scholarly journals Neonatal Mesenchymal Stem Cell Treatment Improves Myelination Impaired by Global Perinatal Asphyxia in Rats

2021 ◽  
Vol 22 (6) ◽  
pp. 3275
Author(s):  
Andrea Tapia-Bustos ◽  
Carolyne Lespay-Rebolledo ◽  
Valentina Vío ◽  
Ronald Pérez-Lobos ◽  
Emmanuel Casanova-Ortiz ◽  
...  
Keyword(s):  
Cell Death ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Perinatal Asphyxia ◽  
Mrna Levels ◽  
Protein Levels ◽  
Delayed Cell Death ◽  
External Capsule ◽  
Stem Cell Treatment ◽  
Main Effects

The effect of perinatal asphyxia (PA) on oligodendrocyte (OL), neuroinflammation, and cell viability was evaluated in telencephalon of rats at postnatal day (P)1, 7, and 14, a period characterized by a spur of neuronal networking, evaluating the effect of mesenchymal stem cell (MSCs)-treatment. The issue was investigated with a rat model of global PA, mimicking a clinical risk occurring under labor. PA was induced by immersing fetus-containing uterine horns into a water bath for 21 min (AS), using sibling-caesarean-delivered fetuses (CS) as controls. Two hours after delivery, AS and CS neonates were injected with either 5 μL of vehicle (10% plasma) or 5 × 104 MSCs into the lateral ventricle. Samples were assayed for myelin-basic protein (MBP) levels; Olig-1/Olig-2 transcriptional factors; Gglial phenotype; neuroinflammation, and delayed cell death. The main effects were observed at P7, including: (i) A decrease of MBP-immunoreactivity in external capsule, corpus callosum, cingulum, but not in fimbriae of hippocampus; (ii) an increase of Olig-1-mRNA levels; (iii) an increase of IL-6-mRNA, but not in protein levels; (iv) an increase in cell death, including OLs; and (v) MSCs treatment prevented the effect of PA on myelination, OLs number, and cell death. The present findings show that PA induces regional- and developmental-dependent changes on myelination and OLs maturation. Neonatal MSCs treatment improves survival of mature OLs and myelination in telencephalic white matter.

scholarly journals FP456CD362+ MESENCHYMAL STEM CELL TREATMENT OF KIDNEY DISEASE IN TYPE 2 DIABETIC LEPR DB/DB MICE

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii223-iii224 ◽  
Author(s):  
Satish Kumar Devarapu ◽  
Xie Junhui ◽  
Murthy Darisipudi ◽  
Anais Rocanin Arjo ◽  
Hans Joachim Anders
Keyword(s):  
Stem Cell ◽  
Kidney Disease ◽  
Mesenchymal Stem Cell ◽  
Stem Cell Treatment ◽  
Mesenchymal Stem Cell Treatment ◽  
Type 2 Diabetic

scholarly journals Gossypol Acetic Acid Attenuates Cardiac Ischemia/Reperfusion Injury in Rats via an Antiferroptotic Mechanism

Biomolecules ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1667
Author(s):  
Jian-Hong Lin ◽  
Kun-Ta Yang ◽  
Pei-Ching Ting ◽  
Yu-Po Luo ◽  
Ding-Jyun Lin ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Acetic Acid ◽  
Ischemia Reperfusion ◽  
Neonatal Rat ◽  
Mrna Levels ◽  
H9c2 Cells ◽  
Rat Cardiomyocytes ◽  
Protein Levels ◽  
Gossypol Acetic Acid

Myocardial ischemia/reperfusion (I/R) injury has been associated with ferroptosis, which is characterized by an iron-dependent accumulation of lipid peroxide to lethal levels. Gossypol acetic acid (GAA), a natural product taken from the seeds of cotton plants, prevents oxidative stress. However, the effects of GAA on myocardial I/R-induced ferroptosis remain unclear. This study investigated the ability of GAA to attenuate I/R-induced ferroptosis in cardiomyocytes along with the underlying mechanisms in a well-established rat model of myocardial I/R and isolated neonatal rat cardiomyocytes. H9c2 cells and cardiomyocytes were treated with the ferroptosis inducers erastin, RSL3, and Fe-SP. GAA could protect H9c2 cells against ferroptotic cell death caused by these ferroptosis inducers by decreasing the production of malondialdehyde and reactive oxygen species, chelating iron content, and downregulating mRNA levels of Ptgs2. GAA could prevent oxygen-glucose deprivation/reperfusion-induced cell death and lipid peroxidation in the cardiomyocytes. Moreover, GAA significantly attenuated myocardial infarct size, reduced lipid peroxidation, decreased the mRNA levels of the ferroptosis markers Ptgs2 and Acsl4, decreased the protein levels of ACSL4 and NRF2, and increased the protein levels of GPX4 in I/R-induced ex vivo rat hearts. Thus, GAA may play a cytoprotectant role in ferroptosis-induced cardiomyocyte death and myocardial I/R-induced ferroptotic cell death.

scholarly journals Successful mesenchymal stem cell treatment of leg ulcers complicated by Behcet disease

Medicine ◽  
2018 ◽  
Vol 97 (16) ◽  
pp. e0515 ◽  
Author(s):  
Yanhong Li ◽  
Zhongming Wang ◽  
Yi Zhao ◽  
Yubin Luo ◽  
Wangdong Xu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Behçet Disease ◽  
Leg Ulcers ◽  
Behcet Disease ◽  
Stem Cell Treatment ◽  
Mesenchymal Stem Cell Treatment

Topically applied adipose-derived mesenchymal stem cell treatment in experimental focal cerebral ischemia

2020 ◽  
Vol 71 ◽  
pp. 226-233
Author(s):  
Ping Kuen Lam ◽  
Kevin Ka Wang Wang ◽  
Don Wai Ching Chin ◽  
Cindy See Wai Tong ◽  
Yixiang Wang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cerebral Ischemia ◽  
Mesenchymal Stem Cell ◽  
Focal Cerebral Ischemia ◽  
Stem Cell Treatment ◽  
Mesenchymal Stem Cell Treatment

scholarly journals Global Hypoxia-Ischemia Induced Inflammation and Structural Changes in the Preterm Ovine Gut Which Were Not Ameliorated by Mesenchymal Stem Cell Treatment

2016 ◽  
Vol 22 (1) ◽  
pp. 244-257 ◽  
Author(s):  
Maria Nikiforou ◽  
Carolin Willburger ◽  
Anja E de Jong ◽  
Nico Kloosterboer ◽  
Reint K Jellema ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Structural Changes ◽  
Hypoxia Ischemia ◽  
Stem Cell Treatment ◽  
Mesenchymal Stem Cell Treatment

scholarly journals Cerebral Ischemia Causes Dysregulation of Synaptic Adhesion in Mouse Synaptosomes

2007 ◽  
Vol 28 (1) ◽  
pp. 99-110 ◽  
Author(s):  
Willard J Costain ◽  
Ingrid Rasquinha ◽  
Jagdeep K Sandhu ◽  
Peter Rippstein ◽  
Bogdan Zurakowski ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Adhesion Molecules ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Synaptic Proteins ◽  
Mrna Levels ◽  
Neuronal Nuclei ◽  
Protein Levels

Synaptic pathology is observed during hypoxic events in the central nervous system in the form of altered dendrite structure and conductance changes. These alterations are rapidly reversible, on the return of normoxia, but are thought to initiate subsequent neuronal cell death. To characterize the effects of hypoxia on regulators of synaptic stability, we examined the temporal expression of cell adhesion molecules (CAMs) in synaptosomes after transient middle cerebral artery occlusion (MCAO) in mice. We focused on events preceding the onset of ischemic neuronal cell death (< 48 h). Synaptosome preparations were enriched in synaptically localized proteins and were free of endoplasmic reticulum and nuclear contamination. Electron microscopy showed that the synaptosome preparation was enriched in spheres (≈650 nm in diameter) containing secretory vesicles and postsynaptic densities. Forebrain mRNA levels of synaptically located CAMs was unaffected at 3 h after MCAO. This is contrasted by the observation of consistent downregulation of synaptic CAMs at 20 h after MCAO. Examination of synaptosomal CAM protein content indicated that certain adhesion molecules were decreased as early as 3 h after MCAO. For comparison, synaptosomal Agrn protein levels were unaffected by cerebral ischemia. Furthermore, a marked increase in the levels of p-Ctnnb1 in ischemic synaptosomes was observed. p-Ctnnb1 was detected in hippocampal fiber tracts and in cornu ammonis 1 neuronal nuclei. These results indicate that ischemia induces a dysregulation of a subset of synaptic proteins that are important regulators of synaptic plasticity before the onset of ischemic neuronal cell death.

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