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The Role of Carotenoids in Health and Disease: From Molecular Mechanism to Clinical Significance

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 19081

Special Issue Editor

Prof. Dr. Tsuguhito Ota

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Guest Editor
Division of Metabolism and Biosystemic Science, Department of Medicine, Asahikawa Medical University, Asahikawa, Japan

Special Issue Information

Dear Colleagues,

In the last 5 years, over 12,000 scientific papers on ‘carotenoids’ have been published. This is an outstanding number of publications, so we can readily understand how important carotenoids are.

Carotenoid deficiencies are associated with the pathogenesis of a wide range of diseases—obesity-related diseases such as insulin resistance, diabetes, NASH/NAFLD and cardiovascular diseases, cancers, and neurodegenerative diseases. By contrast, both preclinical and clinical studies have shown that supplementation or administration of carotenoids such as β-carotene, lycopene, β-cryptoxanthin, and astaxanthin has preventive and therapeutic effects on diseases.

In this Special Issue of IJMS, the research topic is to highlight the carotenoids as bioactives and nutraceuticals for health and disease. Authors are invited to submit their work on the molecular and biochemical mechanisms of carotenoids that contribute to human health and control disease, considering both basic or preclinical and clinical settings. Original research articles and review articles related to any aspects of biochemistry, molecular biology, pharmacology, physiology, and pathology in this topic are welcome.

Prof. Dr. Tsuguhito Ota
Guest Editor

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Keywords

  • Carotenoid
  • Lycopene
  • β-carotene
  • Astaxanthin
  • Obesity and Diabetes
  • NASH/NAFLD
  • Cardiovascular disease
  • Cancers
  • Neurodegenerative disease

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Published Papers (4 papers)

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Research

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14 pages, 30683 KiB  
Article
Astaxanthin Counteracts Vascular Calcification In Vitro Through an Early Up-Regulation of SOD2 Based on a Transcriptomic Approach
by Chia-Ter Chao, Hsiang-Yuan Yeh, You-Tien Tsai, Tzu-Hang Yuan, Min-Tser Liao, Jenq-Wen Huang and Huei-Wen Chen
Int. J. Mol. Sci. 2020, 21(22), 8530; https://doi.org/10.3390/ijms21228530 - 12 Nov 2020
Cited by 17 | Viewed by 3599
Abstract
Vascular calcification (VC) is a critical contributor to the rising cardiovascular risk among at-risk populations such as those with diabetes or renal failure. The pathogenesis of VC involves an uprising of oxidative stress, for which antioxidants can be theoretically effective. However, astaxanthin, a [...] Read more.
Vascular calcification (VC) is a critical contributor to the rising cardiovascular risk among at-risk populations such as those with diabetes or renal failure. The pathogenesis of VC involves an uprising of oxidative stress, for which antioxidants can be theoretically effective. However, astaxanthin, a potent antioxidant, has not been tested before for the purpose of managing VC. To answer this question, we tested the efficacy of astaxanthin against VC using the high phosphate (HP)-induced vascular smooth muscle cell (VSMC) calcification model. RNAs from treated groups underwent Affymetrix microarray screening, with intra-group consistency and inter-group differential expressions identified. Candidate hub genes were selected, followed by validation in experimental models and functional characterization. We showed that HP induced progressive calcification among treated VSMCs, while astaxanthin dose-responsively and time-dependently ameliorated calcification severities. Transcriptomic profiling revealed that 3491 genes exhibited significant early changes during VC progression, among which 26 potential hub genes were selected based on closeness ranking and biologic plausibility. SOD2 was validated in the VSMC model, shown to drive the deactivation of cellular senescence and enhance antioxidative defenses. Astaxanthin did not alter intracellular reactive oxygen species (ROS) levels without HP, but significantly lowered ROS production in HP-treated VSMCs. SOD2 knockdown prominently abolished the anti-calcification effect of astaxanthin on HP-treated VSMCs, lending support to our findings. In conclusion, we demonstrated for the first time that astaxanthin could be a potential candidate treatment for VC, through inducing the up-regulation of SOD2 early during calcification progression and potentially suppressing vascular senescence. Full article
(This article belongs to the Special Issue The Role of Carotenoids in Health and Disease: From Molecular Mechanism to Clinical Significance)
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14 pages, 4223 KiB  
Article
Fucoxanthin Ameliorates Atopic Dermatitis Symptoms by Regulating Keratinocytes and Regulatory Innate Lymphoid Cells
by Chika Natsume, Nao Aoki, Tomoko Aoyama, Keisuke Senda, Mio Matsui, Airi Ikegami, Kosuke Tanaka, Yasu-Taka Azuma and Takashi Fujita
Int. J. Mol. Sci. 2020, 21(6), 2180; https://doi.org/10.3390/ijms21062180 - 22 Mar 2020
Cited by 27 | Viewed by 5860
Abstract
Fucoxanthin (FX) is a xanthophyll that is contained abundantly in marine plants. The biological action of FX includes its antioxidant and anti-lipogenic activities, while the precise action of its mechanisms on skin cells has not yet been clarified. The current study examined the [...] Read more.
Fucoxanthin (FX) is a xanthophyll that is contained abundantly in marine plants. The biological action of FX includes its antioxidant and anti-lipogenic activities, while the precise action of its mechanisms on skin cells has not yet been clarified. The current study examined the effect of FX in comparison with tacrolimus (TAC) on NC/Nga mice, which are an atopic dermatitis (AD) model. FX topical treatment dramatically ameliorated itching behavior over the TAC treatment, which was insufficient for improvement of AD symptoms. In Nc/Nga mice, FX or TAC applied to the skin inhibited eosinophil infiltration with decreased expression of Il-33. FX also stimulated Il-2, Il-5, Il-13, Il-10, and TGF-β expression levels, and Sca1+Il-10+TGF-β+ regulatory innate lymphoid cells (ILCreg) were dominantly observed in FX treated skin epidermal keratinocytes and dermal layers. This combined evidence demonstrated that FX exerts anti-inflammatory effects on keratinocytes and ameliorates AD symptoms by regulating ILCreg to normalize immune responses in an atopic dermatitis model. Full article
(This article belongs to the Special Issue The Role of Carotenoids in Health and Disease: From Molecular Mechanism to Clinical Significance)
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32 pages, 6972 KiB  
Article
Anisotropic Platinum Nanoparticle-Induced Cytotoxicity, Apoptosis, Inflammatory Response, and Transcriptomic and Molecular Pathways in Human Acute Monocytic Leukemia Cells
by Sangiliyandi Gurunathan, Muniyandi Jeyaraj, Hyeonwoo La, Hyunjin Yoo, Youngsok Choi, Jeong Tae Do, Chankyu Park, Jin-Hoi Kim and Kwonho Hong
Int. J. Mol. Sci. 2020, 21(2), 440; https://doi.org/10.3390/ijms21020440 - 9 Jan 2020
Cited by 39 | Viewed by 5263
Abstract
The thermoplasmonic properties of platinum nanoparticles (PtNPs) render them desirable for use in diagnosis, detection, therapy, and surgery. However, their toxicological effects and impact at the molecular level remain obscure. Nanotoxicology is mainly focused on the interactions of nanostructures with biological systems, particularly [...] Read more.
The thermoplasmonic properties of platinum nanoparticles (PtNPs) render them desirable for use in diagnosis, detection, therapy, and surgery. However, their toxicological effects and impact at the molecular level remain obscure. Nanotoxicology is mainly focused on the interactions of nanostructures with biological systems, particularly with an emphasis on elucidating the relationship between the physical and chemical properties such as size and shape. Therefore, we hypothesized whether these unique anisotropic nanoparticles could induce cytotoxicity similar to that of spherical nanoparticles and the mechanism involved. Thus, we synthesized unique and distinct anisotropic PtNPs using lycopene as a biological template and investigated their biological activities in model human acute monocytic leukemia (THP-1) macrophages. Exposure to PtNPs for 24 h dose-dependently decreased cell viability and proliferation. Levels of the cytotoxic markers lactate dehydrogenase and intracellular protease significantly and dose-dependently increased with PtNP concentration. Furthermore, cells incubated with PtNPs dose-dependently produced oxidative stress markers including reactive oxygen species (ROS), malondialdehyde, nitric oxide, and carbonylated protein. An imbalance in pro-oxidants and antioxidants was confirmed by significant decreases in reduced glutathione, thioredoxin, superoxide dismutase, and catalase levels against oxidative stress. The cell death mechanism was confirmed by mitochondrial dysfunction and decreased ATP levels, mitochondrial copy numbers, and PGC-1α expression. To further substantiate the mechanism of cell death mediated by endoplasmic reticulum stress (ERS), we determined the expression of the inositol-requiring enzyme (IRE1), (PKR-like ER kinase) PERK, activating transcription factor 6 (ATF6), and activating transcription factor 4 ATF4, the apoptotic markers p53, Bax, and caspase 3, and the anti-apoptotic marker Bcl-2. PtNPs could activate ERS and apoptosis mediated by mitochondria. A proinflammatory response to PtNPs was confirmed by significant upregulation of interleukin-1-beta (IL-1β), interferon γ (IFNγ), tumor necrosis factor alpha (TNFα), and interleukin (IL-6). Transcriptomic and molecular pathway analyses of THP-1 cells incubated with the half maximal inhibitory concentration (IC50) of PtNPs revealed the altered expression of genes involved in protein misfolding, mitochondrial function, protein synthesis, inflammatory responses, and transcription regulation. We applied transcriptomic analyses to investigate anisotropic PtNP-induced toxicity for further mechanistic studies. Isotropic nanoparticles are specifically used to inhibit non-specific cellular uptake, leading to enhanced in vivo bio-distribution and increased targeting capabilities due to the higher radius of curvature. These characteristics of anisotropic nanoparticles could enable the technology as an attractive platform for nanomedicine in biomedical applications. Full article
(This article belongs to the Special Issue The Role of Carotenoids in Health and Disease: From Molecular Mechanism to Clinical Significance)
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Review

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19 pages, 710 KiB  
Review
The Remedial Potential of Lycopene in Pancreatitis through Regulation of Autophagy
by Suyun Choi and Hyeyoung Kim
Int. J. Mol. Sci. 2020, 21(16), 5775; https://doi.org/10.3390/ijms21165775 - 12 Aug 2020
Cited by 29 | Viewed by 3635
Abstract
Autophagy is an evolutionarily conserved process that degrades damaged organelles and recycles macromolecules to support cell survival. However, in certain disease states, dysregulated autophagy can play an important role in cell death. In pancreatitis, the accumulation of autophagic vacuoles and damaged mitochondria and [...] Read more.
Autophagy is an evolutionarily conserved process that degrades damaged organelles and recycles macromolecules to support cell survival. However, in certain disease states, dysregulated autophagy can play an important role in cell death. In pancreatitis, the accumulation of autophagic vacuoles and damaged mitochondria and premature activation of trypsinogen are shown in pancreatic acinar cells (PACs), which are the hallmarks of impaired autophagy. Oxidative stress mediates inflammatory signaling and cytokine expression in PACs, and it also causes mitochondrial dysfunction and dysregulated autophagy. Thus, oxidative stress may be a mediator for autophagic impairment in pancreatitis. Lycopene is a natural pigment that contributes to the red color of fruits and vegetables. Due to its antioxidant activity, it inhibited oxidative stress-induced expression of cytokines in experimental models of acute pancreatitis. Lycopene reduces cell death through the activation of 5′-AMP-activated protein kinase-dependent autophagy in certain cells. Therefore, lycopene may ameliorate pancreatitis by preventing oxidative stress-induced impairment of autophagy and/or by directly activating autophagy in PACs. Full article
(This article belongs to the Special Issue The Role of Carotenoids in Health and Disease: From Molecular Mechanism to Clinical Significance)
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