scholarly journals Adiponectin Accumulation in the Tetinal Vascular Endothelium and its Possible Role in Preventing Early Diabetic Microvascular Damage

2021 ◽  
Author(s):  
Taka-aki Sakaue ◽  
Yuya Fujishima ◽  
Yoko Fukushima ◽  
Yuri Tsugawa-Shimizu ◽  
Shiro Fukuda ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Vascular Endothelium ◽  
Microvascular Complications ◽  
Diabetic Mouse ◽  
Protective Role ◽  
Cellular Adhesion ◽  
Microvascular Damage ◽  
Cellular Adhesion Molecule ◽  
The Impact

Abstract Adiponectin (APN), a protein abundantly secreted from adipocytes, has been reported to possess beneficial effects on cardiovascular diseases in association with its accumulation on target organs and cells by binding to T-cadherin. However, little is known about the role of APN in the development of diabetic microvascular complications, such as diabetic retinopathy (DR). Here we investigated the impact of APN on the progression of early retinal vascular damage using a streptozotocin (STZ)-induced diabetic mouse model. Our immunofluorescence results clearly showed T-cadherin-dependent localization of APN in the vascular endothelium of retinal arterioles, which was progressively decreased during the course of diabetes. Such reduction of retinal APN accompanied the early features of DR, represented by increased vascular permeability, and was prevented by glucose-lowering therapy with dapagliflozin, a selective sodium-glucose co-transporter 2 inhibitor. In addition, APN deficiency resulted in severe vascular permeability under relatively short-term hyperglycemia, together with a significant increase in vascular cellular adhesion molecule-1 (VCAM-1) and a reduction in claudin-5 in the retinal endothelium. The present study demonstrated a possible protective role of APN against the development of DR.

Comparative Analysis of Autoxidation of Haemoglobin

2001 ◽  
Vol 204 (11) ◽  
pp. 2029-2033
Author(s):  
Frank B. Jensen
Keyword(s):  
Temperature Sensitivity ◽  
Oxidation Rate ◽  
Protective Role ◽  
Yellowfin Tuna ◽  
Histidine Residue ◽  
River Lamprey ◽  
Different Temperatures ◽  
Lower Temperature ◽  
The Impact

SUMMARY Autoxidation of oxyhaemoglobin (oxyHb) to methaemoglobin was measured at different temperatures in haemoglobin solutions from Atlantic hagfish, river lamprey, common carp, yellowfin tuna and pig. The aims were to evaluate the impact of the absent distal histidine in hagfish haemoglobin, the importance of oxyHb being either monomeric (hagfish and lamprey) or tetrameric (carp, tuna and pig) and to gain information on the temperature-sensitivity of autoxidation. The rate of autoxidation was lower in hagfish than in carp, yellowfin tuna and lamprey haemoglobins at any given temperature. Substitution of the distal histidine residue (His E7) with glutamine in hagfish haemoglobin was therefore not associated with an accelerated autoxidation, as might be expected on the basis of the normal protective role of His E7. Glutamine may have similar qualities to histidine and be involved in the low susceptibility to autoxidation. The low oxidation rate of hagfish haemoglobin, together with an oxidation rate of lamprey haemoglobin that did not differ from that of carp and yellowfin tuna haemoglobins, also revealed that autoxidation was not accelerated in the monomeric oxyhaemoglobins. Pig haemoglobin was oxidised more slowly than fish haemoglobins, demonstrating that fish haemoglobins are more sensitive to autoxidation than mammalian haemoglobins. The rate of autoxidation of hagfish haemoglobin was, however, only significantly greater than that of pig haemoglobin at high temperatures. Autoxidation was accelerated by rising temperature in all haemoglobins. Arrhenius plots of carp and yellowfin tuna haemoglobin revealed a break at 25°C, reflecting a lower temperature-sensitivity between 5 and 25°C than between 25 and 40°C.

scholarly journals The Impact of Spaceflight and Simulated Microgravity on Cell Adhesion

2020 ◽  
Vol 21 (9) ◽  
pp. 3031 ◽  
Author(s):  
Xiao Lin ◽  
Kewen Zhang ◽  
Daixu Wei ◽  
Ye Tian ◽  
Yongguang Gao ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Mammalian Cells ◽  
Simulated Microgravity ◽  
General Term ◽  
Cellular Adhesion ◽  
Immunoglobulin Superfamily ◽  
Adhesion Properties ◽  
Cellular Adhesion Molecule ◽  
The Impact ◽  
Cell Cell

Microgravity induces a number of significant physiological changes in the cardiovascular, nervous, immune systems, as well as the bone tissue of astronauts. Changes in cell adhesion properties are one aspect affected during long-term spaceflights in mammalian cells. Cellular adhesion behaviors can be divided into cell–cell and cell–matrix adhesion. These behaviors trigger cell–cell recognition, conjugation, migration, cytoskeletal rearrangement, and signal transduction. Cellular adhesion molecule (CAM) is a general term for macromolecules that mediate the contact and binding between cells or between cells and the extracellular matrix (ECM). In this review, we summarize the four major classes of adhesion molecules that regulate cell adhesion, including integrins, immunoglobulin superfamily (Ig-SF), cadherins, and selectin. Moreover, we discuss the effects of spaceflight and simulated microgravity on the adhesion of endothelial cells, immune cells, tumor cells, stem cells, osteoblasts, muscle cells, and other types of cells. Further studies on the effects of microgravity on cell adhesion and the corresponding physiological behaviors may help increase the safety and improve the health of astronauts in space.

scholarly journals Autophagy plays a protective role during Pseudomonas aeruginosa-induced apoptosis via ROS–MAPK pathway

2020 ◽  
Vol 26 (7) ◽  
pp. 580-591
Author(s):  
Lu Han ◽  
Qinmei Ma ◽  
Jialin Yu ◽  
Zhaoqian Gong ◽  
Chenjie Ma ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Mapk Pathway ◽  
Protective Role ◽  
Vital Role ◽  
Raw264.7 Cells ◽  
Cellular Reactive Oxygen Species ◽  
Induced Apoptosis ◽  
Related Proteins ◽  
The Impact

Pseudomonas aeruginosa infection can induce alveolar macrophage apoptosis and autophagy, which play a vital role in eliminating pathogens. These two processes are usually not independent. Recently, autophagy has been found to interact with apoptosis during pathogen infections. Nevertheless, the role of autophagy in P. aeruginosa-infected cell apoptosis is unclear. In this study, we explored the impact of P. aeruginosa infection on autophagy and apoptosis in RAW264.7 cells. The autophagy activator rapamycin was used to stimulate autophagy and explore the role of autophagy on apoptosis in P. aeruginosa-infected RAW264.7 cells. The results indicated that P. aeruginosa infection induced autophagy and apoptosis in RAW264.7 cells, and that rapamycin could suppress P. aeruginosa-induced apoptosis by regulating the expression of apoptosis-related proteins. In addition, rapamycin scavenged the cellular reactive oxygen species (ROS) and diminished p-JNK, p-ERK1/2 and p-p38 expression of MAPK pathways in RAW264.7 cells infected with P. aeruginosa. In conclusion, the promotion of autophagy decreased P. aeruginosa-induced ROS accumulation and further attenuated the apoptosis of RAW264.7 cells through MAPK pathway. These results provide novel insights into host–pathogen interactions and highlight a potential role of autophagy in eliminating P. aeruginosa.

scholarly journals A Novel STAT3-Mediated GATA6 Pathway Contributes to tert-Butylhydroquinone- (tBHQ-) Protected TNFα-Activated Vascular Cell Adhesion Molecule 1 (VCAM-1) in Vascular Endothelium

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Li Zhou ◽  
Hua Ning ◽  
Haibin Wei ◽  
Tiantian Xu ◽  
Xindi Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Endothelium ◽  
Cell Adhesion Molecule ◽  
Vascular Endothelial Cells ◽  
Protective Role ◽  
Vascular Endothelial ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Cell Adhesion Molecule 1

The activation of vascular cell adhesion molecule 1 (VCAM-1) in vascular endothelial cells has been well considered implicating in the initiation and processing of atherosclerosis. Oxidative stress is mechanistically involved in proatherosclerotic cytokine-induced VCAM-1 activation. tert-Butylhydroquinone (tBHQ), a synthetic phenolic antioxidant used for preventing lipid peroxidation of food, possesses strongly antioxidant capacity against oxidative stress-induced dysfunction in various pathological process. Here, we investigated the protective role of tBHQ on tumor necrosis factor alpha- (TNFα-) induced VCAM-1 activation in both aortic endothelium of mice and cultured human vascular endothelial cells and uncovered its potential mechanisms. Our data showed that tBHQ treatment significantly reversed TNFα-induced activation of VCAM-1 at both transcriptional and protein levels. The mechanistic study revealed that inhibiting neither nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nor autophagy blocked the beneficial role of tBHQ. Alternatively, tBHQ intervention markedly alleviated TNFα-increased GATA-binding protein 6 (GATA6) mRNA and protein expressions and its translocation into nucleus. Further investigation indicated that tBHQ-inhibited signal transducer and activator of transcription 3 (STAT3) but not mitogen-activated protein kinase (MAPK) pathway contributed to its protective role against VCAM-1 activation via regulating GATA6. Collectively, our data demonstrated that tBHQ prevented TNFα-activated VCAM-1 via a novel STAT3/GATA6-involved pathway. tBHQ could be a potential candidate for the prevention of proatherosclerotic cytokine-caused inflammatory response and further dysfunctions in vascular endothelium.

scholarly journals The Impact of Coronavirus Disease 2019 Lockdown on Athletes’ Subjective Vitality: The Protective Role of Resilience and Autonomous Goal Motives

2021 ◽  
Vol 11 ◽  
Author(s):  
Natalia Martínez-González ◽  
Francisco L. Atienza ◽  
Inés Tomás ◽  
Joan L. Duda ◽  
Isabel Balaguer
Keyword(s):  
Linear Models ◽  
Well Being ◽  
Protective Role ◽  
Subjective Vitality ◽  
Huge Impact ◽  
Mediational Role ◽  
The Impact ◽  
The Relationship ◽  
Over Time

The lockdown resulting from coronavirus disease 2019 (COVID-19) has had a huge impact on peoples’ health. In sport specifically, athletes have had to deal with frustration of their objectives and changes in their usual training routines. The challenging and disruptive situation could hold implications for their well-being. This study examined the effect of the COVID-19 lockdown on changes in athletes’ reported eudaimonic well-being (subjective vitality) and goal motives (autonomous and controlled) over time (i.e., pre-lockdown and during lockdown). The relationship of resilience to changes in subjective vitality was also determined, and changes in athletes’ goal motives were examined as potential mediators. Participants were 127 Spanish university athletes aged between 18 and 34 years (M = 21.14; SD = 2.77). Approximately 4 months before the start of the lockdown in Spain (T1), athletes responded to a questionnaire assessing their resilience, goal motives, and subjective vitality. Around 6 months later into the lockdown period (T2), athletes’ goal motives and subjective vitality were assessed again. Growth modeling using hierarchical linear models revealed a significant decrease of autonomous goal motives and subjective vitality during the lockdown, but athletes did not show change over time in controlled goal motives. Path analysis, adjusting T2 measures for their corresponding T1 measures, showed that resilience significantly predicted changes in athletes’ autonomous goal motives, which then accounted for changes in subjective vitality. The indirect effect was significant. Resilience did not predict changes in athletes’ controlled goal motives. However, changes in controlled goal motives negatively predicted changes in subjective vitality during lockdown. The findings suggest negative impacts of the COVID-19 lockdown on athletes’ goal motives and eudaimonic well-being. Results also support the hypothesized mediational role of autonomous goal motives in the relationship between resilience and subjective vitality during the lockdown. As such, findings confirm the relevance of resilience to a key feature of athletes’ eudaimonic well-being and the importance of enhancing their autonomous goal striving.

scholarly journals Infection-induced miR-126 suppresses tsc1- and cxcl12a-dependent permissive macrophages during mycobacterial infection

2021 ◽  
Author(s):  
Kathryn Wright ◽  
Kumudika de Silva ◽  
Karren M. Plain ◽  
Auriol C. Purdie ◽  
Warwick J. Britton ◽  
...  
Keyword(s):  
Immune Response ◽  
Detrimental Effect ◽  
Mycobacterial Infection ◽  
Protective Role ◽  
Zebrafish Embryos ◽  
Zebrafish Model ◽  
Effector Pathways ◽  
The Impact ◽  
Mtor Signalling

AbstractRegulation of host microRNA (miRNA) expression is a contested node that controls the host immune response to mycobacterial infection. The host must overcome concerted subversive efforts of pathogenic mycobacteria to launch and maintain a protective immune response. Here we examine the role of miR-126 in the zebrafish model of Mycobacterium marinum infection and identify a protective role for this infection-induced miRNA through multiple effector pathways. Specifically, we analyse the impact of the miR-126 knockdown-induced tsc1a and cxcl12a/ccl2/ccr2 signalling axes during early host-M. marinum interactions. We find a strong detrimental effect of tsc1a upregulation that renders zebrafish embryos susceptible to higher bacterial burden and increased cell death despite dramatically higher recruitment of macrophages to the site of infection. We demonstrate that infection-induced miR-126 suppresses tsc1 and cxcl12a expression thus improving macrophage function early in infection, partially through activation of mTOR signalling and strongly through preventing the recruitment of Ccr2+ permissive macrophages, resulting in the recruitment of protective tnfa-expressing macrophages. Together our results demonstrate an important role for infection-induced miR-126 in shaping an effective immune response to M. marinum infection in zebrafish embryos.

FGF21 prevents low protein diet-induced renal inflammation in aged mice

2021 ◽  
Author(s):  
Han Fang ◽  
Sujoy Ghosh ◽  
Landon Sims ◽  
Kirsten P. Stone ◽  
Cristal M Hill ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Renal Damage ◽  
Protective Role ◽  
Wild Type ◽  
Kidney Weight ◽  
Albumin Creatinine Ratio ◽  
Low Protein ◽  
The Impact ◽  
Protein Diets

Low protein diets extend lifespan through a comprehensive improvement in metabolic health across multiple tissues and organs. Many of these metabolic responses to protein restriction are secondary to transcriptional activation and release of FGF21 from the liver. However, the effects of a low protein (LP) diet on the kidney in the context of aging has not been examined. Therefore, the goal of the current study was to investigate the impact of chronic consumption of a LP diet on the kidney in aging mice lacking FGF21. Wild type (WT, C57BL/6J) and FGF21 KO mice were fed a normal protein (NP, 20% casein) or a LP (5% casein) diet ad libitum from 3 to19 months of age. The LP diet led to a decrease in kidney weight and urinary albumin/creatinine ratio in both WT and FGF21 KO mice. Although the LP diet produced only mild fibrosis and infiltration of leukocytes in WT kidneys, the effects were significantly exacerbated by the absence of FGF21. Accordingly, transcriptomic analysis showed that inflammation-related pathways were significantly enriched and upregulated in response to LP diet in FGF21 KO but not WT mice. Collectively, these data demonstrate that the LP diet negatively affected the kidney during aging, but in the absence of FGF21, the LP diet-induced renal damage and inflammation were significantly worse, indicating a protective role of FGF21 in the kidney.

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