Papillomavirus-related endocervical adenocarcinoma (a HeLa derivative, ATCC CCL-13TM); Clone 9, typical rat liver epithelial cell line (ATCC CRL-1439TM); FL, epithelial cells derived from human amniotic membrane (a HeLa derivative, RRID:CVCL_1905); G27, rat hepatoma cell line; G401.2/6TG.1, human kidney epithelial cell line; H6c7, human pancreatic ductal epithelial cell line (RRID:CVCL_0P38); HaCaT, aneuploid immortal keratinocyte cell line from adult human skin (RRID:CVCL_0038); HBE1, immortalized human bronchial epithelial cell line (RRID:CVCL_0287; Kerafast #ENC002); HEI-OC1, conditionally immortalized mice cochlear cells (RRID:CVCL_D899); HEL37, mouse epidermal cells (RRID:CVCL_6D73); HepG2, human liver cancer cell line (ATCC HB-8065TM); HL1-1, adult human liver stem cells; HLEC-04, human hepatocyte line derived from SV40 T antigen transfected primary cultured human hepatocytes; Huh-7, adult human hepatocellular carcinoma cell line (RRID:CVCL_0336); IEC-6, rat normal intestinal epithelioid cell line (ATCC CRL-1592TM); IAR-20, non-transformed rat liver epithelial cells (RRID:CVCL_5296); IAR-203, non-transformed rat liver epithelial cells; IAR-6.1, non-transformed rat liver epithelial cells (RRID:CVCL_D613); LC540, rat adult Leydig cell adenoma cell line (ATCC CCL-43TM); MDCK, Madin Darby Canine Kidney (ATCC CCL-34TM); N1S1-67, rat hepatoma cell line; REL, rat liver epithelial cell line; RG2, rat glioma cells (ATCC CRL-2433TM); RGC, rat glial cells; RGC-5, rat/mouse retinal ganglion cell line (RRID:CVCL_4059); mGluR5 Activator drug RWPE-1, human prostate epithelial cells (ATCC CRL-11609TM); T51B, rat liver nonparenchymal cell line; TM3, murine immortalized XIAP Antagonist list immature Leydig cell line (ATCC CRL-1714TM); TM4, murine immortalized immature Sertoli cell line (ATCC CRL-1715TM); V79, Chinese hamster lung fibroblasts (RRID:CVCL_2234; ECACC 86041102); WB F344, typical rat liver epithelial cell line (RRID:CVCL_9806; JCRB0193). Other people: Y, yes.One of several crucial drawbacks for most of your strategies traditionally utilised for GJIC evaluation is their restricted throughput and in some cases a requirement for specific equipment or expertise. However, some of these solutions have been lately adapted into formats compatible using a high throughput screening (HTS) and/or higher content evaluation (HCA)/high content screening (HCS). These adapted methods, with their advantages or disadvantages, are summarized in Table two (modified and updated from [259]). Some HTS and HCA/HCS techniques rely on a fluorometric or luminometric sensing of particular molecules exchanged via gap junctions composed by Cx43 amongst donor and recipient cells, i.e., metabolic cooperation. Having said that, the majority of these setups are determined by dye-transfer techniques, including MI, Par/Pre, microfluidic loading, electroporation loading (EL-DT) or laser perforation (LP-DT). Additionally they include things like the SL-DT assay, most likely essentially the most often made use of assay to study GJIC inside the context of toxicology and toxicant-induced tumor promotion.Int. J. Mol. Sci. 2021, 22,11 ofTable two. Setups compatible for HTS and/or HCA/HCS of gap junctional intercellular communication (GJIC) (adapted from [259]). System Dye transfer assays + Endpoints: GJIC, cell density and viability + Applicable for a assortment of adherent cell varieties + Automated image acquisition and analysis + No specialized cell model, gear or technical capabilities needed – Invasive – For cells forming practically confluent monolayers – Not applicable for Cx channels excluding LY + Precise and quantitative +.
