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35 results on '"Peng, Jiyun"'

14. Microglia are involved in regulating histamine dependent and non-dependent itch transmissions with distinguished signal pathways

Author

Yang, Yuxiu, primary, Mou, Bin, additional, Zhang, Qi-Ruo, additional, Zhao, Hong-Xue, additional, Zhang, Jian-Yun, additional, Yun, Xiao, additional, Xiong, Ming-Tao, additional, Liu, Ying, additional, Liu, Yong U., additional, Pan, Haili, additional, Ma, Chao-Lin, additional, Li, Bao-Ming, additional, and Peng, Jiyun, additional

Published
2022
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21. Microglia Are Indispensable for Synaptic Plasticity in the Spinal Dorsal Horn and Chronic Pain

Author

Zhou, Li-Jun, primary, Peng, Jiyun, additional, Xu, Ya-Nan, additional, Zeng, Wei-Jie, additional, Zhang, Jun, additional, Wei, Xiao, additional, Mai, Chun-Lin, additional, Lin, Zhen-Jia, additional, Liu, Yong, additional, Murugan, Madhuvika, additional, Eyo, Ukpong B., additional, Umpierre, Anthony D., additional, Xin, Wen-Jun, additional, Chen, Tao, additional, Li, Mingtao, additional, Wang, Hui, additional, Richardson, Jason R., additional, Tan, Zhi, additional, Liu, Xian-Guo, additional, and Wu, Long-Jun, additional

Published
2019
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23. Cooperation of luteinizing hormone signaling pathways in preovulatory avian follicles regulates circadian clock expression in granulosa cell

Author

Liang Li, Qing Zhu, Yagang Wang, Zhichao Zhang, and Peng Jiyun

Subjects
Ovulation, medicine.medical_specialty, Time Factors, Transcription, Genetic, Granulosa cell, Clinical Biochemistry, Circadian clock, Estrous Cycle, Biology, p38 Mitogen-Activated Protein Kinases, chemistry.chemical_compound, Internal medicine, Cyclic AMP, medicine, Animals, Cyclic adenosine monophosphate, RNA, Messenger, Circadian rhythm, Extracellular Signal-Regulated MAP Kinases, Protein Kinase Inhibitors, Molecular Biology, Cells, Cultured, Granulosa Cells, Circadian Rhythm Signaling Peptides and Proteins, Cell Biology, General Medicine, Luteinizing Hormone, Circadian Rhythm, PER2, CLOCK, Endocrinology, Gene Expression Regulation, chemistry, cAMP-dependent pathway, Female, Luteinizing hormone, Chickens, Signal Transduction
Abstract

Ovulation in birds is triggered by a surge of luteinizing hormone (LH), and the ovulatory cycle is affected by the circadian rhythms of clock genes transcription levels in follicles. The influence of LH signaling cascades action on circadian clock genes was investigated using granulosa cells of preovulatory follicles from Roman hens cultured in a serum-free system. The expression of core oscillators (Bmal1, Clock, Cry1, Per2, and Rev-erbβ), clock-controlled gene (Star), Egr-1 and LHr was measured by quantitative real-time PCR. Significant changes in clock genes transcription levels were observed in control groups over 24 h, indicating that cell-autonomous rhythms exist in granulosa cells. Intriguingly, the transcript levels of clock genes increased with LH treatment during 24 h of culture; they peaked 4 h in advance of controls and second but weaker oscillations were also observed. It appeared that LH changed the cell-autonomous rhythm and cycle time of clock genes. To further investigate the LH signaling cascades, inhibitors of cyclic adenosine monophosphate (cAMP), p38 mitogen-activated protein kinases (p38MAPK) and extracellular signal-regulated kinases 1 and 2 (ERK1/2) pathways were used. The transcript levels of clock genes were suppressed by blocking cAMP, but increased with similar expression patterns by blocking the p38MPAK and ERK1/2 pathways over 24 h. Thus, the influence of LH signaling cascades in chicken ovulation is mediated by the cAMP pathway and also involves the p38MAPK and ERK1/2 pathways.

Published
2014

27. TNF-α Differentially Regulates Synaptic Plasticity in the Hippocampus and Spinal Cord by Microglia-Dependent Mechanisms after Peripheral Nerve Injury

Author

Liu, Yong, primary, Zhou, Li-Jun, additional, Wang, Jun, additional, Li, Dai, additional, Ren, Wen-Jie, additional, Peng, Jiyun, additional, Wei, Xiao, additional, Xu, Ting, additional, Xin, Wen-Jun, additional, Pang, Rui-Ping, additional, Li, Yong-Yong, additional, Qin, Zhi-Hai, additional, Murugan, Madhuvika, additional, Mattson, Mark P., additional, Wu, Long-Jun, additional, and Liu, Xian-Guo, additional

Published
2017
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28. TNF-α Differentially Regulates Synaptic Plasticity in the Hippocampus and Spinal Cord by Microglia-Dependent Mechanisms after Peripheral Nerve Injury

Author

Liu, Yong, primary, Zhou, Li-Jun, additional, Wang, Jun, additional, Li, Dai, additional, Ren, Wen-Jie, additional, Peng, Jiyun, additional, Wei, Xiao, additional, Xu, Ting, additional, Xin, Wen-Jun, additional, Pang, Rui-Ping, additional, Li, Yong-Yong, additional, Qin, Zhi-Hai, additional, Murugan, Madhuvika, additional, Mattson, Mark P., additional, Wu, Long-Jun, additional, and Liu, Xian-Guo, additional

Published
2016
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33. Neuronal Hyperactivity Recruits Microglial Processes via Neuronal NMDA Receptors and Microglial P2Y12 Receptors after Status Epilepticus.

Author

Eyo, Ukpong B., Peng, Jiyun, Swiatkowski, Przemyslaw, Mukherjee, Aparna, Bispo, Ashley, and Wu, Long-Jun

Subjects
*NEURONS, *MICROGLIA, *METHYL aspartate receptors, *STATUS epilepticus, *HIPPOCAMPUS (Brain), *ADENOSINE triphosphate
Abstract

Microglia are highly dynamic immune cells of the CNS and their dynamism is proposed to be regulated by neuronal activities. However, the mechanisms underlying neuronal regulation of microglial dynamism have not been determined. Here, we found an increased number of microglial primary processes in the hippocampus during KA-induced seizure activity. Consistently, global glutamate induced robust microglial process extension toward neurons in both brain slices and in the intact brain in vivo. The mechanism ofthe glutamate-induced microglialprocess extension involves the activation of neuronal NMDA receptors, calcium influx, subsequent ATP release, and microglial response through P2Y12 receptors. Seizure-induced increases in microglial process numbers were also dependent on NMDA receptor activation. Finally, we found that P2Y12 KO mice exhibited reduced seizure-induced increases in microglial process numbers and worsened KA-induced seizure behaviors. Our results elucidate the molecular mechanisms underlying microglia-neuron communication that may be potentially neuroprotective in the epileptic brain. [ABSTRACT FROM AUTHOR]

Published
2014
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34. Selective deficit in nogo performance induced by blockade of prefrontal cortical 2adrenoceptors in monkeys

Author

Ma, ChaoLin, Qi, XueLian, Peng, JiYun, and Li, BaoMing

Abstract

Two monkeys Macacamulattawere trained tomake a go response go to touch a computer screen when a red signal go signal was presented or a nogo response inhibit the screentouching action when a green signal nogo signal was given. The 2adrenergic antagonist yohimbinewas infused locally, bilaterally and continuously for 8 days into the prefrontal cortex PFC by using miniosmotic pump.The nogo but not go performancewas selectively impaired during the 8 day administration of yohimbine the monkeys showed an inability to inhibit the touching response to the nogo signal, indicating that there was a deficit in the inhibitory ability of the animals. Similar infusion of saline into the same cortical area was without effect. The present study provides behavioral pharmacological evidence that 2adrenoceptors in the PFC are involved in the neural mechanisms underlying response inhibition.

Published
2003
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35. Regulation of Physical Microglia-Neuron Interactions by Fractalkine Signaling after Status Epilepticus.

Author

Eyo UB, Peng J, Murugan M, Mo M, Lalani A, Xie P, Xu P, Margolis DJ, and Wu LJ

Subjects
Animals, Excitatory Amino Acid Agonists administration & dosage, Female, Glutamic Acid administration & dosage, Glutamic Acid metabolism, Interleukin-1beta metabolism, Kainic Acid, Male, Mice, Transgenic, Microglia pathology, Neurons pathology, Neuroprotection physiology, Pilocarpine, Receptors, Interleukin-8A genetics, Receptors, Interleukin-8A metabolism, Receptors, Purinergic P2Y12 genetics, Receptors, Purinergic P2Y12 metabolism, Seizures metabolism, Seizures pathology, Status Epilepticus pathology, Tissue Culture Techniques, Chemokine CX3CL1 metabolism, Microglia metabolism, Neurons metabolism, Status Epilepticus metabolism
Abstract

Microglia, the resident immune cells of the brain, perform elaborate surveillance in which they physically interact with neuronal elements. A novel form of microglia-neuron interaction named microglial process convergence (MPC) toward neuronal axons and dendrites has recently been described. However, the molecular regulators and pathological relevance of MPC have not been explored. Here, using high-resolution two-photon imaging in vivo and ex vivo , we observed a dramatic increase in MPCs after kainic acid- or pilocarpine-induced experimental seizures that was reconstituted after glutamate treatment in slices from mice. Interestingly, a deficiency of the fractalkine receptor (CX3CR1) decreased MPCs, whereas fractalkine (CX3CL1) treatment increased MPCs, suggesting that fractalkine signaling is a critical regulator of these microglia-neuron interactions. Furthermore, we found that interleukin-1β was necessary and sufficient to trigger CX3CR1-dependent MPCs. Finally, we show that a deficiency in fractalkine signaling corresponds with increased seizure phenotypes. Together, our results identify the neuroglial CX3CL1-CX3CR1 communication axis as a modulator of potentially neuroprotective microglia-neuron physical interactions during conditions of neuronal hyperactivity., Competing Interests: Authors report no conflict of interest.

Published
2017
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