Tumor necrosis factor-α disruption of brain endothelial cell barrier is mediated through matrix metalloproteinase-9

Wiggins-Dohlvik, Katie; Merriman, Morgan; Shaji, Chinchusha Anasooya; Alluri, Himakarnika; Grimsley, Marcene; Davis, Matthew L.; Smith, Randall W.; Tharakan, Binu

doi:10.1016/j.amjsurg.2014.08.014

Cited by 44 publications

(30 citation statements)

References 26 publications

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“…The activation of microglia leads to the accumulation of noxious cytokines that are key mediators for brain edema and blood-brain barrier disruption [66,67,68]. The resulting blood-brain barrier disruption and neuroinflammation leads to cognitive and functional deficits in ICH [69].…”

Section: Discussionmentioning

confidence: 99%

Naringin Reverses Neurobehavioral and Biochemical Alterations in Intracerebroventricular Collagenase-Induced Intracerebral Hemorrhage in Rats

et al. 2017

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Intracerebral hemorrhage (ICH) contributes to 10-15% of all strokes and is a high risk factor for morbidity and mortality as compared to other subtypes of stroke, that is, cerebral ischemia and subarachnoid hemorrhage. Oxidative stress (OS)-induced neuroinflammation and neuronal cell death contribute towards the hallmarks of ICH. Spared antioxidant levels, increased inflammatory cytokines and free radicals in ICH lead to neuronal death and exaggerate the hallmarks of ICH. Intracerebroventricular (ICV) collagenase (COL-induced neuronal cell damage and cognitive deficits form a widely recognized experimental model for ICH. Naringin (NGN), a natural antioxidant bioflavonoid, has shown potent neuroprotective effects in different neurodegenerative diseases. However, its potential is least explored in pathological conditions, such as hemorrhagic stroke. This study is aimed at exploring the protective effects of NGN against ICV-COL induced behavioral, neurological and memory deficits in rats. ICV-ICH was induced by single, unilateral intrastriatal injection of COL (1 IU in 2 µL, ICV) over 10 min. From 2nd day onwards, NGN was administered in three different doses (10, 20, and 40 mg/kg; p.o.). Animals were subjected to a battery of behavioral tests to assess behavioral changes, including neurological scoring tests (cylinder test, spontaneous motility, righting reflex, horizontal bar test, forelimb flexion), actophotometer, rotarod, Randall Selitto and von Frey. Poststroke depression and memory deficits were estimated using forced swim test and Morris water maze test, respectively. Poststroke depression, neurological and cognitive deficits were mitigated dose dependently by NGN administration. NGN administration also attenuated the nitro-OS and restored tumor necrosis factor-α and endogenous antioxidant levels. Our research demonstrates that NGN has a protective effect against ICH-induced neurocognitive deficits, along with mitigation of oxido-nitrosative and inflammatory stress.

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Section: Discussionmentioning

confidence: 99%

Naringin Reverses Neurobehavioral and Biochemical Alterations in Intracerebroventricular Collagenase-Induced Intracerebral Hemorrhage in Rats

et al. 2017

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“…At the level of endothelial cells themselves, MMP-2, -9 and -14 all play a role in normal angiogenesis, and a part of that process can include the release of local surface bound growth factors (including VEGF) and TNFα (Pepper 2001). Abnormally elevated TNFα in turn can stimulate damage to cell monolayer integrity of blood brain barrier endothelial cells through ZO-1 breakdown and this effect is apparently mediated by MMP9 (Wiggins-Dohlvik et al 2014). …”

Section: Effects Of Hormones Of Pe On the Endotheliummentioning

confidence: 99%

Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

Boeldt

Bird

2017

Journal of Endocrinology

258

152

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Maternal vascular adaptation to pregnancy is critically important in order to expand the capacity for blood flow through the uteroplacental unit to meet the needs of the developing fetus. Failure of the maternal vasculature to properly adapt can result in hypertensive disorders of pregnancy such as preeclampsia (PE). Herein, we review the endocrinology of maternal adaptation to pregnancy and contrast this with that of PE. Our focus is specifically on those hormones with directly impact endothelial cell function and dysfunction, as endothelial cell dysfunction is a hallmark of PE. A variety of growth factors and cytokines are present in normal vascular adaptation to pregnancy but have also been shown to be circulating at abnormal levels in PE pregnancies. Many of these factors promote endothelial dysfunction when present at abnormal levels by acutely inhibiting key Ca2+ signaling events and chronically promoting the breakdown of endothelial cell-cell contacts. Increasingly, our understanding of how the contributions of the placenta, immune cells, and the endothelium itself promote the endocrine milieu of PE is becoming more clear. We then describe in detail how the complex endocrine environment of PE effects endothelial cell function, why this has contributed to the difficulty in fully understanding and treating this disorder, and how a focus on signaling convergence points of many hormones may be a more successful treatment strategy.

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“…Furthermore, the ability of MMPs to proteolytically process inactive precursors of TNF-α (Gearing et al 1994), IL-1β (Amantea et al 2016) and OPN (Takafuji et al 2007) into biologically active forms can further modulate neuroinflammation. In brain microvascular endothelial cells, TNF-α (Wiggins-Dohlvik et al 2014) and IL-1β (Alluri et al 2016) induced MMP-9 activation leads to the degradation of tight junctions and blood brain barrier hyperpermeability. Similarly, brain pericytes respond to TGF-β by increasing their production of MMP-9 (Takahashi et al 2014).…”

Section: Matrix Metalloproteinases (Mmps)mentioning

confidence: 99%

Extracellular matrix and traumatic brain injury

George

Geller

2018

J of Neuroscience Research

103

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The Brain Extracellular Matrix (ECM) plays a crucial role in both the developing and adult brain by providing structural support and mediating cell-cell interactions. In this review, we focus on the major constituents of the ECM and how they function in both normal and injured brain, and summarize the changes in the composition of the ECM as well as how these changes either promote or inhibit recovery of function following Traumatic Brain Injury (TBI). Modulation of ECM composition to facilitates neuronal survival, regeneration and axonal outgrowth is a potential therapeutic target for TBI treatment.

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Tumor necrosis factor-α disruption of brain endothelial cell barrier is mediated through matrix metalloproteinase-9

Cited by 44 publications

References 26 publications

Naringin Reverses Neurobehavioral and Biochemical Alterations in Intracerebroventricular Collagenase-Induced Intracerebral Hemorrhage in Rats

Naringin Reverses Neurobehavioral and Biochemical Alterations in Intracerebroventricular Collagenase-Induced Intracerebral Hemorrhage in Rats

Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

Extracellular matrix and traumatic brain injury

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