Spatial Trans-Epithelial Electrical Resistance (S-TEER) Integrated in Organs-on-Chips

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Noa Renous ◽  
Mark Dan Kiri ◽  
Ronny Aharon Barnea ◽  
Rossana Rauti ◽  
Yael Leichtamnn-Bardoogo ◽  
...  

Transepithelial/transendothelial electrical resistance (TEER) is a label-free assay that is commonly used to assess tissue barrier integrity. TEER measurement systems have been embedded in Organ-on-a-Chip devices to provide live readouts...

2021 ◽  
Vol 334 ◽  
pp. 129599
Author(s):  
Maider Badiola-Mateos ◽  
Davide Di Giuseppe ◽  
Roberto Paoli ◽  
Maria Jose Lopez-Martinez ◽  
Arianna Mencattini ◽  
...  

2021 ◽  
Vol 141 (7) ◽  
pp. 237-244
Author(s):  
Takashi Miyazaki ◽  
Yoshikazu Hirai ◽  
Ken-ichiro Kamei ◽  
Toshiyuki Tsuchiya ◽  
Osamu Tabata

2001 ◽  
Vol 281 (3) ◽  
pp. L565-L574 ◽  
Author(s):  
Alexander D. Verin ◽  
Anna Birukova ◽  
Peiyi Wang ◽  
Feng Liu ◽  
Patrice Becker ◽  
...  

Endothelial cell (EC) barrier regulation is critically dependent on cytoskeletal components (microfilaments and microtubules). Because several edemagenic agents induce actomyosin-driven EC contraction tightly linked to myosin light chain (MLC) phosphorylation and microfilament reorganization, we examined the role of microtubule components in bovine EC barrier regulation. Nocodazole or vinblastine, inhibitors of microtubule polymerization, significantly decreased transendothelial electrical resistance in a dose-dependent manner, whereas pretreatment with the microtubule stabilizer paclitaxel significantly attenuated this effect. Decreases in transendothelial electrical resistance induced by microtubule disruption correlated with increases in lung permeability in isolated ferret lung preparations as well as with increases in EC stress fiber content and MLC phosphorylation. The increases in MLC phosphorylation were attributed to decreases in myosin-specific phosphatase activity without significant increases in MLC kinase activity and were attenuated by paclitaxel or by several strategies (C3 exotoxin, toxin B, Rho kinase inhibition) to inhibit Rho GTPase. Together, these results suggest that microtubule disruption initiates specific signaling pathways that cross talk with microfilament networks, resulting in Rho-mediated EC contractility and barrier dysfunction.


RSC Advances ◽  
2015 ◽  
Vol 5 (49) ◽  
pp. 39245-39251 ◽  
Author(s):  
Jingfeng Huang ◽  
Hu Chen ◽  
Wenbin Niu ◽  
Derrick W. H. Fam ◽  
Alagappan Palaniappan ◽  
...  

Reduced graphene oxide can be used as a sensitive label-free sensor transducer for detection of Interleukin-6 proteins, by overcoming the variable coverage and high electrical resistance, via ethanol Chemical Vapour Deposition (CVD).


Molecules ◽  
2021 ◽  
Vol 26 (21) ◽  
pp. 6382
Author(s):  
Megumi Watanabe ◽  
Yosuke Ida ◽  
Masato Furuhashi ◽  
Yuri Tsugeno ◽  
Fumihito Hikage ◽  
...  

Effects of a pan-ROCK-inhibitor, ripasudil (Rip), and a ROCK2 inhibitor, KD025 on dexamethasone (DEX)-treated human trabecular meshwork (HTM) cells as a model of steroid-induced glaucoma were investigated. In the presence of Rip or KD025, DEX-treated HTM cells were subjected to permeability analysis of 2D monolayer by transendothelial electrical resistance (TEER) and FITC–dextran permeability, physical properties, size and stiffness analysis (3D), and qPCR of extracellular matrix (ECM), and their modulators. DEX resulted in a significant increase in the permeability, as well as a large and stiff 3D spheroid, and those effects were inhibited by Rip. In contrast, KD025 exerted opposite effects on the physical properties (down-sizing and softening). Furthermore, DEX induced several changes of gene expressions of ECM and their modulators were also modulated differently by Rip and KD025. The present findings indicate that Rip and KD025 induced opposite effects toward 2D and 3D cell cultures of DEX-treated HTM cells.


Author(s):  
Takamasa Iwakura ◽  
Julian A Marschner ◽  
Zhi Bo Zhao ◽  
Monika Katarzyna Świderska ◽  
Hans-Joachim Anders

Abstract Electric cell-substrate impedance sensing (ECIS) is a quantitative, label-free, non-invasive analytical method allowing continuous monitoring of the behaviour of adherent cells by online recording of transcellular impedance. ECIS offers a wide range of practical applications to study cell proliferation, migration, differentiation, toxicity and monolayer barrier integrity. All of these applications are relevant for basic kidney research, e.g. on endothelial cells, tubular and glomerular epithelial cells. This review gives an overview on the fundamental principles of the ECIS technology. We name strengths and remaining hurdles for practical applications, present an ECIS array reuse protocol, and review its past, present and potential future contributions to preclinical kidney research.


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