ArticlebioRxiv : the preprint server for biology2025
Rho-ROCK signaling and α-Catenin mediate β-Catenin-driven hyperplasia in the adrenal via adherens junctions.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
How β-Catenin (βCat) mediates tissue hyperplasia is poorly understood. To explore this, we employed the adrenal cortex as a model system given its stereotypical spatial organization and the important role βCat plays in homeostasis and disease. For example, excessive production of aldosterone by the adrenal cortex (primary aldosteronism, PA) constitutes a significant cause of cardiovascular morbidity, which has been associated with βCat gain-of-function (βCat-GOF). Adherens junctions (AJs) connect the actin cytoskeletons of adjacent zona Glomerulosa (zG) cells via a cadherin/βCat/α-Catenin (αCat) complex and mediate aldosterone production. Whether βCat-GOF drives zG hyperplasia, a key feature of PA, via AJs is unknown. Here, we show that aldosterone secretagogues (K One Sentence Summary: This study demonstrates that β-Catenin-driven hyperplasia in the adrenal cortex, a key feature of primary aldosteronism, is mediated through Rho-ROCK signaling and α-Catenin-dependent stabilization of adherens junctions, with significant implications for patients with primary aldosteronism. Highlights: Rho-ROCK signaling drives AJ enrichment in the adrenalROCK inhibition via fasudil blunts aldosterone productionβCat drives adrenal hyperplasia via enhanced AJ enrichmentROCK inhibition or ɑCat deletion block zG hyperplasia.
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