Objectives: The alteration of vimentin-containing cells (VCCs) proliferation, differentiation and migration in the brain stem of amyotrophic lateral sclerosis (ALS)-like transgenic mice (Tg(SOD1*G93A)1Gur mice) (TG mice) and wild-type mice (WT mice) at the different disease stages of TG mice were studied in this study. The aim of this study was to investigate the change features of proliferation, differentiation and migration of endogenous neural precursor cells (NPCs) and to explore the potential effects of NPCs on restoring degenerated neurons in ALS. Methods: The proliferation, differentiation and migration of VCCs in both different anatomic regions and neural cells of brain stem at the different stages including pre-onset (60-70 days), onset (90-100 days) and progression (120-130 days) stages of TG mice and in WT mice (control) were examined using the immunofluorescence technology. Results: VCCs mainly distributed in the around (peripheral) central canal (CC) and the nuclei of brain stem in adult WT mice. VCCs proliferated and differentiated into astrocytes and directionally migrated from the around CC to the nuclei of brain stem, then to the ventral part of damaged regions in brain stem at the pre-onset, onset and progression stages of TG mice. Conclusions: The data suggest that NPCs widely distribute in the brain stem of adult TG mice can differentiate into astrocytes and migrate into damaged brain regions. This response might be a potential mechanism to repair degenerated motor neurons and restore dysfunctional neural circuitry in ALS.
Heterologous ribonucleoprotein (hnRNP) G protein was found to significantly down-regulated in the spinal cord of amyotrophic lateral sclerosis (ALS) mouse model in our previous study, but the down-regulated effects of hnRNP G in ALS haven’t been known up to now. Therefore, we further studied the possible effects of hnRNP G on spinal neuron death in TG(SOD1*G93A)1Gur (TG) mice. Eighteen TG mice and eighteen SOD1 wild-type (WT) mice were divided into 6 groups. The hnRNP G of the spinal cord was analyzed using immunofluorescent histochemistry and Western blot. hnRNP G-siRNA was transfected into PC12 cells and observed the alteration of proliferation rate and intracellular proteins using the CCK8 and Western blot. We reported that the distribution of hnRNP G positive cells in the posterior horn was more than that in the central canal and its surrounding gray matter more than that in the anterior horn. hnRNP G protein mainly expressed in neurons. hnRNP G expression in the cervical and thoracic segments of TG mice in the pre-onset group was significantly higher than that in the control group. hnRNP G expression in the thoracic and lumbar segments of TG mice in onset group was lower than that in control group. hnRNP G expression in the cervical and thoracic segments of TG mice in progressive group decreased, while that in the lumbar segment of TG mice in progression group significantly increased. After hnRNP G was silenced, the proliferation rate of PC12 cells was slower than that in the control group, SOD1 expression didn’t significantly change, both TDP-43 and Bax expression significantly increased in PC12 cells after silenced. Our study revealed that the distribution of hnRNP G in the spinal cord of ALS mice showed the possible protective effect on the progression of ALS, its mechanism maybe prevent neuron death by reducing abnormal TDP-43 accumulation in the spinal cord of ALS-like mice.
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