ArticleCell proliferation2024
Pcolce2 overexpression promotes supporting cell reprogramming in the neonatal mouse cochlea.
Article in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- PCPE1 and PCPE2: When Sequence Similarity Masks Functional Diversity.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- In Vitro and Animal Studies of Human Natural Killer Cell-Derived Exosomes for the Treatment of Otitis Media.Neuroscience bulletin · 2025Article
- Liquid-Liquid Phase Separation in Hereditary Hearing Loss.Neuroscience bulletin · 2025Review
- Exploring AAV-Mediated Gene Therapy for Inner Ear Diseases: from Preclinical Success to Clinical Potential.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- The predawn dilemma in adeno-associated virus-based gene therapies for hereditary deafness.American journal of stem cells · 2025Review
- Promotion of Cx26 mutants located in TM4 region for membrane translocation successfully rescued hearing loss.Theranostics · 2025Article
- Pcolce2 overexpression promotes supporting cell reprogramming in the neonatal mouse cochlea.Cell proliferation · 2024Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
Abstract
Hair cell (HC) damage is a leading cause of sensorineural hearing loss, and in mammals supporting cells (SCs) are unable to divide and regenerate HCs after birth spontaneously. Procollagen C-endopeptidase enhancer 2 (Pcolce2), which encodes a glycoprotein that acts as a functional procollagen C protease enhancer, was screened as a candidate regulator of SC plasticity in our previous study. In the current study, we used adeno-associated virus (AAV)-ie (a newly developed adeno-associated virus that targets SCs) to overexpress Pcolce2 in SCs. AAV-Pcolce2 facilitated SC re-entry into the cell cycle both in cultured cochlear organoids and in the postnatal cochlea. In the neomycin-damaged model, regenerated HCs were detected after overexpression of Pcolce2, and these were derived from SCs that had re-entered the cell cycle. These findings reveal that Pcolce2 may serve as a therapeutic target for the regeneration of HCs to treat hearing loss.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.