MITF acts as an anti-oxidant transcription factor to regulate mitochondrial biogenesis and redox signaling in retinal pigment epithelial cells

Hua, Jiajia; Chen, Huaicheng; Chen, Yu; Zheng, Guoxiao; Li, Fang; Qu, Jia; Ma, Xiaoyin; Hou, Ling

doi:10.1016/j.exer.2018.02.023

Cited by 20 publications

(19 citation statements)

References 53 publications

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“…Moreover, downregulation of miR-218 can diminish the heart defects induced by overexpression of TBX5, leading to the notion that miR-218 is a candidate mediator of TBX5 in the heart development and possible association with the occurrence of heart malformations [19]. MITF is an anti-oxidant transcription factor, whose deficiency in mice leads to higher levels of reactive oxygen species and oxidative damage [46]. Thus, the treatment of overexpression plasmid of MITF could reduce oxidative stress following MI.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of microRNA-218 is cardioprotective against cardiac fibrosis and cardiac function impairment in myocardial infarction by binding to MITF

Qian

Pan

Shi

et al. 2019

Aging

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Objective: This study is intended to figure out the function of microRNA-218 (miR-218) together with microphthalmia-associated transcription factor (MITF) on the cardiac fibrosis and cardiac function impairment in rat models of myocardial infarction (MI). Results: The rats with MI exhibited cardiac function impairment, cardiac fibrosis, oxidative stress, cardiomyocyte apoptosis, as well as inflammatory injury. Additionally, upregulated miR-218 and downregulated MITF were detected in cardiac tissues of MI rats. MI rats injected with miR-218 inhibitors or overexpressed MITF exhibited elevated MITF expression, improved cardiac function, and diminished pathological damages, infarct size, cardiomyocyte apoptosis, cardiac fibrosis, oxidative stress as well as inflammatory injury in cardiac tissues. Furthermore, downregulated miR-218 and MITF aggravated the conditions than downregulation of miR-218 alone in MI rats. Methods: MI models were performed in rats, and then the rats were injected with miR-218 inhibitors and/or MITF overexpression plasmid to elucidate the role of miR-218 and/or MITF on the cardiac function, pathological damage, cardiac fibrosis, angiogenesis, oxidative stress and inflammatory injury of cardiac tissues in MI rats by performing a series of assays. Conclusion: Collectively, we found that the suppression of miR-218 alleviates cardiac fibrosis and cardiac function impairment, and stimulates angiogenesis in MI rats through inhibiting MITF.

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Section: Discussionmentioning

confidence: 99%

Downregulation of microRNA-218 is cardioprotective against cardiac fibrosis and cardiac function impairment in myocardial infarction by binding to MITF

Qian

Pan

Shi

et al. 2019

Aging

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“…The low level of MITF-M leads to the worst fight with a damage caused by ROS [65,66]. It is well known that increased ROS production directs cells to oncogenic transformation [67]. In our experiments, we detected decreased level of MITF-M in all pT stages of MM.…”

Section: Discussionsupporting

confidence: 59%

Fluorescence biomarkers of malignant melanoma detectable in urine

et al. 2020

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Malignant melanoma (MM) is a cancerous transformation of melanocytes. It is a disease with the worst response to therapy and, compared to other malignancies, presents much earlier with metastases. MM still belongs to relatively late-detected malignant diseases. Even so, the MM mortality rate is up to 96% for a relatively small incidence (5%). The gold standard for MM diagnosis is a histopathological examination that requires invasive surgery. An invasive sampling method of a biological material can be a stressful factor for the patient, which is often the reason why patients do not seek medical assistance as soon as possible. Our goal was to find a link between metabolites in urine and the stage of MM. Two excitation peaks at 360–370 nm and 450 nm were characterised in spectra of urine samples. The emission spectra have shown one significant peak at 410–460 nm. After addition of glutathione reductase to the samples, fluorescence dropped down only in patient samples and hidden fluorophores appeared. Malignant diseases are associated with the presence of specific metabolites that can be detected fluorescently in biological material such as urine, which can be a suitable alternative for an early detection of cancer or for tracking changes during and after treatment.

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“…Nevertheless, the PEDF-mediated rescue of retina structure and gene expression in Mitf -deficient mouse eyes was only partial in Mitf −/− mutant mice. This was not surprising as only the combinations of PEDF with other factors can lead to full rescue (Hua et al, 2018; Wen et al, 2016). Also, it is conceivable that absence of the low levels of MITF normally found in the developing retina might have contributed in a PEDF-resistant way to retinal damage in Mitf −/− mice.…”

Section: Discussionmentioning

confidence: 89%

Photoreceptor degeneration in microphthalmia (Mitf) mice: partial rescue by pigment epithelium-derived factor

Chen

Yang

Geng

et al. 2019

Disease Models &Amp; Mechanisms

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Dysfunction and loss of the retinal pigment epithelium (RPE) are hallmarks of retinal degeneration, but the underlying pathogenetic processes are only partially understood. Using mice with a null mutation in the transcription factor gene Mitf, in which RPE deficiencies are associated with retinal degeneration, we evaluated the role of trophic factors secreted by the RPE in retinal homeostasis. In such mice, the thickness of the outer nuclear layer (ONL) is as in wild type up to postnatal day 10, but then is progressively reduced, associated with a marked increase in the number of apoptotic cells and a decline in staining for rhodopsin. We show that retinal degeneration and decrease in rhodopsin staining can be prevented partially in three different ways: first, by recombining mutant-derived postnatal retina with postnatal wild-type RPE in tissue explant cultures; second, by adding to cultured mutant retina the trophic factor pigment epithelium-derived factor (PEDF; also known as SERPINF1), which is normally produced in RPE under the control of Mitf; and third, by treating the eyes of Mitf mutant mice in vivo with drops containing a bioactive PEDF 17-mer peptide. This latter treatment also led to marked increases in a number of rod and cone genes. The results indicate that RPE-derived trophic factors, in particular PEDF, are instrumental in retinal homeostasis, and suggest that PEDF or its bioactive fragments may have therapeutic potential in RPE deficiency-associated retinal degeneration.

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MITF acts as an anti-oxidant transcription factor to regulate mitochondrial biogenesis and redox signaling in retinal pigment epithelial cells

Cited by 20 publications

References 53 publications

Downregulation of microRNA-218 is cardioprotective against cardiac fibrosis and cardiac function impairment in myocardial infarction by binding to MITF

Downregulation of microRNA-218 is cardioprotective against cardiac fibrosis and cardiac function impairment in myocardial infarction by binding to MITF

Fluorescence biomarkers of malignant melanoma detectable in urine

Photoreceptor degeneration in microphthalmia (Mitf) mice: partial rescue by pigment epithelium-derived factor

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