scholarly journals ω-3 Polyunsaturated fatty acids accelerate airway repair by activating FFA4 in club cells

2017 ◽  
Vol 312 (6) ◽  
pp. L835-L844 ◽  
Author(s):  
Kyoung-Pil Lee ◽  
Soo-Jin Park ◽  
Saeromi Kang ◽  
Jung-Min Koh ◽  
Koichi Sato ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Polyunsaturated Fatty Acids ◽  
Knockout Mice ◽  
Airway Injury ◽  
Club Cells ◽  
And Migration ◽  
Lung Health

A G protein-coupled receptor (GPCR) named free fatty acid receptor 4 (FFA4, also known as GPR120) was found to act as a GPCR for ω-3 polyunsaturated fatty acids. Its expression has been reported in lung epithelial club cells. We investigated whether supplementation of the ω-3 fatty acids benefits lung health. Omacor (7.75 mg/kg), clinically prescribed preparation of ω-3 fatty acids, and FFA4-knockout mice were utilized in a naphthalene-induced mouse model of acute airway injury (1 injection of 30 mg/kg ip). Naphthalene injection induced complete destruction of bronchiolar epithelial cells within a day. Appearance of bronchiolar epithelial cells was observed after 21 days in control mice. It was found, however, that supplementation of Omacor accelerated the recovery. The appearance of bronchiolar epithelial cells was observed between 7 and 14 days after naphthalene injury in Omacor-treated mice. In isolated club cells, ω-3 fatty acids were found to stimulate cell proliferation and migration but to inhibit cell differentiation. With the use of pharmacological tools and FFA4-knockout mice, FFA4 was found to be responsible for ω-3 fatty acids-induced proliferation in vitro in club cells. Furthermore, accelerated recovery from naphthalene-induced airway injury in Omacor-treated mice was not observed in FFA4-knockout mice in vivo. Present findings indicate that ω-3 fatty acids-induced proliferation of bronchiole epithelial cells through FFA4 is responsible for Omacor-induced accelerated recovery from airway injury. Therefore, intermittent administration of Omacor needs to be tested for acute airway injury because ω-3 fatty acids stimulate proliferation but inhibit differentiation of club cells.

scholarly journals n-3 polyunsaturated fatty acids abrogate mTORC1/2 signaling and inhibit adrenocortical carcinoma growth in vitro and in vivo

2016 ◽  
Vol 35 (6) ◽  
pp. 3514-3522 ◽  
Author(s):  
JUN LIU ◽  
MEINIAN XU ◽  
YONGBIN ZHAO ◽  
CHUNPING AO ◽  
YUKUN WU ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Adrenocortical Carcinoma

scholarly journals Role of Omega-3 Polyunsaturated Fatty Acids in the Production of Prostaglandin E2and Nitric Oxide during Experimental Murine Paracoccidioidomycosis

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
S. C. Sargi ◽  
M. M. O. Dalalio ◽  
A. G. Moraes ◽  
J. E. L. Visentainer ◽  
D. R. Morais ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Peritoneal Macrophages ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Potential Health ◽  
Macrophage Activity ◽  
Experimental Paracoccidioidomycosis

There has recently been increased interest in the potential health effects of omega-3 polyunsaturated fatty acids on the immune system. Paracoccidioidomycosis is the most important endemic mycosis in Latin America. Macrophages have a fundamental role and act as first line of organism defense. The purpose of this study was to analyze the effect of n-3 fatty acids on the production of PGE2and NO by mice infected with Pb18 and fed a diet enriched with LNA for 8 weeks. To study the effect of omega-3 fatty acids on macrophage activity during experimental paracoccidioidomycosis, mice were infected with Pb18 and fed a diet supplemented with LNA. PGE2in the serum of animals was analyzed and NO in the supernatants of macrophages cultured and challengedin vitrowith Pb18 was measured. Omega-3 fatty acids seemed to decrease the production of PGE2in vivoin the infected group fed an LNA-supplemented diet during the 4th and 8th weeks of the experiment. At the same time, we observed an increase in synthesis of NO by peritoneal macrophages in this group. Omega-3 fatty acids thus appear to have an immunomodulatory effect in paracoccidioidomycosis.

scholarly journals Supplemental N-3 Polyunsaturated Fatty Acids Limit A1-Specific Astrocyte Polarization via Attenuating Mitochondrial Dysfunction in Ischemic Stroke in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jun Cao ◽  
Lijun Dong ◽  
Jialiang Luo ◽  
Fanning Zeng ◽  
Zexuan Hong ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Ischemic Stroke ◽  
Polyunsaturated Fatty Acids ◽  
Mitochondrial Dysfunction ◽  
Artery Occlusion ◽  
Mice Model ◽  
Neuron Death ◽  
The Impact

Ischemic stroke is one of the leading causes of death and disability for adults, which lacks effective treatments. Dietary intake of n-3 polyunsaturated fatty acids (n-3 PUFAs) exerts beneficial effects on ischemic stroke by attenuating neuron death and inflammation induced by microglial activation. However, the impact and mechanism of n-3 PUFAs on astrocyte function during stroke have not yet been well investigated. Our current study found that dietary n-3 PUFAs decreased the infarction volume and improved the neurofunction in the mice model of transient middle cerebral artery occlusion (tMCAO). Notably, n-3 PUFAs reduced the stroke-induced A1 astrocyte polarization both in vivo and in vitro. We have demonstrated that exogenous n-3 PUFAs attenuated mitochondrial oxidative stress and increased the mitophagy of astrocytes in the condition of hypoxia. Furthermore, we provided evidence that treatment with the mitochondrial-derived antioxidant, mito-TEMPO, abrogated the n-3 PUFA-mediated regulation of A1 astrocyte polarization upon hypoxia treatment. Together, this study highlighted that n-3 PUFAs prevent mitochondrial dysfunction, thereby limiting A1-specific astrocyte polarization and subsequently improving the neurological outcomes of mice with ischemic stroke.

scholarly journals PTH Derivative Promotes Wound Healing via Synergistic Multicellular Stimulating and Exosomal Activities

2020 ◽  
Author(s):  
Yi-Fan Shen ◽  
Jing-Huan Huang ◽  
Kai-Yang Wang ◽  
Jin Zheng ◽  
Lin Cai ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Intercellular Communication ◽  
Indirect Effects ◽  
Clinical Problem ◽  
Therapeutic Effects ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background: Diabetic wounds are a disturbing and rapidly growing clinical problem. A novel peptide, parathyroid hormone related peptide (PTHrP-2), is assumed as multifunctional factor in angiogenesis, fibrogenesis and re-epithelization. This study aims to test PTHrP-2 efficiency and mechanism in wound healing. Methods: Through repair phenomenon in vivo some problems were detected, and further research on their mechanisms was made. In vivo therapeutic effects of PTHrP-2 were determined by HE, Masson, microfil and immunohistochemical staining. In vitro direct effects of PTHrP-2 were determined by proliferation, migration, Vascular Endothelial Grown Factor and collagen I secretion of cells and Akt/ Erk1/2 pathway change. In vitro indirect effects of PTHrP-2 was study via exosomes. Exosomes from PTHrP-2 untreated and treated HUVECs and HFF-1 cells were insolated and identified. Exosomes were co-cultured with original cells, HUVECs or HFF-1 cells, and epithelial cells. Proliferation and migration and pathway change were observed. PTHrP-2-HUVEC-Exos were added into in vivo wound to testify its hub role in PTHrP-2 indirect effects in wound healing. Results: In vivo, PTHrP-2 exerted multifunctional pro-angiogenesis, pro-firbogenesis and re-epithelization effects. In vitro, PTHrP-2 promoted proliferation and migration of endothelial and fibroblast cells, but had no effect on epithelial cells. Therefore, we tested PTHrP-2 indirect effects via exosomes. PTHrP-2 intensified intercellular communication between endothelial cells and fibroblasts and initiated endothelial-epithelial intercellular communication. PTHrP-2-HUVEC-Exos played a hub role in PTHrP-2 indirect effects in wound healing. Conclusion: These findings of this study indicated that PTHrP-2, a multifunctional factor, could promote wound healing via synergistic multicellular stimulating and exosomal activities. Key words PTH, multifunctional factor, diabetic wound, exosomes, synergistic effect

Effect of polyunsaturated fatty acids on diphenyl hydantoin-induced genetic damage in vitro and in vivo

2009 ◽  
Vol 80 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Shivani Ponnala ◽  
Kaipa P. Rao ◽  
Jaideep R. Chaudhury ◽  
Jaleel Ahmed ◽  
B. Rama Rao ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Genetic Damage

scholarly journals n-3 Polyunsaturated Fatty Acids Impede the TCR Mobility and the TCR–pMHC Interaction of Anti-Viral CD8+ T Cells

Viruses ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 639 ◽  
Author(s):  
Younghyun Lim ◽  
Seyoung Kim ◽  
Sehoon Kim ◽  
Dong-In Kim ◽  
Kyung Won Kang ◽  
...  
Keyword(s):  
Fatty Acids ◽  
T Cells ◽  
T Cell ◽  
Polyunsaturated Fatty Acids ◽  
Cd8 T Cells ◽  
Cd8 T Cell ◽  
Omega 3 ◽  
In Vivo Models

The immune-suppressive effects of omega-3 (n-3) polyunsaturated fatty acids (PUFAs) on T cells have been observed via multiple in vitro and in vivo models. However, the precise mechanism that causes these effects is still undefined. In this study, we investigated whether n-3 PUFAs regulated T cell receptor (TCR) and peptide-major histocompatibility complex (pMHC) interactions. The expansion of anti-viral CD8+ T cells that endogenously synthesize n-3 PUFAs (FAT-1) dramatically decreased upon lymphocytic choriomeningitis virus (LCMV) infection in vivo. This decrease was not caused by the considerable reduction of TCR expression or the impaired chemotactic activity of T cells. Interestingly, a highly inclined and laminated optical sheet (HILO) microscopic analysis revealed that the TCR motility was notably reduced on the surface of the FAT-1 CD8+ T cells compared to the wild type (WT) CD8+ T cells. Importantly, the adhesion strength of the FAT-1 CD8+ T cells to the peptide-MHC was significantly lower than that of the WT CD8+T cells. Consistent with this result, treatment with docosahexaenoic acid (DHA), one type of n-3 PUFA, significantly decreased CD8+ T cell adhesion to the pMHC. Collectively, our results reveal a novel mechanism through which n-3 PUFAs decrease TCR-pMHC interactions by modulating TCR mobility on CD8+ T cell surfaces.

scholarly journals Omega-3 Polyunsaturated Fatty Acids and the Intestinal Epithelium—A Review

Foods ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 199
Author(s):  
Luke A. Durkin ◽  
Caroline E. Childs ◽  
Philip C. Calder
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Polyunsaturated Fatty Acids ◽  
Intestinal Barrier ◽  
In Vitro Models ◽  
Omega 3 ◽  
Alpha Linolenic Acid ◽  
Chemical Mediator ◽  
Anti Inflammatory

Epithelial cells (enterocytes) form part of the intestinal barrier, the largest human interface between the internal and external environments, and responsible for maintaining regulated intestinal absorption and immunological control. Under inflammatory conditions, the intestinal barrier and its component enterocytes become inflamed, leading to changes in barrier histology, permeability, and chemical mediator production. Omega-3 (ω-3) polyunsaturated fatty acids (PUFAs) can influence the inflammatory state of a range of cell types, including endothelial cells, monocytes, and macrophages. This review aims to assess the current literature detailing the effects of ω-3 PUFAs on epithelial cells. Marine-derived ω-3 PUFAs, eicosapentaenoic acid and docosahexaenoic acid, as well as plant-derived alpha-linolenic acid, are incorporated into intestinal epithelial cell membranes, prevent changes to epithelial permeability, inhibit the production of pro-inflammatory cytokines and eicosanoids and induce the production of anti-inflammatory eicosanoids and docosanoids. Altered inflammatory markers have been attributed to changes in activity and/or expression of proteins involved in inflammatory signalling including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), peroxisome proliferator activated receptor (PPAR) α and γ, G-protein coupled receptor (GPR) 120 and cyclooxygenase (COX)-2. Effective doses for each ω-3 PUFA are difficult to determine due to inconsistencies in dose and time of exposure between different in vitro models and between in vivo and in vitro models. Further research is needed to determine the anti-inflammatory potential of less-studied ω-3 PUFAs, including docosapentaenoic acid and stearidonic acid.

scholarly journals PTH Derivative Promotes Chronic Wound Healing via Synergistic Multicellular Stimulating and Exosomal Activities

2019 ◽  
Author(s):  
Yi-Fan Shen ◽  
Jing-Huan Huang ◽  
Kai-Yang Wang ◽  
Jin Zheng ◽  
Lin Cai ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Intercellular Communication ◽  
Indirect Effects ◽  
Chronic Wound ◽  
Therapeutic Effects ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background: Chronic diabetic wounds are a disturbing and rapidly growing clinical problem. Parathyroid hormone related peptide (PTHrP-2) was assumed as multifunctional factor in angiogenesis, fibrogenesis and re-epithelization. This study aims to test PTHrP-2 efficiency and mechanism in chronic wound healing. Methods: Through repair phenomenon in vivo some problems were detected, and further research on their mechanisms was made. In vivo therapeutic effects of PTHrP-2 was determined by HE, Masson, microfil and immunohistochemical staining. In vitro direct effects of PTHrP-2 was determined by proliferation, migration, Vascular Endothelial Grown Factor and collagen I secretion of cells and Akt/ Erk1/2 pathway change. In vitro indirect effects of PTHrP-2 was study via exosomes. Exosomes from PTHrP-2 untreated and treated HUVECs and HFF-1 cells were insolated and identified. Exosomes were co-cultured with original cells, HUVECs or HFF-1 cells, and epithelial cells. Proliferation and migration and pathway change were observed. PTHrP-2-HUVEC-Exos was added into in vivo wound to testify its hub role in PTHrP-2 indirect effects in wound healing. Results: In vivo, PTHrP-2 exerted multifunctional pro-angiogenesis, pro-firbogenesis and re-epithelization effects. In vitro, PTHrP-2 promoted proliferation and migration of endothelial and fibroblast cells, but had no effect on epithelial cells. Therefore, we tested PTHrP-2 indirect effects via exosomes. PTHrP-2 intensified intercellular communication between endothelial cells and fibroblasts and initiated endothelial-epithelial intercellular communication. PTHrP-2-HUVEC-Exos played hub role in PTHrP-2 indirect effects in wound healing. Conclusion: The findings of this study indicate that PTHrP-2, a multifunctional factor, can promote chronic wound healing via synergistic multicellular stimulating and exosomal activities.

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