Perilipin 4 Protein: an Impending Target for Amyotrophic Lateral Sclerosis.
Lei ZhuFan HuCheng LiCaixiang ZhangRuiwen HangRen-Shi XuPublished in: Molecular neurobiology (2020)
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.
Keyphrases
- amyotrophic lateral sclerosis
- wild type
- spinal cord
- induced apoptosis
- high fat diet induced
- poor prognosis
- cell proliferation
- minimally invasive
- cell cycle arrest
- signaling pathway
- atrial fibrillation
- binding protein
- oxidative stress
- cell death
- metabolic syndrome
- quantum dots
- cell cycle
- machine learning
- spinal cord injury
- pi k akt
- adipose tissue
- small molecule
- artificial intelligence