aPKC/Par3/Par6 polarity complexes regulate podocyte motility and crescent formation in the progression of ANCA-associated vasculitis
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A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
Post-publication record
- Nature
- Retraction
- Reason
- Concerns/Issues about Data;Investigation by Journal/Publisher;Unreliable Results and/or Conclusions;
- Date
- 4/6/2025 0:00
- Flagged by OpenAlex?
- Yes
Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.
Machine scores (provisional)
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
- Teacher spread
- 0.276 · how far apart the two teachers sit on this one work
- Validation status
score_only:v0-immature-baseline· verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it
Abstract
OBJECTIVES: Podocyte bridging may be a key initial event occurring early in crescent formation. This study aims to probe the underlying mechanism of atypical protein kinase C (aPKC)/protease-activated receptor 3(Par3)/Par6 polarity complexes on podocyte motility and crescent formation during the progression of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). METHODS: The effects of anti-TNF-α monoclonal antibody (mAb) on the crescent formation, localization and expression of aPKC/Par3/Par6 polarity complexes, and activities of small GTPases (Rho/Rac1/Cdc42) were explored in an AAV mouse model. Podocytes were stimulated in vitro by TNF-α and myeloperoxidase (MPO)-ANCA positive serum collected from patients with microscopic polyangiitis (MPA). Then, podocyte motility, aPKC/Par3/Par6 polarity protein expression and small GTPases activity were measured. The impacts of heat shock protein 70 (HSP70), a type of molecular chaperone, on the phosphorylation of aPKC was evaluated. RESULTS: Anti-TNF-α mAb inhibited crescent formation and restored the localization of aPKC/Par3/Par6 polarity complexes in the glomerulus of the AAV mouse model. Both MPO-ANCA-positive serum and TNF-α stimulation significantly induced podocyte motility by inhibiting of aPKC phosphorylation and detachment of aPKC/Par3/Par6 polarity complexes. Overexpression of HSP70 increased p-aPKC level and inhibited podocyte motility stimulated by either MPO-ANCA-positive serum or TNF-α. CONCLUSION: The podocyte polarity preserved by aPKC/Par3/Par6 polarity complexes, especially the phosphorylation status of aPKC, may play an important role in the crescent formation of AAV. The inhibition of TNF-α prevents the crescent formation in AAV via, at least partly, inhibiting podocyte polarity loss and motility.
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
The record
- Venue
- Lara D. Veeken
- Topic
- Renal Diseases and Glomerulopathies
- Field
- Medicine
- Canadian institutions
- Trinity College
- Funders
- National Key Research and Development Program of ChinaPeking University
- Keywords
- Cell biologyPodocytePhosphorylationMotilitySignal transducing adaptor proteinChemistryCell polarityBiologyBiochemistryEndocrinologyKidneyCell
- Has abstract in OpenAlex
- yes