Metformin inhibits polyphosphate-induced hyper-permeability and inflammation

Asgharzadeh, Fereshteh; Barneh, Farnaz; Fakhraie, Maryam; barkhordar, Seyede leili Adel; Shabani, Mohammad; Soleimani, Atena; Rahmani, Farzad; Ariakia, Fatemeh; Mehraban, Saeedeh; Avan, Amir; Hashemzehi, Milad; Arjmand, Mohammad-Hassan; Behnam-Rassouli, Reyhaneh; Jaberi, Najmeh; Sayyed-Hosseinian, Sayyed-Hadi; Ferns, Gordon A.; Ryzhikov, Mikhail; Jafari, Mohieddin; Hassanian, Seyed Mahdi

doi:10.1016/j.intimp.2021.107937

Cited by 6 publications

(3 citation statements)

References 63 publications

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“…Our data using heat-killed C. albicans indicate that live C. albicans infection is required to disrupt the RPE layer’s cell-cell junction integrity, also demonstrated in the case of bacterial endophthalmitis ( 24 ). Since AMPK has been shown to play a role in regulating the barrier integrity, we postulate that reduced AMPK levels in our study might be contributing to the breach of outer BRB ( 57 , 68 ). Hence, our study warrants further in-depth investigation of the role of AMPK in regulating the host response against C. albicans endophthalmitis to unravel a novel therapeutic approach to limit ocular candidiasis.…”

Section: Discussionmentioning

confidence: 84%

“…Our prior studies demonstrate an essential role of AMPK in regulating the retinal innate immune response to ocular infection by modulating both residential (glial) and infiltrating immune cells. Therefore, pharmacological AMPK activators such as 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) and metformin can be potentially used to promote the inflammation resolution in C. albicans endogenous endophthalmitis ( 54 – 57 ).…”

Section: Discussionmentioning

confidence: 99%

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Systemic Candida albicans Infection in Mice Causes Endogenous Endophthalmitis via Breaching the Outer Blood-Retinal Barrier

Singh

Kumar

2022

Microbiol Spectr

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Systemic Candida albicans Infection in Mice Causes Endogenous Endophthalmitis via Breaching the Outer Blood-Retinal Barrier

Singh

Kumar

2022

Microbiol Spectr

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“…However, the glycemic value of rats receiving the metformin treatment was not staticticaly different from saline treatment in our experiment. Metformin also was known to protect endothelial barrier and decrease permeability via junction reinforcement, anti-inflammation, anti-autophagy, and anti-oxidant [ 53 , 54 , 55 , 56 ]. Moreover, some studies revealed that metformin treatment could protect BBB [ 57 ].…”

Section: Discussionmentioning

confidence: 99%

Metformin Preserves VE–Cadherin in Choroid Plexus and Attenuates Hydrocephalus via VEGF/VEGFR2/p-Src in an Intraventricular Hemorrhage Rat Model

Shen

et al. 2022

IJMS

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Hydrocephalus induced by intraventricular hemorrhage (IVH) is associated with unfavorable prognosis. The increased permeability of choroid plexus and breakdown of the blood–brain barrier (BBB) was reported as a prominent mechanism of IVH-induced hydrocephalus, and vascular endothelial–cadherin (VE–cadherin) was demonstrated to be relevant. Metformin was reported to protect endothelial junction and preserve permeability widely; however, its role in hydrocephalus remains unclear. In this study, the decreased expression of VE–cadherin in the choroid plexus, accompanied with ventricle dilation, was investigated in an IVH rat model induced by intraventricular injection of autologous blood. Metformin treatment ameliorated hydrocephalus and upregulated VE–cadherin expression in choroid plexus meanwhile. We then observed that the internalization of VE–cadherin caused by the activation of vascular endothelial growth factor (VEGF) signaling after IVH was related to the occurrence of hydrocephalus, whereas it can be reversed by metformin treatment. Restraining VEGF signaling by antagonizing VEGFR2 or inhibiting Src phosphorylation increased the expression of VE–cadherin and decreased the severity of hydrocephalus after IVH. Our study demonstrated that the internalization of VE–cadherin via the activation of VEGF signaling may contribute to IVH-induced hydrocephalus, and metformin may be a potential protector via suppressing this pathway.

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Mechanism of metformin regulation in central nervous system: Progression and future perspectives

Cao¹,

Gong²,

Du³

et al. 2022

Biomedicine & Pharmacotherapy

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Metformin inhibits polyphosphate-induced hyper-permeability and inflammation

Cited by 6 publications

References 63 publications

Systemic Candida albicans Infection in Mice Causes Endogenous Endophthalmitis via Breaching the Outer Blood-Retinal Barrier

Systemic Candida albicans Infection in Mice Causes Endogenous Endophthalmitis via Breaching the Outer Blood-Retinal Barrier

Metformin Preserves VE–Cadherin in Choroid Plexus and Attenuates Hydrocephalus via VEGF/VEGFR2/p-Src in an Intraventricular Hemorrhage Rat Model

Mechanism of metformin regulation in central nervous system: Progression and future perspectives

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