MedElevator Войти в исследования
← Поиск публикаций

DOI 10.1093/brain/awac015

Медицинская библиотека · Brain : a journal of neurology · 2022

A neuron-to-astrocyte Wnt5a signal governs astrogliosis during HIV-associated pain pathogenesis.

Liu Xin, Bae Chilman, Gelman Benjamin B, Chung Jin Mo, Tang Shao-Jun

СтатьяПоддержка NIH: внешняя программаПеревод в очереди

Аннотация

Chronic pain is the most common neurological disorder of HIV patients. Multiple neuropathologies were identified in the pain pathway. Among them is the prominent astrocytic reaction (also know an astrogliosis). However, the pathogenic role and mechanism of the astrogliosis are unclear. Here, we show that the astrogliosis is crucial for the pain development induced by a key neurotoxic HIV protein gp120 and that a neuron-to-astrocyte Wnt5a signal controls the astrogliosis. Ablation of astrogliosis blocked the development of gp120-induced mechanical hyperalgesia, and concomitantly the expression of neural circuit polarization in the spinal dorsal horn. We demonstrated that conditional knockout of either Wnt5a in neurons or its receptor ROR2 in astrocytes abolished not only gp120-induced astrogliosis but also hyperalgesia and neural circuit polarization. Furthermore, we found that the astrogliosis promoted expression of hyperalgesia and NCP via IL-1β regulated by a Wnt5a-ROR2-MMP2 axis. Our results shed light on the role and mechanism of astrogliosis in the pathogenesis of HIV-associated pain.

Для цитирования: Liu Xin, Bae Chilman, Gelman Benjamin B, Chung Jin Mo, Tang Shao-Jun. A neuron-to-astrocyte Wnt5a signal governs astrogliosis during HIV-associated pain pathogenesis.. Brain : a journal of neurology. 2022. DOI: 10.1093/brain/awac015.

Предметные рубрики MeSH

Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

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.

Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.