Potential role of heme metabolism in the inducible expression of heme oxygenase-1

Takeda, Tomotaka; Sasai, Machiko; Adachi, Yuka; Ohnishi, Keiko; Fujisawa, Jun–ichi; Izawa, Shingo; Taketani, Shigeru

doi:10.1016/j.bbagen.2017.03.018

Cited by 18 publications

(19 citation statements)

References 49 publications

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“…Researchers propose that the antioxidative capacity of HO-1 should be ascribed to its end products such as ferrous free iron, CO, and biliverdin. 14,[62][63][64] Biliverdin is metabolized further by biliverdin reductase to the bile pigment (bilirubin), a potent antioxidant molecule. 65 Biological effects of these products are complex, and they may act cooperatively to alleviate photoreceptors from oxidative insults.…”

Section: Discussionmentioning

confidence: 99%

“…These end products have shown potent antiapoptotic and antioxidant ability under pathologic conditions. 14 HO-1 is reactive to external insults including inflammation, heat shock, oxidative damage, and ischemia-reperfusion injury. [14][15][16] For instance, HO-1 expression in Müller cells increases significantly during retinal ischemic injury.…”

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confidence: 99%

“…14 HO-1 is reactive to external insults including inflammation, heat shock, oxidative damage, and ischemia-reperfusion injury. [14][15][16] For instance, HO-1 expression in Müller cells increases significantly during retinal ischemic injury. Conversely, inhibiting HO-1 expression with HO-1 short-interfering RNA (siRNA) causes severe inflammatory reaction and retinal damage.…”

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confidence: 99%

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CoPP-Induced-Induced HO-1 Overexpression Alleviates Photoreceptor Degeneration With Rapid Dynamics: A Therapeutic Molecular Against Retinopathy

Tao

Cai

Zhou

et al. 2019

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Retinitis pigmentosa (RP) causes progressive photoreceptor degeneration in the retina. The N-methyl-N-nitrosourea (MNU)-administered mouse is used as a chemically induced RP model with rapid progression rate. This study was designed to study heme oxygenase-1 (HO-1) expression in the MNU-administered mice, and to explore the therapeutic effects of cobalt protoporphyrin (CoPP). METHODS. The HO-1 expression in the retina of MNU-administered mice was analyzed. CoPP was injected intravenously into the MNU-administered mice. Subsequently, the CoPP-treated mice were subjected to functional and morphologic examinations. RESULTS. HO-1 was involved in the MNU-induced photoreceptor degeneration. CoPP treatment enhanced retinal HO-1 expression in the MNU-administered mice. Electroretinogram (ERG) examination and behavioral tests showed that CoPP treatment improved the retinal responsiveness of MNU-administered mice. Histologic analysis and optical coherence tomography (OCT) examination showed that retinal architecture of the CoPP-treated mice was more intact than that of the MNUþvehicle group. Cone photoreceptors in the MNUadministered mice were rescued efficiently by CoPP treatment. Furthermore, multielectrode array (MEA) recording showed that CoPP treatment mitigated the spontaneous firing response, enhanced the light-induced firing response, and preserved the basic configurations of visual signal pathway in the MNU-administered mice. Mechanism studies suggested that CoPP afforded these therapeutic effects by modulating the apoptosis cascades and alleviating the oxidative stress in degenerative retinas. CONCLUSIONS. CoPP alleviated photoreceptor degeneration and rectified the signaling abnormities in MNU-administered mice. CoPP may serve as a potential medication against degenerative retinopathy.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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CoPP-Induced-Induced HO-1 Overexpression Alleviates Photoreceptor Degeneration With Rapid Dynamics: A Therapeutic Molecular Against Retinopathy

Tao

Cai

Zhou

et al. 2019

Invest. Ophthalmol. Vis. Sci.

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“…This results in the production of cytokines such as (TNF-α, IL-1B, IL-6, IL-2) and causes a cytokine storm that results in necrosis and cell death. In COVID-19 patients it is observed that there is an inhibition in the production of heme, as it is responsible for the production of biliverdin, ferrous iron and carbon mono-oxide which could limit the inflammation and stress caused due to SARS-CoV-2 viral infection [ [37] , [38] , [39] ]. If the BS is provided to the COVID-19 patients, then it could suppress the production of NF-κB by stimulating the HO-1 and TH1 macrophage cells [ 40 ].…”

Section: Bss Anti-inflammatory Role Against Covid-19mentioning

confidence: 99%

Biosurfactants and anti-inflammatory activity: A potential new approach towards COVID-19

Subramaniam

Venkatesan

Iyer

et al. 2020

Current Opinion in Environmental Science & Health

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Coronavirus Disease 2019 (COVID-19) has grown to be global public health emergency. The biosurfactants (BSs) are surface-active biomolecules with unique properties and wide applications. Several microbes synthesize secondary metabolites with surface-active properties which has wide range of anti-inflammatory and anti-viral role.. The monocytes and neutrophils are activated by bacteria which subsequently result in high secretion of pro-inflammatory cytokines (TNF-α, IL-6, IL-8, IL-12, Il-18 and IL-1β) and toll-like receptors-2 (TLR-2). Following the inflammatory response, BSs induce the production of cationic proteins, reactive oxygen species (ROS) and lysozyme, and thus can be utilized for therapeutic purposes. This review provides recent advances in the anti-inflammatory and antiviral activities of biosurfactants and discusses the potential use of these compounds against COVID-19, highlighting the need for in-vitro and in-vivo approaches to confirm this hypothesis. This suggestion is necessary because there are still no studies that have focused on the use of biosurfactants against COVID-19.

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“…Carbon monoxide (CO) is an endogenously produced gas molecule causing relaxation of the vessels [ 7 ]. Heme oxygenase (HO) is a critical cytoprotective enzyme that degrades cytotoxic free heme and produces the potent vasodilator CO and the antioxidant bilirubin [ 7 , 8 ]. Three isoforms of HO are known.…”

Section: Introductionmentioning

confidence: 99%

Contribution of Heme Oxygenase 2 to Blood Pressure Regulation in Response to Swimming Exercise and Detraining in Spontaneously Hypertensive Rats

et al. 2018

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BackgroundWe aimed to determine the effects of exercise followed by detraining on systolic blood pressure (SBP), heme oxygenase 2 (HO-2) expression, and carboxyhemoglobin (COHb) concentration in spontaneously hypertensive rats (SHR) to explain the role of carbon monoxide (CO) in this process.Material/MethodsAnimals were randomized into exercised and detrained groups. Corresponding sedentary rats were grouped as Time 1–2. Swimming of 60 min/5 days/week for 10 weeks was applied. Detraining rats discontinued training for an additional 5 weeks. Gene and protein expressions were determined by real-time PCR and immunohistochemistry.ResultsAorta HO-2 histological scores (HSCORE) of hypertensive rats were lower, while SBP was higher. Swimming caused enhancement of HO-2 immunostaining in aorta endothelium and adventitia of SHR. Exercise induced elevation of blood COHb index in SHR. Synchronous BP lowering effect of exercise was observed. HO-2 mRNA expression, HSCORE, and blood COHb index were unaltered during detraining, while SBP was still low in SHR.ConclusionsCO synthesized by HO-2 at least partly plays a role in SBP regulation in the SHR- and BP-lowering effect of exercise. Regular exercise with short-term pauses may be advised to both hypertensives and individuals who are at risk.

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Potential role of heme metabolism in the inducible expression of heme oxygenase-1

Cited by 18 publications

References 49 publications

CoPP-Induced-Induced HO-1 Overexpression Alleviates Photoreceptor Degeneration With Rapid Dynamics: A Therapeutic Molecular Against Retinopathy

CoPP-Induced-Induced HO-1 Overexpression Alleviates Photoreceptor Degeneration With Rapid Dynamics: A Therapeutic Molecular Against Retinopathy

Biosurfactants and anti-inflammatory activity: A potential new approach towards COVID-19

Contribution of Heme Oxygenase 2 to Blood Pressure Regulation in Response to Swimming Exercise and Detraining in Spontaneously Hypertensive Rats

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