their basic properties.

scholarly journals Synthesis and cellular labeling of multifunctional phosphatidylinositol bis‐ and trisphosphate derivatives

2021 ◽  
Author(s):  
Rainer Mueller ◽  
Ana Kojic ◽  
Mevlut Citir ◽  
Carsten Schultz
Keyword(s):  
Cellular Labeling

Curauá-derived carbon dots: Fluorescent probes for effective Fe(III) ion detection, cellular labeling and bioimaging

2021 ◽  
pp. 112409
Author(s):  
Sebastian Raja ◽  
Eva Miriam Buhl ◽  
Stephan Dreschers ◽  
Carmen Schalla ◽  
Martin Zenke ◽  
...  
Keyword(s):  
Fluorescent Probes ◽  
Carbon Dots ◽  
Ion Detection ◽  
Cellular Labeling

Secondary regulatory volume increase conferred on Xenopus oocytes by expression of AE2 anion exchanger

1997 ◽  
Vol 272 (1) ◽  
pp. C191-C202 ◽  
Author(s):  
L. Jiang ◽  
M. N. Chernova ◽  
S. L. Alper
Keyword(s):  
Volume Regulation ◽  
Xenopus Oocytes ◽  
Disulfonic Acid ◽  
Functional Coupling ◽  
Intrinsic Volume ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Hypertonic Stimulation ◽  
Shrinkage Prior ◽  
Hypotonic Swelling

Xenopus oocytes lack volume regulation and Cl/anion-exchange (AE) activity but express endogenous Na+/H+ exchange (NHE). We postulated that expression in oocytes of heterologous anion exchangers might allow regulatory volume increase (RVI) via functional coupling with endogenous NHE. Expression of neither erythroid nor kidney isoforms of AE1 conferred any form of RVI. In contrast, although AE2 expression did not confer primary RVI, it did confer on oocytes secondary RVI, with a requirement for hypotonic swelling before hypertonic shrinkage. This secondary RVI required extracellular Cl- and Na+, was blocked by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and amiloride, was bumetanide insensitive, and was blocked by prevention of intracellular alkalinization, all properties consistent with functional coupling of AE2-mediated Cl-/HCO3- exchange and endogenous NHE. RVI was unaffected by CO2-HCO3- or by partial oocyte Cl- depletion and was unrelated to the rate of oocyte shrinkage. Prior hypotonic swelling did not significantly alter subsequent hypertonic stimulation of AE2-mediated 36Cl influx or efflux. We conclude that heterologous AE2 expression suffices to confer volume regulation on Xenopus oocytes that lack intrinsic volume-regulatory mechanisms.

scholarly journals Cellular labeling with Gd(III) chelates: only high thermodynamic stabilities prevent the cells acting as ‘sponges’ of Gd3+ ions

2006 ◽  
Vol 1 (1) ◽  
pp. 23-29 ◽  
Author(s):  
C. Cabella ◽  
S. Geninatti Crich ◽  
D. Corpillo ◽  
A. Barge ◽  
C. Ghirelli ◽  
...  
Keyword(s):  
Cellular Labeling

Abstract 99: Hypotonic Swelling Promotes Nitric Oxide Release in Cardiac Ventricular Myocytes

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Luis Gonano ◽  
Malena Morell ◽  
Juan I Burgos ◽  
Martin Vila Petroff
Keyword(s):  
Nitric Oxide ◽  
Cardiac Myocytes ◽  
Cardiac Myocyte ◽  
Contractile Function ◽  
Cell Swelling ◽  
Contractile Dysfunction ◽  
Ischemia And Reperfusion ◽  
Hypotonic Solution ◽  
No Release ◽  
Hypotonic Swelling

Cardiac myocyte swelling occurs in multiple pathological situations and in particular contributes to the deleterious effects of ischemia and reperfusion by promoting contractile dysfunction. We investigated whether hypotonic swelling promotes nitric oxide (NO) release in cardiac myocytes and if so, whether it impacts on swelling induced contractile dysfunction. Perfusing rat cardiac myocytes, loaded with the NO sensor DAF-FM, with a hypotonic solution (HS; 217 mOsm), increased cell volume, reduced myocyte contraction and Ca2+ transient amplitude and significantly increased DAF-FM fluorescence. When cells were exposed to the HS supplemented with 2.5 mM of the NO synthase inhibitor L-NAME, cell swelling occurred in the absence of NO release. Swelling-induced NO release was also prevented by the NOS1 inhibitor, Nitroguanidine. In addition, Colchicine (an inhibitor of microtubule polymerization) prevented the increase in DAF-FM fluorescence induced by HS indicating that microtubule integrity is necessary for swelling-induced NO release. The swelling-induced negative inotropic effect was exacerbated in the presence of either L-NAME, Nitroguandine or the guanylate cyclase inhibitor, ODQ, suggesting that NOS1-derived NO provides contractile support via a GMP-dependent mechanism. Indeed, ODQ reduced Ca2+ wave velocity and the HS-induced increment in ryanodine receptor (RyR2) phosphorylation at site Ser2808 suggesting that in the context of hypotonic swelling, cGMP may contribute to preserve contractile function by enhancing SR Ca2+ release. Our findings suggest a novel mechanism for NO release in cardiac myocytes with putative pathophysiological relevance in the context of ischemia and reperfusion, where it may be cardioprotective by reducing the extent of contractile dysfunction associated with hypotonic swelling.

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