Perilipin 4 Protein: an Impending Target for Amyotrophic Lateral Sclerosis
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Perilipin 4 Protein: an Impending Target for Amyotrophic Lateral Sclerosis Lei Zhu 1 & Fan Hu 1 & Cheng Li 1 & Caixiang Zhang 1 & Ruiwen Hang 1 & Renshi Xu 1 Received: 15 July 2020 / Accepted: 16 November 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract The pathogenesis of amyotrophic lateral sclerosis (ALS) might exist some relationships with the abnormal lipidomic metabolisms. Therefore, we observed and analyzed the alteration of perilipin 4 (PLIN 4) distribution in the anterior horns (AH); the central canals (CC) and its surrounding gray matter; the posterior horns (PH); and the anterior, lateral, and posterior funiculus (AF, LF, and PF) of the cervical, thoracic, and lumbar segments, as well as the alteration of PLIN 4 expression in the entire spinal cords at the pre-onset, onset, and progression stages of Tg(SOD1*G93A)1Gur (TG) mice and the same period of wild-type(WT) by fluorescent immunohistochemistry, the Western blot, and the image analysis. Results showed that the PLIN 4 distributions in the spinal AH, CC and its surrounding gray matter, PH, AF, and PF of the cervical, thoracic, and lumbar segments in the TG mice at the pre-onset, onset, and progression stages significantly increased compared with those at the same periods of WT mice; the gray matter was especially significant. No significant changes were detected in the LF. PLIN 4 extensively distributed in the neurons and the proliferation neural cells. The PLIN 4 distributions significantly gradually increased from the pre-onset to onset to progression stages, and significantly correlated with the gradual increase death of neural cells. Total PLIN 4 expression in the spinal cords of TG mice significantly increased from the pre-onset, to onset, and to progression stages compared with that in the WT mice. Our data suggested that the PLIN 4 distribution and expression alterations might participate in the death of neural cells in the pathogenesis of ALS through modulating the lipidomic metabolisms and the neural cell proliferation. Keywords Amyotrophic lateral sclerosis . Perilipin 4 . Spinal cord . Pathogenesis . Tg(SOD1*G93A)1Gur mice
Introduction
Lei Zhu, Fan Hu and Cheng Li contributed equally to this work. * Renshi Xu [email protected] Lei Zhu [email protected] Fan Hu [email protected] Cheng Li [email protected] Caixiang Zhang [email protected] Ruiwen Hang [email protected] 1
Department of Neurology, Jiangxi Provincial People’s Hospital, Affiliated People’s Hospital of Nanchang University, Nanchang, China
Lipid droplet (LD) is an organelle of neutral lipid core, is sequestered by a phospholipid monolayer, and is wrapped up by the LD-binding proteins [1, 2]. LD distributes in the fiber of skeletal muscle of both the subsarcolemmal region and the center of the intermyofibrillar region [3, 4]. The size and number of intracellular LD are regulated by the availability of lipid and the activity of LD metabolized enzymes, the co-activators required for the LD synthesis, and the degradation of LD. Many of LD meta
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