Recombinant osteopontin attenuates experimental cerebral vasospasm following subarachnoid hemorrhage in rats through an anti-apoptotic mechanism

He, Junchi; Liu, Mindi; Liu, Zhen; Luo, Lixia

doi:10.1016/j.brainres.2015.03.015

Cited by 17 publications

(17 citation statements)

References 30 publications

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“…There were also drugs with anti-apoptotic effects, including proanthocyanidin, N-acetylcysteine, mexiletine, immunoglobulin, telmisartan, 2,2 0 -dipyridyl, recombinant human erythropoietin, human tissue kallikrein, alpha lipoic acid and so on. 6,[42][43][44][45][46][47][48][49][50] Signalling pathways participating in the anti-apoptotic effects include the Akt pathway, JAK2/STAT3 pathway, and others. Based on the above results, we could conclude that anti-apoptotic and anti-inammatory mechanisms play an important role in the attenuation of CVS aer SAH.…”

Section: Discussionmentioning

confidence: 99%

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Ethyl pyruvate attenuates delayed experimental cerebral vasospasm following subarachnoid haemorrhage in rats: possible role of JNK pathway

et al. 2018

RSC Adv.

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Section: Discussionmentioning

confidence: 99%

“…1 The pathophysiology of CVS is multifaceted and involves both endothelial apoptosis and inammation. [2][3][4][5][6][7] However, the development of therapeutic interventions has been largely hindered by the fact that the underlying pathological mechanisms of CVS remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Ethyl pyruvate attenuates delayed experimental cerebral vasospasm following subarachnoid haemorrhage in rats: possible role of JNK pathway

et al. 2018

RSC Adv.

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“…Intra-accumbens injection was performed according to previously described methods 31,48,49 , with minor modifications. Mice were microinjected with OPN (0.03 μg) or PBS (vehicle) in a total volume of 0.25 μL/side at a rate of 0.25 μL/min using a microdrive pump (ESP-64; EICOM, Kyoto, Japan), and injectors were left in the NAc for an additional 30 sec to allow for diffusion after the 1 min infusion period.…”

Section: Methodsmentioning

confidence: 99%

Involvement of the accumbal osteopontin-interacting transmembrane protein 168 in methamphetamine-induced place preference and hyperlocomotion in mice

Miyamoto

Otake

et al. 2017

Sci Rep

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Chronic exposure to methamphetamine causes adaptive changes in brain, which underlie dependence symptoms. We have found that the transmembrane protein 168 (TMEM168) is overexpressed in the nucleus accumbens of mice upon repeated methamphetamine administration. Here, we firstly demonstrate the inhibitory effect of TMEM168 on methamphetamine-induced behavioral changes in mice, and attempt to elucidate the mechanism of this inhibition. We overexpressed TMEM168 in the nucleus accumbens of mice by using an adeno-associated virus vector (NAc-TMEM mice). Methamphetamine-induced hyperlocomotion and conditioned place preference were attenuated in NAc-TMEM mice. Additionally, methamphetamine-induced extracellular dopamine elevation was suppressed in the nucleus accumbens of NAc-TMEM mice. Next, we identified extracellular matrix protein osteopontin as an interacting partner of TMEM168, by conducting immunoprecipitation in cultured COS-7 cells. TMEM168 overexpression in COS-7 cells induced the enhancement of extracellular and intracellular osteopontin. Similarly, osteopontin enhancement was also observed in the nucleus accumbens of NAc-TMEM mice, in in vivo studies. Furthermore, the infusion of osteopontin proteins into the nucleus accumbens of mice was found to inhibit methamphetamine-induced hyperlocomotion and conditioned place preference. Our studies suggest that the TMEM168-regulated osteopontin system is a novel target pathway for the therapy of methamphetamine dependence, via regulating the dopaminergic function in the nucleus accumbens.

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“…Osteopontin (OPN) is a secreted extracellular matrix glycoprotein with roles in a variety of physiological and pathological processes, including cerebral vascular remodeling, cell migration, and antiapoptotic processes. 13 In previous studies, administration of recombinant OPN (rOPN) has shown promising neuroprotective effects 14 such as stabilizing vascular smooth muscle cell phenotype after subarachnoid hemorrhage, 15 and attenuating inflammation after intracerebral hemorrhage. 16 Interestingly, recent studies showed that OPN was a potential enhancer of autophagy in an in-vitro model of abdominal aorta aneurysm 17 and human hepatocellular carcinoma.…”

Section: Introductionmentioning

confidence: 99%

Osteopontin attenuates early brain injury through regulating autophagy‐apoptosis interaction after subarachnoid hemorrhage in rats

et al. 2019

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Aim To determine the effect of osteopontin (OPN) on autophagy and autophagy‐apoptosis interactions after SAH. Methods The endovascular perforation model of SAH or sham surgery was performed in a total of 86 Sprague‐Dawley male rats. The temporal expressions of endogenous OPN and autophagy‐related proteins (Beclin 1, ATG5, LC3 II to I ratio) were measured in sham and SAH rats at different time points (3, 6, 12, 24, and 72 hours). Rats were randomly divided into three groups: Sham, SAH + Vehicle (PBS, phosphate‐buffered saline), and SAH + rOPN (5 μg/rat recombinant OPN). Neurobehavioral tests were performed 24 hours after SAH, followed by the collection of brain samples for assessment of autophagy and apoptosis proteins. These tests assessed whether an autophagy‐apoptosis relationship existed on the histological level in the brain. Results Endogenous OPN and autophagy‐related proteins all increased after SAH. rOPN administration improved neurological dysfunction, increased the expression of autophagy‐related proteins (Beclin 1, ATG5, LC3 II to I ratio) and antiapoptotic protein Bcl‐2, while decreasing the expression of proapoptotic proteins (cleaved Caspase‐3 and Bax). rOPN also regulated autophagy‐apoptosis interactions 24 hours after SAH. Conclusion rOPN attenuates early brain injury and inhibits neuronal apoptosis by activating autophagy and regulating autophagy‐apoptosis interactions.

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Recombinant osteopontin attenuates experimental cerebral vasospasm following subarachnoid hemorrhage in rats through an anti-apoptotic mechanism

Cited by 17 publications

References 30 publications

Ethyl pyruvate attenuates delayed experimental cerebral vasospasm following subarachnoid haemorrhage in rats: possible role of JNK pathway

Ethyl pyruvate attenuates delayed experimental cerebral vasospasm following subarachnoid haemorrhage in rats: possible role of JNK pathway

Involvement of the accumbal osteopontin-interacting transmembrane protein 168 in methamphetamine-induced place preference and hyperlocomotion in mice

Osteopontin attenuates early brain injury through regulating autophagy‐apoptosis interaction after subarachnoid hemorrhage in rats

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