Increased CD147 (EMMPRIN) expression in the rat brain following traumatic brain injury

Wei, Ming; Li, Hong; Shang, Yanguo; Zhou, Ziwei; Zhang, Jianning

doi:10.1016/j.brainres.2014.06.018

Cited by 11 publications

(3 citation statements)

References 37 publications

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“…Studies have shown that the brain water content and the content of Evans blue dye in the brain following TBI are significantly high in comparison with control group, 48 h post-trauma [37,38], in accordance with our present findings. Administration of genistein resulted in inhibiting the brain edema development and the BBB disruption.…”

Section: Discussionsupporting

confidence: 92%

Is genistein neuroprotective in traumatic brain injury?

Soltani

Khaksari

Jafari

et al. 2015

Physiology & Behavior

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The concerns about negative consequences of estrogen therapy have led to introduce other strategies to obtain estrogen's benefits in the brain. The present study tests the hypothesis that a major isoflavone of soy; genistein with estrogen-like activity can be neuroprotective in traumatic brain injury (TBI). The male Wistar rats were randomly divided to four groups: sham, TBI, vehicle and genistein. The TBI was induced by Marmarou method. The brain edema and the disruption of blood-brain-barrier (BBB) were evaluated 48 h post-TBI. Genistein (15 mg/kg) or dimethyl sulfoxide (DMSO) was injected i.p., twice after TBI. The intracranial pressure (ICP), the motor performance, and the beam-walk task (WB) were determined before trauma, on trauma day (D0), and first (D1) and second (D2) days post-TBI. Genistein inhibited a development of brain edema and a BBB permeability in TBI animals. An increase of ICP and a defect in motor and WB performance were showed following TBI, in all times evaluated. An increase of ICP induced by TBI was suppressed by genistein on D1 and D2 times. Genistein improved a motor disorder induced by TBI, on D1 and D2 times. Also an increase of traversal time in WB task was suppressed by genistein in TBI animals, on D1 and D2 times. The results of this study demonstrated that genistein can be neuroprotective in TBI. Genistein inhibited the disruption of BBB, the brain edema and the increase of ICP, and the disturbance of neurobehavioral performance in TBI.

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Section: Discussionsupporting

confidence: 92%

Is genistein neuroprotective in traumatic brain injury?

Soltani

Khaksari

Jafari

et al. 2015

Physiology & Behavior

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“…The cerebrovasculature becomes leakier, with reduced capillary density, glucose transport and cerebral blood flow [ 105 , 234 ]. Increased cerebrovascular MMP activities via CD147/ADAM17 breakdown the basement membrane and contribute to the vascular dysfunction [ 235 , 236 ]. Proinflammatory cytokines, such as TNFα could stimulate ADAM17[ 69 ].…”

Section: Co-morbidities Increase Risk Of Death From Covid-19: Outlinedmentioning

confidence: 99%

SARS-CoV-2: is there neuroinvasion?

McQuaid

Brady

Deane

2021

Fluids Barriers CNS

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Background SARS-CoV-2, a coronavirus (CoV), is known to cause acute respiratory distress syndrome, and a number of non-respiratory complications, particularly in older male patients with prior health conditions, such as obesity, diabetes and hypertension. These prior health conditions are associated with vascular dysfunction, and the CoV disease 2019 (COVID-19) complications include multiorgan failure and neurological problems. While the main route of entry into the body is inhalation, this virus has been found in many tissues, including the choroid plexus and meningeal vessels, and in neurons and CSF. Main body We reviewed SARS-CoV-2/COVID-19, ACE2 distribution and beneficial effects, the CNS vascular barriers, possible mechanisms by which the virus enters the brain, outlined prior health conditions (obesity, hypertension and diabetes), neurological COVID-19 manifestation and the aging cerebrovascualture. The overall aim is to provide the general reader with a breadth of information on this type of virus and the wide distribution of its main receptor so as to better understand the significance of neurological complications, uniqueness of the brain, and the pre-existing medical conditions that affect brain. The main issue is that there is no sound evidence for large flux of SARS-CoV-2 into brain, at present, compared to its invasion of the inhalation pathways. Conclusions While SARS-CoV-2 is detected in brains from severely infected patients, it is unclear on how it gets there. There is no sound evidence of SARS-CoV-2 flux into brain to significantly contribute to the overall outcomes once the respiratory system is invaded by the virus. The consensus, based on the normal route of infection and presence of SARS-CoV-2 in severely infected patients, is that the olfactory mucosa is a possible route into brain. Studies are needed to demonstrate flux of SARS-CoV-2 into brain, and its replication in the parenchyma to demonstrate neuroinvasion. It is possible that the neurological manifestations of COVID-19 are a consequence of mainly cardio-respiratory distress and multiorgan failure. Understanding potential SARS-CoV-2 neuroinvasion pathways could help to better define the non-respiratory neurological manifestation of COVID-19.

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“…Кроме того, повреждение гена CD147 у мышей и дрозофил (D. melanogaster) приводит к нечувствительности к раздражающим запахам [54]. Особого внимания заслуживает экспрессия CD147 на клетках церебрального эндотелия, которая, вероятно, участвует в регуляции проницаемости гематоэнцефалического барьера (ГЭБ) и, как свидетельствуют экспериментальные данные, увеличивается после повреждения головного мозга [55]. С учетом предполагаемой роли лактата, продуцируемого периваскулярной астроглией, в контроле структурно-функциональной целостности ГЭБ, весьма логичным представляется участие CD147, сопряженного с MCT клеток эндотелия, в регуляции астроцит-эндотелиального взаимодействия.…”

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Cd147 Polyfunctionality and New Diagnostic and Therapy Opportunities

Uspenskaya¹,

Kоmleva²,

Gorina³

et al. 2018

SMR

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НИИ молекулярной медицины и патобиохимии, Красноярск 660022, Российская Федерация 2 Красноярский государственный медицинский университет имени профессора В. Ф. Войно-Ясенецкого, Красноярск 660022, Российская Федерация Резюме. В обзоре представлены современные представления об открытии, характеристике, молекулярной структуре, особенностях экспрессии в клетках различной природы, биологических функциях и регуляторных механизмах CD147 у человека в физиологических и патологических условиях. Обсуждается роль CD147 в регуляции активности клеток центральной нервной системы в норме и при нейродегенерации. Рассматривается участие CD147 в патологии центральной нервной системы, в частности в патогенезе болезни Альцгеймера. Описаны механизмы, с помощью которых CD147 регулируют уровень бета-амилоида. Представлены сведения о возможности применения CD147 в качестве мишени для фармакотерапии заболеваний центральной нервной системы. Ключевые слова: CD147, матриксные металлопротеиназы, сигнальная трансдукция, центральная нервная система, нейродегенерация, болезнь Альцгеймера, γ-секретазный комплекс. Конфликт интересов. Авторы декларируют отсутствие явных и потенциальных конфликтов интересов, связанных с публикацией настоящей статьи.

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Increased CD147 (EMMPRIN) expression in the rat brain following traumatic brain injury

Cited by 11 publications

References 37 publications

Is genistein neuroprotective in traumatic brain injury?

Is genistein neuroprotective in traumatic brain injury?

SARS-CoV-2: is there neuroinvasion?

Cd147 Polyfunctionality and New Diagnostic and Therapy Opportunities

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