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Frontiers | Neurons Release Injured Mitochondria as "Help-Me" Signaling After Ischemic Stroke

Mitochondrial dysfunction has been regarded as one of the major contributors of ischemic neuronal death after stroke. Recently, intercellular mitochondria transfer between different cell types has been widely studied and suggested as a potential therapeutic approach. However, whether mitochondria are involved in the neuron-glia crosstalk following ischemic stroke and the underlying mechanisms have not been explored yet. In this study, we demonstrated that under physiological condition, neurons release few mitochondria into the extracellular space, and the mitochondrial release increased when subjected to the challenges of acidosis, hydrogen peroxide (H2O2), N-methyl-D-aspartate (NMDA) or glutamate. Acidosis reduced the mitochondrial basal respiration and lowered the membrane potential in primary cultured mouse cortical neurons. These defective mitochondria were prone to be expelled to the extracellular space by the injured neurons, and were engulfed by adjacent astrocytes, leading to i ....

United States , United Kingdom , South Korea , Takara Bio , Rho Gtpase , Franklin Lakes , Savic Azoulay , Beit Haemek , Tukey Kramer , Acta Neuropathol , Ben Kasus Nissim , Shanghai Jiao Tong University School Of Medicine , National Natural Science Foundation Of China , Doccol Corp , Promotion Program Of Renji Hospital , Cell Bank Stem , American Heart Association Stroke , Shanghai Chinese Academy Of Sciences , Thermo Fisher Scientific , Biological Industries , Kibbutz Beit Haemek , Hyclone Life Science , Stem Cell , Shanghai Chinese Academy , Reperfusion Cell , Animal Care ,