Tricellular tight junction-associated angulins in the gill epithelium of rainbow trout

Abstract

Molecular physiology of the tricellular tight junction (tTJ)-associated proteins lipolysis-stimulated lipoprotein receptor ( lsr, = angulin-1) and an immunoglobulin-like domain-containing receptor ( ildr2, ≈angulin-3) was examined in model trout gill epithelia. Transcripts encoding lsr and ildr2 are broadly expressed in trout organs. A reduction in lsr and ildr2 mRNA abundance was observed during and after confluence in flask-cultured gill cells. In contrast, as high-resistance and low-permeability characteristics developed in a model gill epithelium cultured on permeable polyethylene terephthalate membrane inserts, lsr and ildr2 transcript abundance increased. However, as epithelia entered the developmental plateau phase, lsr abundance returned to initial values, while ildr2 transcript abundance remained elevated. When mitochondrion-rich cells were introduced to model preparations, lsr mRNA abundance was unaltered and ildr2 mRNA abundance significantly increased. Transcript abundance of ildr2 was not altered in association with corticosteroid-induced tightening of the gill epithelium, while lsr mRNA abundance decreased. Transcriptional knockdown of the tTJ protein tricelluin (Tric) reduced Tric abundance, increased gill epithelium permeability, and increased lsr without significantly altering ildr2 transcript abundance. Data suggest that angulins contribute to fish gill epithelium barrier properties but that Lsr and Ildr2 seem likely to play different roles. This is because ildr2 typically exhibited increased abundance in association with decreased model permeability, while lsr abundance changed in a manner that suggested a role in Tric recruitment to the tTJ.

Corticosteroid enhances epithelial barrier function in intestinal organoids derived from patients with Crohn’s disease

“…Mutations in ILDR-1 were found to be associated with nonsyndromic autosomal recessive hearing impairment [ 53 ]. Another report showed that ILDR-1 contributes to fish gill epithelium barrier properties [ 54 ]. Herein, our data revealed that ILDR-1 transcripts were detected in patient-derived intestinal organoids.…”

Tight Junctions as Targets and Effectors of Mucosal Immune Homeostasis

“…[16][17][18] This includes discovery of zonula occludens (ZO)-1 19 and the related cytoplasmic scaffolding proteins ZO-2 20 and ZO-3 21 ; cingulin 22 ; the tight junction associated Marvel proteins occludin, 23 tricellulin, 24 and marvelD3 25,26 ; claudins [27][28][29][30][31] ; and others. 32,33 Beyond these compositional proteins, the tight junction is functionally and structurally linked to the subcortical terminal web of actin microfilaments and the perijunctional actomyosin ring. [34][35][36][37][38][39] Solutes and water cross the tight junction by two distinct pathways that can be distinguished on the basis of their size-selectivity, charge-selectivity, and capacity (Figure 1A).…”

Claudins of sea lamprey (Petromyzon marinus) – organ‐specific expression and transcriptional responses to water of varying ion content

“…In the gill and skin of teleosts, the regulated movement of solutes across epithelia has been linked to changes in the transcript and protein abundance of select Cldns and other TJ proteins (Bagherie-Lachidan et al, 2008Chasiotis & Kelly, 2008;Bui & Kelly, 2014;Gauberg et al, 2017;Tacchi et al, 2015;Kolosov and Kelly, 2016). Furthermore, functional knockdown of select cldns (i.e., cldn-8d and -31) as well as ocln and tric in cultured gill epithelium models has been reported to increase paracellular solute permeability, indicating a barrier role for these proteins Kolosov and Kelly, 2018). In contrast, some Cldns, such as members of the Cldn-10 subfamily, have been linked to "selectively permeable" TJs and enhanced Na + secretion across branchial epithelia of teleosts Bui & Kelly, 2014;Loh et al, 2004;Marshall et al, 2018).…”