Nerve Growth Factor is a Potential Treated Target in Tg(SOD1*G93A)1Gur Mice
- PDF / 1,839,555 Bytes
- 12 Pages / 595.276 x 790.866 pts Page_size
- 92 Downloads / 187 Views
ORIGINAL RESEARCH
Nerve Growth Factor is a Potential Treated Target in Tg(SOD1*G93A)1Gur Mice Zhenzhen Xu1,2 · Jianxiang Jiang1 · Shengyuan Xu1 · Zunchun Xie1,2 · Pei He1 · Shishi Jiang1 · Renshi Xu1 Received: 19 June 2020 / Accepted: 28 October 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Nerve growth factor (NGF) is a protective factor of neural cells; the possible relationship between the NGF and the pathogenesis of amyotrophic lateral sclerosis (ALS) hasn’t been completely known. In this study, we observed and analyzed the expression and distribution of NGF, as well as the possible relationship between the NGF expression and distribution and the neural cell death in both SOD1 wild-type (WT) and Tg(SOD1*G93A)1Gur (TG) mice applying the fluorescence immunohistochemistry method. The results showed that the expression and distribution of NGF in the anterior horn (AH), the lateral horn (LH), and the surrounding central canal (CC) significantly increased at the supper early stage of ALS (Pre-onset stage) and the early stage (Onset stage), but the NGF expression and distribution in the AH, the LH, and the surrounding CC significantly reduced at the progression stage. The astrocyte, neuron, and oligodendrocyte produced the NGF and the neural precursor cells (NPCs) produced the NGF. The neural cell death gradually increased accompanying with the reduction of NGF expression and distribution. Our data suggested that the NGF was a protective factor of neural cells, because the neural cells in the AH, the LH, and the surrounding CC produced more NGF at the supper early and early stage of ALS; moreover, the NPCs produced the NGF. It implied that the NGF exerted the protective effect of neural cells, prevented from the neural cell death and aroused the potential of self-repair in the development of ALS. Keywords Amyotrophic lateral sclerosis · Nerve growth factor · Spinal cord · Pathogenesis · Tg(SOD1*G93A)1Gur mice Zhenzhen Xu, Jianxiang Jiang, Shengyuan Xu and Zunchun Xie have common contribution in this study. * Renshi Xu [email protected]; [email protected] Zhenzhen Xu [email protected] Jianxiang Jiang [email protected] Shengyuan Xu [email protected] Zunchun Xie [email protected] Pei He [email protected] Shishi Jiang [email protected] 1
Department of Neurology, Jiangxi Provincial People’s Hospital, Affiliated People’s Hospital of Nanchang University, Nanchang 330006, Jiangxi, China
Department of Neurology, First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China
2
Background Amyotrophic lateral sclerosis (ALS) is the commonest adultonset motor neuron disease, which ultimately leads to death because of the respiratory failure at usually 3–5 years after the appearance of first symptom. The exact etiology and pathogenesis of ALS still haven’t been completely clear up to now (Ludolph et al. 2012; Salameh et al. 2015; Zarei et al. 2015). The current researches are considered that the development of ALS might be closely related
Data Loading...
