Carbon monoxide releasing molecule improves structural and functional cardiac recovery after myocardial injury

Segersvärd, Heli; Lakkisto, Päivi; Hänninen, Mikko; Forsten, Hanna; Siren, Juuso; Immonen, Katariina; Kosonen, Riikka; Sarparanta, Mirkka; Laine, Mika; Tikkanen, Ilkka

doi:10.1016/j.ejphar.2017.10.031

Cited by 23 publications

(20 citation statements)

References 46 publications

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“…This hypothesis is supported by Soni et al, who have shown that exogenous CO mitigates doxorubicin-induced cardiotoxicity [85]. CORM-3 improves structural and functional cardiac recovery after myocardial injury [86]. In addition, CORM-2 reduces endothelial cell apoptosis triggered by ox-LDL [87].…”

Section: Atherosclerosismentioning

confidence: 85%

Heme, Heme Oxygenase, and Endoplasmic Reticulum Stress—A New Insight into the Pathophysiology of Vascular Diseases

Gáll

Balla

2019

IJMS

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The prevalence of vascular disorders continues to rise worldwide. Parallel with that, new pathophysiological pathways have been discovered, providing possible remedies for prevention and therapy in vascular diseases. Growing evidence suggests that endoplasmic reticulum (ER) stress is involved in a number of vasculopathies, including atherosclerosis, vascular brain events, and diabetes. Heme, which is released from hemoglobin or other heme proteins, triggers various pathophysiological consequence, including heme stress as well as ER stress. The potentially toxic free heme is converted by heme oxygenases (HOs) into carbon monoxide (CO), iron, and biliverdin (BV), the latter of which is reduced to bilirubin (BR). Redox-active iron is oxidized and stored by ferritin, an iron sequestering protein which exhibits ferroxidase activity. In recent years, CO, BV, and BR have been shown to control cellular processes such as inflammation, apoptosis, and antioxidant defense. This review covers our current knowledge about how heme induced endoplasmic reticulum stress (HIERS) participates in the pathogenesis of vascular disorders and highlights recent discoveries in the molecular mechanisms of HO-mediated cytoprotection in heme stress and ER stress, as well as crosstalk between ER stress and HO-1. Furthermore, we focus on the translational potential of HIERS and heme oxygenase-1 (HO-1) in atherosclerosis, diabetes mellitus, and brain hemorrhage.

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Section: Atherosclerosismentioning

confidence: 85%

Heme, Heme Oxygenase, and Endoplasmic Reticulum Stress—A New Insight into the Pathophysiology of Vascular Diseases

Gáll

Balla

2019

IJMS

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“…CORM-2 prevents TNF-α-induced endothelial nitric oxide synthase downregulation by inhibiting miR-155-5p biogenesis (Choi et al , 2017). CORM-3 improves structural and functional cardiac recovery after myocardial injury via decreasing miR-206 expression (Segersvard et al , 2018). However, little is known about CORMs and miR-195-5p.…”

Section: Discussionmentioning

confidence: 99%

“…CO, which is a gasotransmitter, displays many physiological roles in several organs and tissues. CO administration has therapeutic potential in many diseases (Gullotta et al , 2012;Mitchell et al , 2010;Segersvard et al , 2018). CO has already been evaluated in phase I clinical testing and the feasibility and anti-inflammatory effects of low-dose CO inhalation in patients with chronic obstructive pulmonary disease have been demonstrated (Bathoorn et al , 2007).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-195-5p regulates carbon monoxide releasing molecule-3-induced osteogenic differentiation of rat bone marrow mesenchymal stem cells by targeting Wnt3a

Han

Chen

et al. 2020

Preprint

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Background and Purpose: Bone marrow-derived mesenchymal stem cells (BMSCs) are potential in promoting bone regeneration for their multipotential differentiation capacity. Our previous study showed that carbon monoxide releasing molecule-3 (CORM-3) promoted the osteogenic differentiation of rat BMSCs. However, the mechanism was not clearly understood. MicroRNAs (miRNAs) play a critical role in regulating the osteogenic differentiation of BMSCs. We therefore investigated the role of miR-195-5p in CORM-3-induced osteogenic differentiation. Experimental Approach: The rat BMSCs were transfected with miR-195-5p mimics, miR-195-5p inhibitor, pcDNA3.1-Wnt3a, Wnt3a siRNA or their corresponding controls. The rat BMSCs osteogenic differentiation was assessed by quantitative real-time polymerase chain reaction, Western blot and alizarin red staining. In addition, dual luciferase assay was used for the verification of targeting relationship between miR-195-5p and Wnt3a. Key Results: miR-195-5p was down-regulated during the CORM-3-induced osteogenic differentiation of rat BMSCs.Overexpression of miR-195-5p inhibited CORM-3-induced osteogenic differentiation of rat BMSCs, evidenced by significantly decreased mRNA and protein expressions of runt-related transcription factor 2 and osteopontin, and matrix mineralization demonstrated. Whereas, inhibition of miR-195-5p expression enhanced osteogenic differentiation. miR-195-5p directly targeted Wnt3a. Overexpression of Wnt3a increased CORM-3-induced osteogenic differentiation of rat BMSCs, the opposite effect was observed in Wnt3a-deficient cells. Moreover, the inhibitory effect of miR-195-5p overexpression on CORM-3-induced osteogenic differentiation was rescued by Wnt3a overexpression. Conclusion and Implications: These results demonstrated that miR-195-5p may negatively regulate CORM-3-induced osteogenic differentiation of rat BMSCs by targeting Wnt3a, which provided insight into new mechanism of CORM-3, and theoretical basis for bone regeneration.

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“…But when CORMs were utilized, different effects were observed due to their low concentration and controlled targeting in the body. For instance, a recent investigation by Segersvärd et al has shown CORM-3 (but not iCORM-3) improves cardiac structure and function of rats following experimentally induced myocardial infarction [ 79 ]. CORM-2 has also displayed cardioprotective behaviour.…”

Section: Cardiovascular Effects Of Cormsmentioning

confidence: 99%

An Overview of the Potential Therapeutic Applications of CO-Releasing Molecules

Ismailova

Kuter

Bohle

et al. 2018

Bioinorganic Chemistry and Applications

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Carbon monoxide (CO) has long been known as the “silent killer” owing to its ability to form carboxyhemoglobin—the main cause of CO poisoning in humans. Its role as an endogenous neurotransmitter, however, was suggested in the early 1990s. Since then, the biological activity of CO has been widely examined via both the direct administration of CO and in the form of so-called “carbon monoxide releasing molecules (CORMs).” This overview will explore the general physiological effects and potential therapeutic applications of CO when delivered in the form of CORMs.

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Carbon monoxide releasing molecule improves structural and functional cardiac recovery after myocardial injury

Cited by 23 publications

References 46 publications

Heme, Heme Oxygenase, and Endoplasmic Reticulum Stress—A New Insight into the Pathophysiology of Vascular Diseases

Heme, Heme Oxygenase, and Endoplasmic Reticulum Stress—A New Insight into the Pathophysiology of Vascular Diseases

MicroRNA-195-5p regulates carbon monoxide releasing molecule-3-induced osteogenic differentiation of rat bone marrow mesenchymal stem cells by targeting Wnt3a

An Overview of the Potential Therapeutic Applications of CO-Releasing Molecules

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