Receptors, Opioid, delta

Publication Title: 
The Journal of Biological Chemistry

The detrimental effect of severe hypoxia (SH) on neurons can be mitigated by hypoxic preconditioning (HPC), but the molecular mechanisms involved remain unclear, and an understanding of these may provide novel solutions for hypoxic/ischemic disorders (e.g. stroke). Here, we show that the delta-opioid receptor (DOR), an oxygen-sensitive membrane protein, mediates the HPC protection through specific signaling pathways.

Author(s): 
Ma, Ming-Chieh
Qian, Hong
Ghassemi, Farshid
Zhao, Peng
Xia, Ying
Publication Title: 
BMC biology

BACKGROUND: We have recently shown that delta-opioid receptors (DORs) play an important role in neuroprotection from hypoxic injury via the regulation of extracellular signaling-regulated kinase (ERK) and cytochrome c release. Since ERK and cytochrome c are differentially involved in caspase signaling of oxidative injury that significantly contributes to neuronal damage in ischemia/reperfusion, we considered if DOR activation protects the ischemic brain by attenuating oxidative injury.

Author(s): 
Yang, Yilin
Xia, Xiwei
Zhang, Yi
Wang, Qiang
Li, Lu
Luo, Guanghua
Xia, Ying
Publication Title: 
Cellular and molecular life sciences: CMLS

Hypoxic/ischemic disruption of ionic homeostasis is a critical trigger of neuronal injury/death in the brain. There is, however, no promising strategy against such pathophysiologic change to protect the brain from hypoxic/ischemic injury. Here, we present a novel finding that activation of delta-opioid receptors (DOR) reduced anoxic Na+ influx in the mouse cortex, which was completely blocked by DOR antagonism with naltrindole.

Author(s): 
Kang, Xuezhi
Chao, Dongman
Gu, Quanbao
Ding, Guanghong
Wang, Yingwei
Balboni, Gianfranco
Lazarus, Lawrence H.
Xia, Ying
Publication Title: 
Sheng Li Xue Bao: [Acta Physiologica Sinica]

The use of opioid analgesics has a long history in clinical settings, although the functions of opioid receptors, especially their role in the brain, are not well understood yet. Recent studies have generated abundant new data on opioid receptor-mediated functions and the underlying mechanisms. The most exciting finding in the past decade is probably the neuroprotection against hypoxic/ischemic stress mediated by delta-opioid receptors (DOR). An up-regulation of DOR expression and the release of endogenous opioids may increase neuronal tolerance to hypoxic/ischemic stress.

Author(s): 
Feng, Yuan
Chao, Dongman
He, Xiaozhou
Yang, Yilin
Kang, Xuezhi
H Lazarus, Lawrence
Xia, Ying
Publication Title: 
The Chinese Journal of Physiology

Recent studies show that both delta-opioid receptors (DOR) and GABA receptors play a neuroprotective role in the mature cortex. Since we have observed that DOR over-expression renders the cortex more tolerant to hypoxic stress, we asked whether DOR over-expression affects GABA receptors expression in the cortex under hypoxia. As the first step, we investigated the expression of GABAA receptor alpha1-subunit (GABAA Ralpha1, the most abundant alpha-subunit of GABA receptors in the adult brain) in the mouse cortex with transgenic DOR over-expression after hypoxia.

Author(s): 
Feng, Yuan
He, Xiaozhou
Yang, Yilin
Chen, Jingshan
Yin, Kaisheng
Xia, Ying
Publication Title: 
Experimental Neurology

Activation of delta-opioid receptors (DOR) is neuroprotective against hypoxic/ischemic injury in the cortex, which is at least partially related to its action against hypoxic/ischemic disruption of ionic homeostasis that triggers neuronal injury. Na(+) influx through TTX-sensitive voltage-gated Na(+) channels may be a main mechanism for hypoxia-induced disruption of K(+) homeostasis, with DOR activation attenuating the disruption of ionic homeostasis by targeting voltage-gated Na(+) channels.

Author(s): 
Chao, Dongman
He, Xiaozhou
Yang, Yilin
Bazzy-Asaad, Alia
Lazarus, Lawrence H.
Balboni, Gianfranco
Kim, Dong H.
Xia, Ying
Publication Title: 
PloS One

Prolonged hypoxic/ischemic stress may cause cortical injury and clinically manifest as a neurological disability. Activation of the δ-opioid receptor (DOR) may induce cortical protection against hypoxic/ischemic insults. However, the mechanisms underlying DOR protection are not clearly understood. We have recently found that DOR activation modulates the expression of microRNAs (miRNAs) in the kidney exposed to hypoxia, suggesting that DOR protection may involve a miRNA mechanism.

Author(s): 
Yang, Yilin
Zhi, Feng
He, Xiaozhou
Moore, Meredith L.
Kang, Xuezhi
Chao, Dongman
Wang, Rong
Kim, Dong H.
Xia, Ying
Publication Title: 
PloS One

Hypoxic/ischemic injury to kidney is a frequently encountered clinical problem with limited therapeutic options. Since microRNAs are differentially involved in hypoxic/ischemic events and δ-opioid receptor (DOR) activation is known to protect against hypoxic/ischemic injury, we speculated on the involvement of DOR activation in altering the microRNA (miRNA) expression in kidney under hypoxic condition. We selected 31 miRNAs based on microarray data for quantitative PCR analysis.

Author(s): 
He, Xiaozhou
Yang, Yilin
Zhi, Feng
Moore, Meredith L.
Kang, Xuezhi
Chao, Dongman
Wang, Rong
Balboni, Gianfranco
Salvadori, Severo
Kim, Dong H.
Xia, Ying
Publication Title: 
PloS One

OBJECTIVES: δ-opioid receptor (DOR) activation reduced brain ischemic infarction and attenuated neurological deficits, while DOR inhibition aggravated the ischemic damage. The underlying mechanisms are, however, not well understood yet. In this work, we asked if DOR activation protects the brain against ischemic injury through a brain-derived neurotrophic factor (BDNF) -TrkB pathway. METHODS: We exposed adult male Sprague-Dawley rats to focal cerebral ischemia, which was induced by middle cerebral artery occlusion (MCAO).

Author(s): 
Tian, Xuesong
Guo, Jingchun
Zhu, Min
Li, Minwei
Wu, Gencheng
Xia, Ying
Publication Title: 
International Journal of Molecular Sciences

We investigated whether δ-opioid receptor (DOR)-induced neuroprotection involves the brain-derived neurotrophic factor (BDNF) pathway. We studied the effect of DOR activation on the expression of BDNF and other proteins in the cortex of C57BL/6 mice exposed to hypoxia (10% of oxygen) for 1-10 days.

Author(s): 
Tian, Xuesong
Hua, Fei
Sandhu, Harleen K.
Chao, Dongman
Balboni, Gianfranco
Salvadori, Severo
He, Xiaozhou
Xia, Ying

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