LncRNA LOC102176306 plays important roles in goat testicular development

Reproduction ◽  
2021 ◽  
Vol 161 (5) ◽  
pp. 523-537
Author(s):  
Shi-Yu An ◽  
Zi-Fei Liu ◽  
El-Samahy M A ◽  
Ming-Tian Deng ◽  
Xiao-Xiao Gao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Molecular Mechanisms ◽  
Complex Iii ◽  
Testicular Development ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Atp Production ◽  
Positive Effects ◽  
And Oxidative Stress

Long ncRNAs regulate a complex array of fundamental biological processes, while its molecular regulatory mechanism in Leydig cells (LCs) remains unclear. In the present study, we established the lncRNA LOC102176306/miR-1197-3p/peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PPARGC1A) regulatory network by bioinformatic prediction, and investigated its roles in goat LCs. We found that lncRNA LOC102176306 could efficiently bind to miR-1197-3p and regulate PPARGC1A expression in goat LCs. Downregulation of lncRNA LOC102176306 significantly supressed testosterone (T) synthesis and ATP production, decreased the activities of antioxidant enzymes and mitochondrial complex I and complex III, caused the loss of mitochondrial membrane potential, and inhibited the proliferation of goat LCs by decreasing PPARGC1A expression, while these effects could be restored by miR-1197-3p inhibitor treatment. In addition, miR-1197-3p mimics treatment significantly alleviated the positive effects of lncRNA LOC102176306 overexpression on T and ATP production, antioxidant capacity and proliferation of goat LCs. Taken together, lncRNA LOC102176306 functioned as a sponge for miR-1197-3p to maintain PPARGC1A expression, thereby affecting the steroidogenesis, cell proliferation and oxidative stress of goat LCs. These findings extend our understanding of the molecular mechanisms of T synthesis, cell proliferation and oxidative stress of LCs.

scholarly journals Molecular Mechanisms of Obesity-Linked Cardiac Dysfunction: An Up-Date on Current Knowledge

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 629
Author(s):  
Jorge Gutiérrez-Cuevas ◽  
Ana Sandoval-Rodriguez ◽  
Alejandra Meza-Rios ◽  
Hugo Christian Monroy-Ramírez ◽  
Marina Galicia-Moreno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Peroxisome Proliferator ◽  
White Adipocyte ◽  
Peroxisome Proliferator Activated Receptors ◽  
And Oxidative Stress

Obesity is defined as excessive body fat accumulation, and worldwide obesity has nearly tripled since 1975. Excess of free fatty acids (FFAs) and triglycerides in obese individuals promote ectopic lipid accumulation in the liver, skeletal muscle tissue, and heart, among others, inducing insulin resistance, hypertension, metabolic syndrome, type 2 diabetes (T2D), atherosclerosis, and cardiovascular disease (CVD). These diseases are promoted by visceral white adipocyte tissue (WAT) dysfunction through an increase in pro-inflammatory adipokines, oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and adverse changes in the gut microbiome. In the heart, obesity and T2D induce changes in substrate utilization, tissue metabolism, oxidative stress, and inflammation, leading to myocardial fibrosis and ultimately cardiac dysfunction. Peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of carbohydrate and lipid metabolism, also improve insulin sensitivity, triglyceride levels, inflammation, and oxidative stress. The purpose of this review is to provide an update on the molecular mechanisms involved in obesity-linked CVD pathophysiology, considering pro-inflammatory cytokines, adipokines, and hormones, as well as the role of oxidative stress, inflammation, and PPARs. In addition, cell lines and animal models, biomarkers, gut microbiota dysbiosis, epigenetic modifications, and current therapeutic treatments in CVD associated with obesity are outlined in this paper.

Anti-adipogenesis and antioxidative defense status of a crude extract of ‘Kalasin 2’ peanut sprouts in 3T3-L1 mouse adipocytes

2019 ◽  
Vol 97 (6) ◽  
pp. 740-749
Author(s):  
Tantip Boonsong ◽  
Siriporn Pakwan ◽  
Wanida Chawnawa
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Oxidative Status ◽  
Peroxisome Proliferator ◽  
Antioxidative Defense ◽  
Peroxisome Proliferator Activated Receptor ◽  
Defense Systems ◽  
Treatment Of Obesity ◽  
Mouse Adipocytes ◽  
And Oxidative Stress

The aim of this study was to investigate the effects of extracts from germinated (GPE) and non-germinated peanuts (NGPE) on adipogenesis and oxidative status in normal and oxidative-stress-induced 3T3-L1 mouse adipocytes. The treated cells were analysed for cell growth, lipid accumulation, levels of intracellular reactive oxygen species (ROS), and the expression levels of mRNAs and proteins related to adipogenesis and antioxidative defense systems. The results indicated that an extract from peanuts made 9 days after germination (9GPE) reduced lipid contents and mRNA expression of adipogenesis-related genes to a greater extent than an extract from peanuts made 1-day after germination (1GPE) or from NGPE, respectively. In oxidative-stress-induced adipocytes, 9GPE decreased ROS levels, lipid content, and the protein expression of peroxisome-proliferator-activated receptor gamma, and also increased the protein expression of antioxidants. These results illustrate the anti-adipogenic capacity and oxidative status improvement achievable with GPE, and that it could be used as a putative therapeutic agent in the prevention of and (or) treatment of obesity and diseases associated with oxidative stress.

Activation of peroxisome proliferator-activated receptor–γ by a 12/15-lipoxygenase product of arachidonic acid: a possible neuroprotective effect in the brain after experimental intracerebral hemorrhage

2017 ◽  
Vol 127 (3) ◽  
pp. 522-531 ◽  
Author(s):  
Ruobing Xu ◽  
Shu Wang ◽  
Weishan Li ◽  
Zhen Liu ◽  
Jiaxin Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intracerebral Hemorrhage ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Peroxisome Proliferator ◽  
Double Labeling ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pparγ Agonist ◽  
Autologous Whole Blood ◽  
The Brain ◽  
And Oxidative Stress

OBJECTIVEIn this study, the authors investigated the involvement of 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE) in the regulation of peroxisome proliferator-activated receptor–γ (PPARγ) after intracerebral hemorrhage (ICH) and its effects on hemorrhage-induced inflammatory response and oxidative stress in an experimental rodent model.METHODSTo simulate ICH in a rat model, the authors injected autologous whole blood into the right striatum of male Sprague-Dawley rats. The distribution and expression of 12/15-lipoxygenase (12/15-LOX) were determined by immunohistochemistry and Western blot analysis, respectively. Immunofluorescent double labeling was used to study the cellular localization of 12/15-LOX, and 15(S)-HETE was measured with a 15(S)-HETE enzyme immunoassay kit. Neurological deficits in the animals were assessed through behavioral testing, and apoptotic cell death was determined with terminal deoxynucleotidyl transferase–mediated biotinylated dUTP nick-end labeling.RESULTSRats with ICH had increased expression of 12/15-LOX predominantly in neurons and also in oligodendrocytes, astrocytes, and microglia. Moreover, ICH elevated production of 15(S)-HETE in the brain area ipsilateral to the blood injection. The PPARγ agonist, exogenous 15(S)-HETE, significantly increased PPARγ protein levels and increased PPARγ-regulated gene (i.e., catalase) expression in the ICH rats. Reduced expression of the gene for the proinflammatory protein nuclear factor κB coincided with decreased neuron damage and improved functional recovery from ICH. A PPARγ antagonist, GW9662, reversed the effects of exogenous 15(S)-HETE on the PPARγ-regulated genes.CONCLUSIONSThe induction of 15(S)-HETE during simulated ICH suggests generation of endogenous signals of neuroprotection. The effects of exogenous 15(S)-HETE on brain hemorrhage–induced inflammatory responses and oxidative stress might be mediated via PPARγ.

Oxidative stress-induced alterations in PPAR-γ and associated mitochondrial destabilization contribute to kidney cell apoptosis

2014 ◽  
Vol 307 (7) ◽  
pp. F814-F822 ◽  
Author(s):  
David M. Small ◽  
Christudas Morais ◽  
Jeff S. Coombes ◽  
Nigel C. Bennett ◽  
David W. Johnson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Cell Viability ◽  
Mitochondrial Biogenesis ◽  
Peroxisome Proliferator ◽  
Western Blots ◽  
Positive Effects ◽  
Ppar Γ ◽  
Mitotracker Red ◽  
And Oxidative Stress

The mechanism(s) underlying renoprotection by peroxisome proliferator-activated receptor (PPAR)-γ agonists in diabetic and nondiabetic kidney disease are not well understood. Mitochondrial dysfunction and oxidative stress contribute to kidney disease. PPAR-γ upregulates proteins required for mitochondrial biogenesis. Our aim was to determine whether PPAR-γ has a role in protecting the kidney proximal tubular epithelium (PTE) against mitochondrial destabilisation and oxidative stress. HK-2 PTE cells were subjected to oxidative stress (0.2–1.0 mM H2O2) for 2 and 18 h and compared with untreated cells for apoptosis, mitosis (morphology/biomarkers), cell viability (MTT), superoxide (dihydroethidium), mitochondrial function (MitoTracker red and JC-1), ATP (luminescence), and mitochondrial ultrastructure. PPAR-γ, phospho-PPAR-γ, PPAR-γ coactivator (PGC)-1α, Parkin (Park2), p62, and light chain (LC)3β were investigated using Western blots. PPAR-γ was modulated using the agonists rosiglitazone, pioglitazone, and troglitazone. Mitochondrial destabilization increased with H2O2 concentration, ATP decreased (2 and 18 h; P < 0.05), Mitotracker red and JC-1 fluorescence indicated loss of mitochondrial membrane potential, and superoxide increased (18 h, P < 0.05). Electron microscopy indicated sparse mitochondria, with disrupted cristae. Mitophagy was evident at 2 h (Park2 and LC3β increased; p62 decreased). Impaired mitophagy was indicated by p62 accumulation at 18 h ( P < 0.05). PPAR-γ expression decreased, phospho-PPAR-γ increased, and PGC-1α decreased (2 h), indicating aberrant PPAR-γ activation and reduced mitochondrial biogenesis. Cell viability decreased (2 and 18 h, P < 0.05). PPAR-γ agonists promoted further apoptosis. In summary, oxidative stress promoted mitochondrial destabilisation in kidney PTE, in association with increased PPAR-γ phosphorylation. PPAR-γ agonists failed to protect PTE. Despite positive effects in other tissues, PPAR-γ activation appears to be detrimental to kidney PTE health when oxidative stress induces damage.

scholarly journals Role of Peroxisome Proliferator-Activated Receptorγin Ocular Diseases

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Su Zhang ◽  
Hongwei Gu ◽  
Nan Hu
Keyword(s):  
Oxidative Stress ◽  
Eye Diseases ◽  
Age Related Macular Degeneration ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Physiological Processes ◽  
Age Related ◽  
Potential Benefits ◽  
And Oxidative Stress

Peroxisome proliferator-activated receptorγ(PPARγ), a member of the nuclear receptor superfamily, is a ligand-activated transcription factor that plays an important role in the control of a variety of physiological processes. The last decade has witnessed an increasing interest for the role played by the agonists of PPARγin antiangiogenesis, antifibrosis, anti-inflammation effects and in controlling oxidative stress response in various organs. As the pathologic mechanisms of major blinding diseases, such as age-related macular degeneration (AMD), diabetic retinopathy (DR), keratitis, and optic neuropathy, often involve neoangiogenesis and inflammation- and oxidative stress-mediated cell death, evidences are accumulating on the potential benefits of PPARγto improve or prevent these vision threatening eye diseases. In this paper we describe what is known about the role of PPARγin the ocular pathophysiological processes and PPARγagonists as novel adjuvants in the treatment of eye diseases.

Sign in / Sign up

Export Citation Format

Share Document