Acetazolamide ameliorates the severity of collagen-induced arthritis in rats: Involvement of inducing synovial apoptosis and inhibiting Wnt/β-catenin pathway

Mu, Yu-rong; Cai, Li; Zhou, Meng-Yuan; Liu, Mingming; Zeng, Li; Li, Rong

doi:10.1016/j.intimp.2020.107214

Cited by 8 publications

(1 citation statement)

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“…While inhibiting water transportation by reducing AQP1, the water content of the intervertebral disc and nutrient permeability are also reduced, thereby affecting the nutrient supply and then affecting cell function until apoptosis. Furthermore, the suppression of AQP1 would lead the excessive activation of Wnt/β-catenin signaling [28]. Wnt/β-catenin is a classic Wnt signaling pathway closely related to various diseases and participates in regulating various life processes [29].…”

Section: Discussionmentioning

confidence: 99%

Hypo-osmolality activates Wnt/β-catenin mediated by AQP1 in nucleus pulposus cells degeneration

Xiao Zhang,

Zheng Lv,

Chengjian Wei

2024

Cell Mol Biol (Noisy-le-grand)

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The goals of this study were to investigate whether Wnt/β-catenin signaling plays a role in hypo-osmolalityrelated degeneration of nucleus pulposus (NP) cells, and if so, to define the mechanism underlying AQP1 in this effect. Human NP cells were cultured under hypo-osmotic (300/350/400 mOsm) and iso-osmotic (450 mOsm) conditions. The cell viability, AQP1, the expression of Wnt/β-catenin signaling, collagen II/I, and MMP3/9 were evaluated. To determine the effects of the Wnt/β-catenin signaling, we used the inhibitor and the activator of Wnt during the hypo-osmotic culture of NP cells. We also examined whether the silencing and overexpressing of the AQP1 gene would affect the Wnt/β-catenin expression in NP cells. Hypo-osmolality caused NP cell degeneration and activated the Wnt/β-catenin signaling but suppressed the AQP1 level. Inhibiting the Wnt/β-catenin signaling alleviated the hypo-osmolality-induced NP cell degeneration. On the contrary, activating Wnt/β-catenin aggravated the NP cell degeneration under hypo-osmotic conditions, which did not affect AQP1 expression. AQP1-overexpressed NP cells exhibited decreased Wnt/β-catenin signaling and alleviated cell degeneration under the hypo-osmotic condition. Besides, AQP1 silencing accelerated NP cell degeneration and activated Wnt/β-catenin expression compared with untreated control. Hypo-osmolality promotes NP cell degeneration via activating Wnt/β-catenin signaling, which is suppressed by AQP1 expression. The upregulation of AQP1 suppressed the Wnt/β-catenin signaling and alleviated the hypo-osmolality induced by the NP cell degeneration.

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Section: Discussionmentioning

confidence: 99%