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Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
UCP2 is a member of a family of mitochondrial uncoupling proteins that are homologous to UCP1. Although UCP2 shares 60% sequence identity with UCP1 and both proteins localize to the IM, UCP2 exhibits a broad tissue distribution and is abundantly expressed in monocytes and macrophages,732 whereas UCP1 expression is restricted to brown adipose tissue. UCP2 has been shown to induce mild mitochondrial uncoupling, which increases the rate of respiration and is thought to reduce electron leak from oxidative phosphorylation complexes, thereby decreasing mitochondrial superoxide generation.733
Mitochondrial uncoupling protein 2 is regulated through heterogeneous nuclear ribonucleoprotein K in lead exposure models
Published in Journal of Environmental Science and Health, Part C, 2020
Gaochun Zhu, Qian Zhu, Wei Zhang, Chen Hui, Yuwen Li, Meiyuan Yang, Shimin Pang, Yaobing Li, Guoyong Xue, Hongping Chen
Recent studies have showed that uncoupling protein 2 (UCP2) is vital for the adaptation of synaptic plasticity in learning and memory.14 UCP2 is a member of mitochondrial uncoupling proteins (UCPs) which include UCP1, UCP2, UCP3, UCP4 and UCP5. UCP2 is abundantly expressed in hypothalamic nuclei, substantia nigra, and especially in the hippocampus of rats.14 UCP2, an inner mitochondrial membrane anion carrier which is encoded by nuclear genome but functions exclusively in mitochondria,15 is activated by free radicals and free fatty acids.16 And UCP2 plays an important role in uncoupling oxidative phosphorylation from ATP synthesis via controlling proton reentry into the mitochondrial matrix. Therefore, uncoupled neurons can adapt rapidly and efficiently changeable neuronal activities through regulating synaptic plasticity.14 Recently, UCP2 has been shown to play a critical role in protecting the body from neurological diseases such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, temporal lobe epilepsy, brain trauma, stroke and ischemia.14,16–19. Taken together, UCP2 can affect synaptic plasticity and neurodegenerative processes, and maintain learning and memory functions in the hippocampus by regulating mitochondrial biogenesis, calcium efflux, free radical production and local temperature.20 But the mechanism that regulates its expression in lead exposure models remains to be illuminated.