Acta oto-laryngologica · 2026
Proteomic characterization of cochlea vascular injury and PVM/Ms-associated repair using iTRAQ and PRM approaches.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Qin, Zhang Tong, Tang Chaoying, Fan Shuhang, Sai Na, Sun Jianbin, Guo Weiwei, Yang Shiming, Han Weiju
Аннотация
BACKGROUND: Noise exposure (NE) disrupts blood-labyrinth barrier (BLB), damaging cell junctions and perivascular macrophage-like melanocytes (PVM/Ms), causing hair cell loss.
OBJECTIVE: To determine vascular endothelial growth factor (VEGF)/pigment epithelium-derived factor (PEDF) signaling and PVM/Ms dysfunction contribute to BLB breakdown and repair following NE.
MATERIAL AND METHODS: Proteomic profiling of the stria vascularis (SV) from control and NE mice was performed using Isobaric Tags for Relative and Absolute Quantitation (iTRAQ) and Parallel Reaction Monitoring (PRM). Immunofluorescence, qPCR, and ect. were used to assess changes in PVM/Ms distribution, VEGF/PEDF signaling, and junctional proteins.
RESULTS: Nine altered proteins mapped to four functional modules: junctional stability, metabolic/vesicular regulation, ion homeostasis, and immune modulation. PPI-GO analysis identified 'regulation of cell junction assembly' as a pathway linking these proteins with VEGF/PEDF. NE induced an acute reduction in PVM/Ms coverage and early downregulation of VEGF, PEDF, and junctional proteins. VEGF and VEGFR2 peaked at 2 days after NE (NE2d), while PEDF and VEGFR1 peaked at 7 days after NE (NE7d), paralleling recovery of VE-Cadherin and ZO-1 and a compensatory rise in Occludin.
CONCLUSIONS AND SIGNIFICANCE: NE triggers a coordinated, time-dependent disruption of the PVM/Ms-VEGF/PEDF-junctional protein axis, driving BLB instability and repair.
OBJECTIVE: To determine vascular endothelial growth factor (VEGF)/pigment epithelium-derived factor (PEDF) signaling and PVM/Ms dysfunction contribute to BLB breakdown and repair following NE.
MATERIAL AND METHODS: Proteomic profiling of the stria vascularis (SV) from control and NE mice was performed using Isobaric Tags for Relative and Absolute Quantitation (iTRAQ) and Parallel Reaction Monitoring (PRM). Immunofluorescence, qPCR, and ect. were used to assess changes in PVM/Ms distribution, VEGF/PEDF signaling, and junctional proteins.
RESULTS: Nine altered proteins mapped to four functional modules: junctional stability, metabolic/vesicular regulation, ion homeostasis, and immune modulation. PPI-GO analysis identified 'regulation of cell junction assembly' as a pathway linking these proteins with VEGF/PEDF. NE induced an acute reduction in PVM/Ms coverage and early downregulation of VEGF, PEDF, and junctional proteins. VEGF and VEGFR2 peaked at 2 days after NE (NE2d), while PEDF and VEGFR1 peaked at 7 days after NE (NE7d), paralleling recovery of VE-Cadherin and ZO-1 and a compensatory rise in Occludin.
CONCLUSIONS AND SIGNIFICANCE: NE triggers a coordinated, time-dependent disruption of the PVM/Ms-VEGF/PEDF-junctional protein axis, driving BLB instability and repair.