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Ning, T.

Publications and source records attributed to Ning, T..

2 recordsLinked to original sources

Hsp22 is the key sensor and balancer in mitochondrial dynamic associated metabolic reprogramming

Altered mitochondrial dynamics are commonly seen in tumors and Parkinsons disease (PD), but the exact mechanism is unclear. We observed in tumor and PD flies, interference of mitochondrial fission or fusion reverses metabolic reprogramming and attenuates pathogenic phenotypes, indicating the rebalanced mitochondrial dynamics can re-establish cellular homeostasis. Surprisingly, we found Hsp22 is highly induced in tumor and PD flies. Hence, Hsp22 overexpression, not only suppressed RAS tumor flies, hepatocellular carcinoma mice, but also rescued PINK1B9 PD flies associating with restored mitochondrial homeostasis and reversing metabolic reprogramming. We speculate that mitochondrial dynamics is normally in a constant dynamic equilibrium, as if on a continually oscillating seesaw, tumor and PD are like the two extreme states of the seesaw which can be corrected by the promising target, Hsp22. One Sentence SummaryMitochondrial dynamics defects including tumor and PD lead to metabolic reprogramming accompanied with Hsp22 induction, vice versa, overexpression of Hsp22 reverses the mitochondrial dynamic dysfunction caused pathogenic metabolism.

cancer biology↗

Gut microbiota analysis in rats with methamphetamine-induced conditioned place preference

Methamphetamine abuse is a major public health crisis. Because accumulating evidence supports the hypothesis that the gut microbiota plays an important role in central nervous system (CNS) function, and research on the roles of the microbiome in CNS disorders holds conceivable promise for developing novel therapeutic avenues for treating CNS disorders, we sought to determine whether administration of methamphetamine leads to alterations in the intestinal microbiota. In this study, the gut microbiota profiles of rats with methamphetamine-induced conditioned place preference (CPP) were analysed through 16S rRNA gene sequencing. The faecal microbial diversity was slightly higher in the METH CPP group. The propionate-producing genus Phascolarctobacterium was attenuated in the METH CPP group, and the family Ruminococcaceae was elevated in the METH CPP group. Short chain fatty acid analysis revealed that the concentrations of propionate were decreased in the faecal matter of METH-administered rats. These findings provide direct evidence that administration of METH causes gut dysbiosis, enable a better understanding of the function of gut microbiota in the process of drug abuse, and provide a new paradigm for addiction treatment.

microbiology↗