What does this research mean for the field?

Soluble adenylyl cyclase (sAC) bidirectionally controls the ionic permeability of tight junctions in human intestinal epithelial cells by regulating claudin-4 protein expression via the EPAC1 pathway. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To characterize the regulatory role and underlying molecular mechanisms of soluble adenylyl cyclase in modulating tight junctions in human intestinal epithelial cells.

September 5, 2026AJP Gastrointestinal and Liver Physiology

Soluble adenylyl cyclase regulates tight junctions of human intestinal epithelial cells via claudin-4

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Authors

HLHang Lam Li KHKam Ho-Mok AVArthur Verhoeven

Discussion

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Overview

In vitro study reveals that soluble adenylyl cyclase regulates tight junction permeability in intestinal epithelial cells via claudin-4, highlighting a novel mechanism for gut barrier control.

Key Points

To characterize the regulatory role and underlying molecular mechanisms of soluble adenylyl cyclase in modulating tight junctions in human intestinal epithelial cells.
Assessed ionic and paracellular permeability across human intestinal epithelial (Caco2Bbe1) cell monolayers by measuring transepithelial electrical resistance (TEER) and lucifer yellow flux.
Manipulated soluble adenylyl cyclase (sAC), EPAC1, and ERK signaling pathways through pharmacological inhibition, targeted genetic knockdown, and sAC overexpression, followed by Western blot analysis.
Pharmacological inhibition or knockdown of sAC increased TEER and claudin-4 protein abundance, whereas sAC overexpression led to reciprocal reductions in both measures without affecting paracellular lucifer yellow permeability.
EPAC1 functioned as the sole downstream cAMP effector mediating sAC-driven changes in TEER and claudin-4 protein expression.
Inhibition of sAC induced phosphorylated ERK expression, but ERK inhibition reduced TEER without altering claudin-4 expression.

Cite This Study

Li et al. (2026) studied this question.

synapsesocial.com/papers/6a9bd4536b95aff0620ebf96 https://doi.org/10.1152/ajpgi.00316.2025

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September 5, 2026AJP Gastrointestinal and Liver Physiology

Soluble adenylyl cyclase regulates tight junctions of human intestinal epithelial cells via claudin-4

View Full Paper

Ask AI

Bookmark

Authors

HLHang Lam Li KHKam Ho-Mok AVArthur Verhoeven

Discussion

Member takes

Overview

In vitro study reveals that soluble adenylyl cyclase regulates tight junction permeability in intestinal epithelial cells via claudin-4, highlighting a novel mechanism for gut barrier control.

Key Points

To characterize the regulatory role and underlying molecular mechanisms of soluble adenylyl cyclase in modulating tight junctions in human intestinal epithelial cells.
Assessed ionic and paracellular permeability across human intestinal epithelial (Caco2Bbe1) cell monolayers by measuring transepithelial electrical resistance (TEER) and lucifer yellow flux.
Manipulated soluble adenylyl cyclase (sAC), EPAC1, and ERK signaling pathways through pharmacological inhibition, targeted genetic knockdown, and sAC overexpression, followed by Western blot analysis.
Pharmacological inhibition or knockdown of sAC increased TEER and claudin-4 protein abundance, whereas sAC overexpression led to reciprocal reductions in both measures without affecting paracellular lucifer yellow permeability.
EPAC1 functioned as the sole downstream cAMP effector mediating sAC-driven changes in TEER and claudin-4 protein expression.
Inhibition of sAC induced phosphorylated ERK expression, but ERK inhibition reduced TEER without altering claudin-4 expression.

Cite This Study

Li et al. (2026) studied this question.

synapsesocial.com/papers/6a9bd4536b95aff0620ebf96 https://doi.org/10.1152/ajpgi.00316.2025

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