Réabsorption du sel et sécrétion du potassium par le néphron distal

Rafael, Chloé; Chávez-Canales, María; Hadchouel, Juliette

doi:10.1051/medsci/20163203012

Cited by 3 publications

(1 citation statement)

References 34 publications

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“…Therefore, our results imply that CYLD is an important factor in the osteogenic differentiation of BMSCs and OP progression. WNK1 plays a vital role in maintaining ion homeostasis by regulating the trafficking or activity of various membrane transport proteins [43]. Multiple studies have highlighted the contribution of WNK1 in regulating blood pressure and electrolyte balance through its modulation of multiple ion channels and ion transporters [44].…”

Section: Discussionmentioning

confidence: 99%

CYLD alleviates NLRP3 inflammasome-mediated pyroptosis in osteoporosis by deubiquitinating WNK1

Jiang,

Cai,

Cheng

et al. 2024

J Orthop Surg Res

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Background Osteoporosis (OP) is the result of bone mass reduction and bone structure disorder. Bone marrow mesenchymal stem cells (BMSCs) are the main source of osteogenic precursor cells involved in adult bone remodeling. The involvement of the deubiquitinating enzyme CYLD in OP has recently been discovered. However, the detailed role and mechanism of CYLD remain unknown. Methods The OP mouse model was established by performing ovariectomy (OVX) on mice. Hematoxylin and eosin staining, Masson and Immunohistochemical staining were used to assess pathologic changes. Real-time quantitative PCR, Western blot, and immunofluorescence were employed to assess the expression levels of CYLD, WNK1, NLRP3 and osteogenesis-related molecules. The binding relationship between CYLD and WNK1 was validated through a co-immunoprecipitation assay. The osteogenic capacity of BMSCs was determined using Alkaline phosphatase (ALP) and alizarin red staining (ARS). Protein ubiquitination was evaluated by a ubiquitination assay. Results The levels of both CYLD and WNK1 were decreased in bone tissues and BMSCs of OVX mice. Overexpression of CYLD or WNK1 induced osteogenic differentiation in BMSCs. Additionally, NLRP3 inflammation was activated in OVX mice, but its activation was attenuated upon overexpression of CYLD or WNK1. CYLD was observed to reduce the ubiquitination of WNK1, thereby enhancing its protein stability and leading to the inactivation of NLRP3 inflammation. However, the protective effects of CYLD on osteogenic differentiation and NLRP3 inflammation inactivation were diminished upon silencing of WNK1. Conclusion CYLD mitigates NLRP3 inflammasome-triggered pyroptosis in osteoporosis through its deubiquitination of WNK1.

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Section: Discussionmentioning

confidence: 99%

CYLD alleviates NLRP3 inflammasome-mediated pyroptosis in osteoporosis by deubiquitinating WNK1

Jiang,

Cai,

Cheng

et al. 2024

J Orthop Surg Res

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Mécanismes de l’effet diurétique de la caféine

et al. 2016

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Sévérité de l’hypertension hyperkaliémique familiale causée par les mutations de CUL-3

Rafael

Hadchouel

2020

Med Sci (Paris)

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> L'hypertension hyperkaliémique familiale (HHF) est une forme mendélienne rare d'hypertension artérielle associée à une hyperkaliémie et une acidose métabolique hyperchlorémique. Ces troubles sont corrigés par les diurétiques thiazidiques, inhibiteurs du cotransporteur Na + / Cl-(Na +-Cl − cotransporter, NCC) exprimé dans le tube contourné distal du néphron. Les premières analyses génétiques ont mis en évidence des mutations dans les gènes codant les sérine-thréonine kinases WNK1 et WNK4 (with no (K) lysine) chez une minorité (8,5 %) de patients HHF [1]. De multiples études in vitro et in vivo ont permis de montrer que ces kinases stimulent l'activité du cotransporteur NCC grâce à une cascade de phosphorylations [2] (➜). En 2012, des nouvelles mutations dans les gènes CUL3 (cullin-3) et KLHL3 (kelch-like family member 3) ont été identifiées chez 47 % des patients [3]. Les protéines CUL3 et KLHL3 font partie d'un complexe ubiquitine-ligase E3 permettant l'ubiquitination de protéines cibles en vue de leur dégradation par le protéasome. WNK1 et WNK4 sont des substrats de ce complexe enzymatique [4] (Figure 1).

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Réabsorption du sel et sécrétion du potassium par le néphron distal

Cited by 3 publications

References 34 publications

CYLD alleviates NLRP3 inflammasome-mediated pyroptosis in osteoporosis by deubiquitinating WNK1

CYLD alleviates NLRP3 inflammasome-mediated pyroptosis in osteoporosis by deubiquitinating WNK1

Mécanismes de l’effet diurétique de la caféine

Sévérité de l’hypertension hyperkaliémique familiale causée par les mutations de CUL-3

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