scholarly journals Role of Resveratrol in Regulating Cutaneous Functions

2020 ◽  
Vol 2020 ◽  
pp. 1-20 ◽  
Author(s):  
Si Wen ◽  
Jiechen Zhang ◽  
Bin Yang ◽  
Peter M. Elias ◽  
Mao-Qiang Man
Keyword(s):  
Protective Role ◽  
The Body ◽  
Sirtuin 1 ◽  
Mitogen Activated Protein Kinase ◽  
Keratinocyte Differentiation ◽  
Related Factor ◽  
Keratinocyte Proliferation ◽  
Mitogen Activated Protein ◽  
Peptide Expression

Protective role of the skin is against external insults and maintenance of electrolyte homeostasis of the body. Cutaneous dysfunction can account for the development of both cutaneous and systemic disorders. Thus, improvements in cutaneous functions can benefit a number of extracutaneous and cutaneous functions. Resveratrol, a natural ingredient, displays multiple benefits for various systems/organs, including the skin. The benefits of resveratrol for cutaneous functions include stimulation of keratinocyte differentiation and antimicrobial peptide expression, inhibition of keratinocyte proliferation and cutaneous inflammation, UV protection, anticancer, antiaging, and inhibition of melanogenesis. The mechanisms of action of resveratrol include activation of sirtuin 1 and nuclear factor erythroid 2-related factor 2, and inhibition of mitogen-activated protein kinase signaling. Evidence suggests that topical resveratrol could be a valuable alternative not only for daily skin care, but also for the prevention and treatment of various cutaneous disorders. This review summarizes the benefits of resveratrol for cutaneous functions.

Melatonin plays a pivotal role in conferring tolerance against endoplasmic reticulum stress via mitogen-activated protein kinases and bZIP60 in Arabidopsis thaliana

2018 ◽  
Vol 1 (1) ◽  
pp. 94-108 ◽  
Author(s):  
Hyoung Yool Lee ◽  
Kyoungwhan Back
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Secretory Protein ◽  
Protective Role ◽  
Mitogen Activated Protein Kinase ◽  
Ion Leakage ◽  
Defense Systems ◽  
Mitogen Activated Protein ◽  
Stress Damage

Melatonin has diverse roles as a signaling molecule that activates a number of downstream defense systems against various biotic and abiotic stresses in plants. However, there have been no reports regarding a direct protective role of melatonin against endoplasmic reticulum (ER) stress. Here, we report that exogenous melatonin treatment attenuated ER stress damage by preserving ER structure and enhancing secretory protein folding capacity in response to tunicamycin treatment. Further transgenic experiments indicated that melatonin-deficient snat1 mutant was hypersensitive to ER stress, whereas melatonin-proficient SNAT1 overexpression (OE) was tolerant to ER stress, as evidenced by reduced ion leakage and higher transcript levels of ER chaperones, including luminal binding protein (BIP) 2, BIP3, and CNX1, compared to wild-type controls. Moreover, this melatonin-mediated ER stress tolerance was dependent on the bZIP60 transcription factor and mitogen-activated protein kinase. Our data suggest that melatonin is actively involved in maintaining homeostasis of the ER during normal plant growth, and also has a protective effect against many environmental stressors that induce ER stress.

Role of signaling pathway in biological cause of Rheumatoid arthritis

2020 ◽  
Vol 12 ◽  
Author(s):  
Rakesh Kumar Chauhan ◽  
Pramod Kumar Sharma ◽  
Shikha Srivastava
Keyword(s):  
Rheumatoid Arthritis ◽  
Protein Kinase ◽  
Signaling Pathways ◽  
Interleukin 1 ◽  
Development Stage ◽  
The Body ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Heart Blood

Abstract:: Rheumatoid Arthritis is a chronic progressive inflammatory auto-immune disease in which the immune system of the body attacks its cartilage and joints lining. It not only affects synovial joints but also many other sites including heart, blood vessels, and skins. It is more common in females than in males. The exact cause of rheumatoid arthritis is not well established but the hypothesis reported in the literature is that in the development stage of the disease, both genetics and environmental factors can play an inciting role. Along with these factors alteration in the normal physiology of enzymatic action, acts as a trigger to develop this condition. Numerous signaling pathways involved in the pathogenesis of Rheumatoid Arthritis involves activation of mitogen-activated protein kinase, kinases Janus family, P-38 Mitogen-Activated Protein Kinase, Nuclear Factor-kappa B. Interleukin-1 to play a proinflammatory cytokine that plays an important role in inflammation in RA. These are also associated with an increase in neutrophil, macrophage and lymphocytic chemotaxis, mast cell degranulation, activation, maturation and survival of T-cells and B-cells activated. These signaling pathways also show that p38α downregulation in myeloid cells exacerbates the severity of symptoms of arthritis. Thus, present review carters about the detail of different signaling pathways and their role in rheumatoid arthritis.

scholarly journals Supplementation of 17β-Estradiol Normalizes Rapid Gastric Emptying by Restoring Impaired Nrf2 and nNOS Function in Obesity-Induced Diabetic Ovariectomized Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 582 ◽  
Author(s):  
Jeremy C. Sprouse ◽  
Chethan Sampath ◽  
Pandu R. Gangula
Keyword(s):  
Nitric Oxide ◽  
Gastric Emptying ◽  
Mitogen Activated Protein Kinase ◽  
Related Factor ◽  
Metabolic Homeostasis ◽  
Ovariectomized Mice ◽  
Mitogen Activated Protein ◽  
17Β Estradiol ◽  
Oxide Synthase

Gastroparesis (Gp) is a multifactorial condition commonly observed in females and is characterized by delayed or rapid gastric emptying (GE). The role of ovarian hormones on GE in the pathogenesis of obesity induced type 2 diabetes mellitus (T2DM) is completely unknown. The aims of our study are to investigate whether supplementation of 17β-estradiol (E2) or progesterone (P4) restores impaired nuclear factor erythroid 2-related factor 2 (Nrf2, an oxidative stress-responsive transcription factor) and nitric oxide (NO)-mediated gastric motility in ovariectomized (OVX) mice consuming a high-fat diet (HFD, a model of T2DM). Groups of OVX+HFD mice were administered daily subcutaneous doses of either E2 or P4 for 12 weeks. The effects of E2 and P4 on body weight, metabolic homeostasis, solid GE, gastric antrum NO-mediated relaxation, total nitrite levels, neuronal nitric oxide synthase (nNOSα), and its cofactor expression levels were assessed in OVX+HFD mice. HFD exacerbated hyperglycemia and insulinemia while accelerating GE (p < 0.05) in OVX mice. Exogenous E2, but not P4, attenuated rapid gastric emptying and restored gastric nitrergic relaxation, total nitrite levels, nNOSα, and cofactor expression via normalizing Nrf2-Phase II enzymes, inflammatory response, and mitogen-activated protein kinase (MAPK) protein expression in OVX+HFD mice. We conclude that E2 is beneficial in normalizing metabolic homeostasis and gastric emptying in obese, diabetic OVX mice consuming a fat-rich diet.

scholarly journals Protective role of PI3-kinase/Akt/eNOS signaling in mechanical stress through inhibition of p38 mitogen-activated protein kinase in mouse lung

2010 ◽  
Vol 31 (2) ◽  
pp. 175-183 ◽  
Author(s):  
Xin-qi Peng ◽  
Mahendra Damarla ◽  
Jarrett Skirball ◽  
Stephanie Nonas ◽  
Xiao-ying Wang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mechanical Stress ◽  
Protective Role ◽  
Pi3 Kinase ◽  
Mitogen Activated Protein Kinase ◽  
Mouse Lung ◽  
Mitogen Activated Protein

scholarly journals Differential Role of Threonine and Tyrosine Phosphorylation in the Activation and Activity of the Yeast MAPK Slt2

2021 ◽  
Vol 22 (3) ◽  
pp. 1110
Author(s):  
Gema González-Rubio ◽  
Ángela Sellers-Moya ◽  
Humberto Martín ◽  
María Molina
Keyword(s):  
Cell Wall ◽  
Biological Activity ◽  
Biological Significance ◽  
Mitogen Activated Protein Kinase ◽  
Activation Loop ◽  
High Increase ◽  
Dual Specificity ◽  
Mitogen Activated Protein ◽  
Full Activation

The Mitogen-Activated Protein Kinase (MAPK) Slt2 is central to signaling through the yeast Cell Wall Integrity (CWI) pathway. MAPKs are regulated by phosphorylation at both the threonine and tyrosine of the conserved TXY motif within the activation loop (T190/Y192 in Slt2). Since phosphorylation at both sites results in the full activation of MAPKs, signaling through MAPK pathways is monitored with antibodies that detect dually phosphorylated forms. However, most of these antibodies also recognize monophosphorylated species, whose relative abundance and functionality are diverse. By using different phosphospecific antibodies and phosphate-affinity (Phos-tag) analysis on distinct Slt2 mutants, we determined that Y192- and T190-monophosphorylated species coexist with biphosphorylated Slt2, although most of the Slt2 pool remains unphosphorylated following stress. Among the monophosphorylated forms, only T190 exhibited biological activity. Upon stimulation, Slt2 is first phosphorylated at Y192, mainly by the MAPKK Mkk1, and this phosphorylation is important for the subsequent T190 phosphorylation. Similarly, dephosphorylation of Slt2 by the Dual Specificity Phosphatase (DSP) Msg5 is ordered, with dephosphorylation of T190 depending on previous Y192 dephosphorylation. Whereas Y192 phosphorylation enhances the Slt2 catalytic activity, T190 is essential for this activity. The conserved T195 residue is also critical for Slt2 functionality. Mutations that abolish the activity of Slt2 result in a high increase in inactive Y192-monophosphorylated Slt2. The coexistence of different Slt2 phosphoforms with diverse biological significance highlights the importance of the precise detection of the Slt2 phosphorylation status.

ERK5 and its role in tumour development

2012 ◽  
Vol 40 (1) ◽  
pp. 251-256 ◽  
Author(s):  
Pamela A. Lochhead ◽  
Rebecca Gilley ◽  
Simon J. Cook
Keyword(s):  
Mitogen Activated Protein Kinase ◽  
Invasion And Migration ◽  
Extracellular Signal Regulated Kinase ◽  
Protein Levels ◽  
Extracellular Signal ◽  
Mapk Signalling ◽  
Mitogen Activated Protein ◽  
Tumour Cell Invasion ◽  
And Migration

The MEK5 [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase 5]/ERK5 pathway is the least well studied MAPK signalling module. It has been proposed to play a role in the pathology of cancer. In the present paper, we review the role of the MEK5/ERK5 pathway using the ‘hallmarks of cancer’ as a framework and consider how this pathway is deregulated. As well as playing a key role in endothelial cell survival and tubular morphogenesis during tumour neovascularization, ERK5 is also emerging as a regulator of tumour cell invasion and migration. Several oncogenes can stimulate ERK5 activity, and protein levels are increased by a novel amplification at chromosome locus 17p11 and by down-regulation of the microRNAs miR-143 and miR-145. Together, these finding underscore the case for further investigation into understanding the role of ERK5 in cancer.

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