glial scars  (R&D Systems)

Journal: Molecular Neurobiology

Article Title: Tauroursodeoxycholic Acid Inhibited Apoptosis and Oxidative Stress in H 2 O 2 -Induced BMSC Death via Modulating the Nrf-2 Signaling Pathway: the Therapeutic Implications in a Rat Model of Spinal Cord Injury

doi: 10.1007/s12035-023-03754-5

Figure Lengend Snippet: The combined treatment of TUDCA and BMSC transplantation accelerated the regeneration of tissues and motor functional recovery after SCI. a Images of behavioral observation showing the characteristics of hind limb movement of rats across different groups. b Footprint analyses of different groups on day 28 after SCI. c Representative images from H&E staining in longitudinal section on day 28 after SCI. d , e The survived neurons following Nissl staining and relative quantification at the lesion area from different groups on day 28 after SCI. f The Basso, Beattie, and Bresnahan (BBB) locomotor scores of different groups. g The Immunofluorescence staining of MAP2(green), MBP (green), TUJ1 (red), and GFAP (red) from different groups on day 28 post-SCI. Data are presented as mean ± SD. * P < 0.05 vs. the SHAM group. # P < 0:05 vs. the SCI group. & P < 0.05 vs. the BMSC group ( n = 6)

Article Snippet: According to a previous study [ ], the tissues were subjected to overnight incubation at the temperature of 4 °C with microtubule-associated protein 2 (MAP2) (1:200, Boster Biological Engineering Co.), glial scar formation (GFAP) (1:200, Boster Biological Engineering Co.), myelin basic protein (MBP) (1:200, Boster Biological Engineering Co.), and beta-tubulin III (TUJ1) (1:200, CST) as primary antibodies.

Techniques: Transplantation Assay, Functional Assay, Staining, Quantitative Proteomics, Immunofluorescence

Journal: Advanced Science

Article Title: Transplanting Human Neural Stem Cells with ≈50% Reduction of SOX9 Gene Dosage Promotes Tissue Repair and Functional Recovery from Severe Spinal Cord Injury

doi: 10.1002/advs.202205804

Figure Lengend Snippet: SOX9 KD grafts exhibit efficient distribution into lesion cavities and integration in the absence of growth factors in the SCI model. A) Representative immunofluorescence images for GFP, MAP2 (red), and GFAP (Blue) in sagittal sections with scramble and SOX9 KD grafts at 1 month (1 m ) post‐graft. The cystic lesion cavity (LC) is surrounded by dense GFAP immunoreactivity (blue) in scramble control, whereas GFP + SOX9 KD grafts extend across GFAP barriers. White box shows a magnified view with indicated markers (Scale bar, 100 µm). Lower panel shows the line scan of fluorescence intensity with indicated markers across the lesion cavity of recipients with scramble and SOX9 KD grafts. ( n = 7 rats per group, 4–5 sections per rat) B) Representative immunofluorescence images for GFP, CSPG (red), and DAPI (Blue) in spinal cord sagittal sections grafted with the scramble and SOX9 KD hNSCs at 1‐month post‐graft. The cystic lesion cavity (LC) formed with surrounding dense CSPG immunoreactivity (red). White box shows a zoomed‐in view with indicated markers. SOX9 KD grafts attenuated CSPG graft/host interface (Scale bar, 500 µm). C) Relative fluorescence intensity analysis of CSPG surrounding the lesion cavity that normalized to the uninjured region ( n = 7 rats per group, 4–5 sections per rat). ** p < 0.05. D) Representative images of host serotonergic axons immunolabeled with 5‐HT (red) extending into the scramble and SOX9 KD grafts at 2 months post‐transplantation. a‐a’’ and b‐b’’ show high magnification of 5‐HT + fibers innervating into the graft at different regions from rostral to caudal (Scale bar, 100 µm). E) Quantification of the portion of host 5‐HT + serotonergic axons in the scramble and SOX9 KD grafts, normalized to the total number of 5‐HT + axons located 0.5 mm rostral to the lesion site ( n = 6 rats per group, 3–4 sections per rat). One‐way ANOVA. ** p < 0.05, *** p < 0.005. F) Triple immunolabeling of host 5‐HT + fibers, proximal hsyn, and GFP‐terminals indicating the establishment of synaptic contacts between the host raphespinal fibers and SOX9 KD grafted cells ( n = 6 rats per group, 3–4 sections per rat, Scale bar, 50 µm).

Article Snippet: As expected, a lesion control without grafts showed the formation of cystic cavitation surrounded by a glial scar expressing both GFAP and CSPG, which prevents axons and corticospinal tract fibers (CST) from penetrating through the lesion cavity that disrupts neuronal connectivity (Figure , Supporting Information).

Techniques: Immunofluorescence, Control, Fluorescence, Immunolabeling, Transplantation Assay