Protective Functions of PJ34, a Poly(ADP-ribose) Polymerase Inhibitor, Are Related to Down-Regulation of Calpain and Nuclear Factor-κB in a Mouse Model of Traumatic Brain Injury

Xue, Tao; Chen, Xuetao; Hou, Zhiyong; Hao, Shuyu; Liu, Baiyun

doi:10.1016/j.wneu.2017.06.076

Cited by 6 publications

(3 citation statements)

References 67 publications

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“…142 Moreover, adhesive and chemotactic properties of OPN exert function in the lateral migration of neuroblasts from the subventricular zone to the injured region following focal cerebral ischaemia and ICH. 143,144 OPN also reportedly enhances the sensitivity of adult corticospinal neurons to insulin-like growth factor 1, 145 ameliorates cerebral vasospasm 109,[146][147][148] and stabilizes smooth muscle cell phenotype 57 following acute brain injury.…”

Section: Additional Aspects Of Opnmentioning

confidence: 97%

Osteopontin as a candidate of therapeutic application for the acute brain injury

Zhou

Yao

Sheng

et al. 2020

J Cellular Molecular Medi

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Acute brain injury is the leading cause of human death and disability worldwide, which includes intracerebral haemorrhage, subarachnoid haemorrhage, cerebral ischaemia, traumatic brain injury and hypoxia‐ischaemia brain injury. Currently, clinical treatments for neurological dysfunction of acute brain injury have not been satisfactory. Osteopontin (OPN) is a complex adhesion protein and cytokine that interacts with multiple receptors including integrins and CD44 variants, exhibiting mostly neuroprotective roles and showing therapeutic potential for acute brain injury. OPN‐induced tissue remodelling and functional repair mainly rely on its positive roles in the coordination of pro‐inflammatory and anti‐inflammatory responses, blood‐brain barrier maintenance and anti‐apoptotic actions, as well as other mechanisms such as affecting the chemotaxis and proliferation of nerve cells. The blood OPN strongly parallel with the OPN induced in the brain and can be used as a novel biomarker of the susceptibility, severity and outcome of acute brain injury. In the present review, we summarized the molecular signalling mechanisms of OPN as well as its overall role in different kinds of acute brain injury.

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Section: Additional Aspects Of Opnmentioning

confidence: 97%

Osteopontin as a candidate of therapeutic application for the acute brain injury

Zhou

Yao

Sheng

et al. 2020

J Cellular Molecular Medi

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“…Similarly, in the N -methyl- d -aspartic acid (NMDA) toxicity model in rat primary cortical neurons, PARP and calpain were found to be linked via PARP-1 induced alterations in mitochondrial Ca 2+ homeostasis [ 104 ]. In a mouse model of controlled cortical impact (CCI), the PARP inhibitor PJ34 suppressed the over-activation of calpain [ 97 ]. Hence, in hereditary retinal degeneration, PARP may be linked directly to calpain activity or vice versa .…”

Section: Ca 2+ and Calpain-type Proteasesmentioning

confidence: 99%

The role of cGMP-signalling and calcium-signalling in photoreceptor cell death: perspectives for therapy development

Das

Chen

Yan

et al. 2021

Pflugers Arch - Eur J Physiol

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The second messengers, cGMP and Ca2+, have both been implicated in retinal degeneration; however, it is still unclear which of the two is most relevant for photoreceptor cell death. This problem is exacerbated by the close connections and crosstalk between cGMP-signalling and calcium (Ca2+)-signalling in photoreceptors. In this review, we summarize key aspects of cGMP-signalling and Ca2+-signalling relevant for hereditary photoreceptor degeneration. The topics covered include cGMP-signalling targets, the role of Ca2+ permeable channels, relation to energy metabolism, calpain-type proteases, and how the related metabolic processes may trigger and execute photoreceptor cell death. A focus is then put on cGMP-dependent mechanisms and how exceedingly high photoreceptor cGMP levels set in motion cascades of Ca2+-dependent and independent processes that eventually bring about photoreceptor cell death. Finally, an outlook is given into mutation-independent therapeutic approaches that exploit specific features of cGMP-signalling. Such approaches might be combined with suitable drug delivery systems for translation into clinical applications.

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“…At the subcellular level (in the particular case of ionic homeostasis), primary damage strongly influences Ca 2+ homeostasis, which is a known second messenger, hence its disruption generates a wide scope of negative effects in the brain, 13 such as the deregulated release of neurotransmitters (mainly glutamate), which unchains the additional release of Ca 2+ found in the intracellular reserves 14 giving way to reactions that can lead to a cytotoxic injury, oxidative stress, 15 proteolysis 16 and, finally, to programmed (apoptosis) and not programmed (necrosis) cell death. 17,18 Derived from the TBI-induced primary damage events are the secondary effects on the brain's physiology; these effects are known as secondary damage, and occur on a greater temporal scale than those of primary damage. 12 The secondary damage processes can include traumatic hematomas, focal or diffuse brain edema, elevated intracranial pressure, obstructive hydrocephaly, hypoxia, ischemic lesion and infections.…”

Section: Primary and Secondary Damagementioning

confidence: 99%

Neuroimmunological phenomena involved in chronic traumatic brain injury

Velasco-González

Vargas‐Castro

Mendoza‐Negrete

et al. 2019

Clinical & Exp Neuroim

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Currently, chronic traumatic encephalopathy (CTE) is widely recognized as a neurodegenerative syndrome caused by constant exposure to events of acceleration and deceleration. CTE produces a myriad of neurological alterations in both the short-and long term; some of these alterations disturb the homeostasis of the central nervous system, and trigger several behavioral and cognitive deficits. The pathology of CTE resembles that of Alzheimer's, Parkinson's and Huntington's disease (among many others), which are characterized by the important role of the immune response in the development of the disease and the deposition of proteins, such as amyloid beta and tau. In the present article, we review the succession of events that develop after exposure to acceleration/deceleration events, and how such events affect the distinct cellular types in the central nervous system and their role in the activation of the immune system. We also review how the activation of the immune system affects mechanisms, such as neurogenesis and neurodegeneration, and how this in turn could generate the behavioral and cognitive deficits associated with this pathology. ClassificationChronic traumatic encephalopathy, such as posttraumatic encephalopathy, is part of TBI, the latter is

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Protective Functions of PJ34, a Poly(ADP-ribose) Polymerase Inhibitor, Are Related to Down-Regulation of Calpain and Nuclear Factor-κB in a Mouse Model of Traumatic Brain Injury

Cited by 6 publications

References 67 publications

Osteopontin as a candidate of therapeutic application for the acute brain injury

Osteopontin as a candidate of therapeutic application for the acute brain injury

The role of cGMP-signalling and calcium-signalling in photoreceptor cell death: perspectives for therapy development

Neuroimmunological phenomena involved in chronic traumatic brain injury

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