bluuebunny/crossref_metadata_2025_split huggingface dataset:
Avocado Oil Alleviates Renal Damage and decreases NADPH Oxidase Activity, Peroxynitrite Production and Mitochondrial Calcium Uptake in Hypertension Rats
Authors: Olmos‐Orizaba Berenice Eridani , Márquez‐Ramírez Cristian Adrián , Garcia‐Berumen Claudia Isabel , Villagómez Ana Victoria Hurtado , Calderón‐Cortés Elizabeth , Saavedra‐Molina Alfredo , Montoya‐Pérez Rocio 
Published: June 2021

Hypertension (HT) has been associated with mitochondrial dysfunction due to both nitrosative and oxidative stresses that are generated by increased activity of NADPH oxidase (Nox), defective calcium transport and enhanced ROS generation by reverse electron transfer (RET) at complex I. These factors contribute to the pathogenesis of endothelial dysfunction and to the progress of hypertensive complications. Previously, we have shown that avocado oil, a rich source of bioactive compounds and antioxidants, decreases blood pressure and ameliorates both mitochondrial dysfunction and oxidative stress in kidney from hypertensive rats. However, it is unknown whether the effects of avocado oil on renal mitochondria are attributable to decreased activity of NADPH oxidase, lowered levels of reactive nitrogen species (RNS) and improved calcium uptake by mitochondria. Thus, we analyzed Nox activity and peroxynitrite (ONOO‐) levels in kidney cytosolic fractions of L‐NAME – induced hypertensive rats as well as mitochondrial calcium uptake and complex I activity. After 60‐days of L‐NAME administration, the hypertensive rats exhibited enhanced Nox activity and ONOO‐ levels, as well as increased complex I activity and excessive calcium uptake. All these alterations were prevented by co‐administration of L‐NAME with avocado oil. Moreover, the kidneys from hypertensive rats shown histological manifestations of renal damage that were also corrected by avocado oil. These data suggest that avocado oil could be beneficial to decrease hypertensive nephropathy progression by improving mitochondrial function, diminishing RNS production and normalizing Nox activity.Support or Funding InformationThis work was supported by a Coordinación de la Investigación Científica‐UMSNH grant (to CCR)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Gas7 regulates mitochondrial morphology and physiology
Authors: Bhupana Jagannatham Naidu , Huang Bo‐Tsang , Chang Yu‐Ling , Chao Sue Lin 
Published: June 2021

Gas7 belongs to the F‐BAR family of proteins and has been shown to be involved in actin and microtubule dynamics. Gas7 is mainly expressed in mouse brain and testicular tissues. In primary cultured neurons, Gas7 enhances actin polymerization and neurite outgrowth. Mutations in PARKIN and PINK1 genes, which play major roles in mitochondrial quality control and mitochondrial autophagy, are often associated with Parkinson's disease. Here, we report a role of Gas7 in mitochondrial distribution, physiological functions, and enhancement of PINK1‐parkin‐mediated mitochondrial autophagy. In the brain of gas7 knockout mice, the mitochondrial aspect ratio is elevated, suggesting a decrease in the level of mitochondrial fragmentation, resulting in an elongated shape. Furthermore, in primary neuronal cultured cells, we found that mitochondrial distribution was restricted around the nucleus, tubular mitochondrial subtypes increased, indicating decreased mitochondrial division, and increased mitochondrial fusion in Gas7 knockout neurons. Gas7 ectopic‐expression in these primary cultured neurons can restore normal morphology and distribution of mitochondria. Overall, our data suggest that Gas7 is required for normal mitochondrial dynamics and therefore may be important for cerebral neurons to maintain mitochondrial function.Support or Funding InformationThis work was supported by an intramural fund from the Institute of Molecular Biology, Academia Sinica and a theme project of Academia Sinica (2323)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Leptin Delivers β‐cell‐derived C‐peptide to Red Blood Cells
Authors: Meints Lisa , Keshavarz Hamideh , Kauffman Nate , Geiger Morgan , Zinn Kurt , Spence Dana 
Published: June 2021

It was recently reported that C‐peptide, the connecting peptide of proinsulin, binds to red blood cells (RBCs) when delivered by albumin. Additionally, treatment of RBCs with C‐peptide, zinc, and albumin results in an increase in ATP release from the RBC and downstream production of endothelium‐derived nitric oxide. Here, we report leptin, an adipocyte‐derived cytokine known for its importance for energy balance and potential glucoregulatory effects, as a potential drug carrier for C‐peptide. Here, we report that C‐peptide increases GLUT1 translocation and ATP release from RBCs, but only in the presence of leptin and zinc. To investigate the nature of the interaction of C‐peptide and leptin with RBCs we have utilized leptin labeled with technetium‐99m (99mTc) to perform saturation binding studies. Samples containing 7% RBCs were treated with different concentrations of labeled leptin and 20 nM C‐peptide. Samples were then incubated, centrifuged, and washed several times prior to quantitative determination of gamma emission from the 99mTc‐labeled leptin bound to the RBCs. Data was correlated back to a standard curve of labeled leptin, and a saturation binding curve was generated. Initial results suggest that total binding of labeled leptin, in the presence of C‐peptide, begins to saturate when 200 picomoles of labeled leptin are added to the RBCs.Support or Funding InformationNational Institutes of HealthThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effects of melatonin on neural reconstruction after acute spinal cord injury through regulation of endoplasmic reticulum stress response and autophagy
Authors: Jin Yunho , Hong Yonggeun 
Published: June 2021

It has been reported that autophagy and endoplasmic reticulum (ER) stress response cause improved hindlimb motor function and reduced damage of axons in spinal cord injured animals, respectively. However, the effects of melatonin on neural reconstruction and motor recovery through regulation of ER stress response and autophagy have not been well described. Therefore, the purpose of this study is to elucidate the effects of melatonin treatment on neural reconstruction and motor recovery through regulation of ER stress response and autophagy.To verify the effect of melatonin injection on post‐SCI alterations regarding neural cells, autophagy, and ER stress response, we analyzed markers at protein level, and morphological changes. At day 3 after SCI, melatonin did not cause behavioral improvement (p<.05). At molecular levels, melatonin suppressed the loss of astrocytes after SCI (p<.05). Beclin‐1 expression was decreased by melatonin treatment (p<.05). In other words, autophagy activation in SCI+MT was lower than that of SCI group, indicating melatonin‐mediated suppression of autophagic cell death. In addition, GRP78 expression was preserved in SCI+MT group with no difference compared to non‐injured groups. Namely, ER stress response was advanced by melatonin. In histological analysis, it was proved that dendritic branches were preserved by melatonin treatment.In conclusion, exogenous treatment of melatonin may result in neural reconstruction after SCI through regulating autophagy and ER stress response at the injured spinal segments.Support or Funding InformationNRF‐2017R1A2A2A01067169, KGM4611821, 2016 Creative Research Program of Inje University, Republic of KoreaThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Compared to liver, bile duct and skeletal muscle, garlic stimulates only pancreatic insulinogenesis in early streptozotocin‐induced diabetic rats
Authors: Al‐Qattan Khaled K , Al‐Adsani Amani M 
Published: June 2021

BackgroundStreptozotocin (STZ) induces diabetes mellitus (DM: STZ‐DM) type‐1 in rats by pancreatic β‐cells DNA alkylation and consequently reduction in insulin circulating concentration. Garlic aqueous extract (GE) increases insulin circulating concentration in the STZ‐DM rat model.ObjectiveThis study investigated the insulinogenic mechanisms of GE in the pancreas, liver, bile duct and gastrocnemius skeletal muscle (GSM) of STZ‐DM rats.MethodThe body weight, food and water intake, urine output, fasting blood glucose (FBG), serum insulin (SI) in addition to insulin m‐RNA expression, immunohistochemical localization (IHC) and concentration were investigated before (basal level = BL) and after 1, 4 and 8 weeks of oral treatment in normal rats treated with normal saline (NR‐NS), diabetic rats treated with normal saline (DR‐NS) and diabetic rats treated with GE (DR‐GE).ResultsCompared to NRNS, DR‐NS showed significant typical diabetic behaviors and biophysical symptoms including progressive increases in FBG and reductions in SI, in addition to reductions in pancreatic insulin m‐RNA expression, IHC and concentration. Conversely, and in comparison to DR‐NS, DR‐GE showed significant amelioration of diabetic behaviors and biophysical symptoms, including progressive decreases in FBG and increases in SI, in addition to timely‐progressive increases in pancreatic insulin m‐RNA expression, IHC labeling and concentration. The remaining investigated tissues did not show any advent changes in insulin m‐RNA and IHC in response to GE treatment.ConclusionGarlic's short‐term treatment induced hyperinsulinemia observed in the early STZ‐DM type‐1 rat model may result from augmented pancreatic insulinogenesis.Support or Funding InformationResearch Sector ‐ Kuwait University (SL04/14)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Lin28a Regulates Pathological Cardiac Hypertrophic Growth through Pck2‐mediated Enhancement of Anabolic Synthesis
Authors: Ma Hong , Yu Shuo , Liu Xiaojing , Zhang Yingao , Fakadej Thomas , Liu Ziqing , Yin Chaoying , Shen Weining , Locasale Jason W , Taylor Joan M , Qian Li , Liu Jiandong 
Published: June 2021

During pathological hypertrophy, the heart undergoes extensive metabolic changes prior to the onset of structural remodeling, yet, it remains largely unexplored whether and how this metabolic remodeling could contribute to cardiac hypertrophic growth. Here, we identified the RNA‐binding protein Lin28a as a critical regulator of pathological cardiac hypertrophy and metabolic re‐patterning. Cardiac‐specific deletion of Lin28a attenuated pressure overload‐induced hypertrophic growth, cardiac dysfunction and alterations in cardiac transcriptome. Mechanistically, Lin28a directly bound to mitochondrial phosphoenolpyruvate carboxykinase 2 (Pck2) mRNA and positively modulated its level. Manipulation of Pck2 expression phenocopied hypertrophic growth phenotypes of manipulating Lin28a expression. Epistatic analysis demonstrated that Pck2 mediated, at least in part, the role of Lin28a in cardiac hypertrophic growth. Furthermore, metabolomic analyses highlighted role for Lin28a and Pck2 in promoting cardiac anabolic biosynthesis required for cell growth. Thus, our study revealed a critical role of Lin28a in the regulation of pathological cardiac hypertrophic growth through Pck2‐mediated regulation of cardiac metabolism.Support or Funding InformationThis study was supported by AHA 13SDG17060010, Ellison Medical Foundation (EMF) AGNS‐13 1064‐, and NIH/NHLBI R01HL128331 to L.Q., NIH/NHLBI R00 HL109079, R56HL133081, and American Heart Association (AHA) 15GRNT25530005 to J.L.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Cyclic stretching establishes cardiac model expressing ANF and β‐MHC that responds to anti‐oxidizing drug
Authors: Wong Tzyy‐Yue , Tseng Yu‐Kai , Jhong Rong‐Chang , Lee Wen‐Hsien , Cheng Pei‐Wen 
Published: June 2021

The road to drug discovery for heart‐related diseases is challenged by advancement in whole‐heart and reliable animal heart models. In vitro model is a solution to replacing the unpredictable in vivo heart models. However, the techniques are time‐ and cost‐consuming. Cardiomyocyte cell line that expands in culture can be trained by mechanical stimulation to express cardiac biomarkers. The use of mechanical stimulation such as cyclic stretching can be more predictable, reliable in terms of cardiac marker expressions. The heart is an organ that is in constant dynamic which requires regulation for reactive oxygen species (ROS) to prevent pathological process. Here, we used cyclic stretching to stimulate cardiomyocytes with mild (5%), and aggressive (25%) strains at 1Hz. The stimulated cardiomyocytes expressed the cardiac characteristic markers Atrial natriuretic factor (ANF), and β‐myosin heavy chain (β‐MHC) after 24h of stretching. The 3H‐1,2‐dithiole‐3‐thione (D3T) has been reported to be a potent inducer of antioxidant genes through activation of the transcription factor Nrf2, and Nrf2 has been reported to play a role in cardiac remodeling.In this study, we investigated the effect of the D3T on the cardiomyocytes stimulated at mild, or aggressive strain. Results show that the aggressive strain reduced the β‐MHC expression, and the D3T enhanced the β‐MHC expression in cardiomyocytes that were stimulated with aggressive strain.Support or Funding InformationThis research is supported by VGHKS107‐076, VGHKS107‐168, VGHKS107‐175, MOST104‐2320‐B‐0751B‐003‐MY3, and MOST106‐2320‐B‐075B‐001.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Plakophilin‐dependent Dsg3 oligomerization and binding properties are involved in desmosomal hyper‐adhesion
Authors: Fuchs Michael Tobias , Foresti Marco , Vielmuth Franzsika , Waschke Jens 
Published: June 2021

Under mechanical stress, intercellular adhesion of keratinocytes is critically dependent on desmosomes which, during maturation, acquire a hyper‐adhesive state – at which desmosomal cadherins become independent from Calcium (Ca2+). The desmosomal plaque proteins plakophilins (Pkps) are known to be involved in desmosomal turnover and hyper‐adhesion. However, the molecular mechanism underlying is not elucidated yet. Thus, we here used atomic force microscopy (AFM) in combination with biochemical approaches in murine keratinocytes lacking either Pkp1 or Pkp3 to dissect the underlying mechanism by which Pkps regulate desmosomal cadherin binding properties and desmosomal hyper‐adhesion. Intercellular adhesion was impaired in Pkp3‐ and more severe in Pkp1‐deficient keratinocytes as revealed by keratinocytes dissociation assay. In accordance, Pkps regulated the single molecule binding properties of desmoglein 3 in a manner that Pkp loss led to decreased binding frequency and strength. This was further accompanied by compromised oligomerization of Dsg3. Furthermore, loss of Pkp1 but not Pkp3 causes increased lateral mobility and impaired cluster size of Dsg3. Thus, we questioned whether Pkp‐dependent changes in Dsg clustering and mobility participate in development of a hyper‐adhesive state in those keratinocytes. Interestingly, in keratinocyte dissociation assays wt keratinocytes become partly hyper‐adhesive after 72h whereas Pkp‐loss abolished the development of Ca2+‐independency. Further, Pkp1‐deficiency reduced development of Ca2+‐independent Dsg3 oligomers on the contrary to wt and Pkp3 k.o. keratinocytes. Furthermore, in wt but not in Pkp‐deficient keratinocytes, Dsg3 single molecule binding strength was increased in wt keratinocytes when cells where hyper‐adhesive. Whereas this increase was missing in Pkp‐deficient keratinocytes, which could serve as a molecular explanation for their failure to reach a proper hyper‐adhesive state. In summary, the data provided show that Pkp‐dependent changes in Dsg3 oligomerization as well as binding properties provide a new concept of the molecular mechanism of hyper‐adhesion.Support or Funding InformationElse‐Kröner‐Fresenius‐Stiftung 2016_AW157DFG SPP1782This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Synonymous Changes in Specific Leucine Codons Impact Morbilliviral Protein Production from Human & Canine Codon Optimized Constructs
Authors: Uhl Elizabeth W , Osborn Michelle L , Michel Frank , Jelesijevic Tomislav , Hogan Robert J 
Published: June 2021

Protein expression is increased by optimization of human measles virus (HMV) & canine distemper virus (CDV) nucleoprotein (N) gene to human or canine codon usage bias (CUB) and decreased by suboptimization. Six leucine codons were all replaced by CTG in human CUB optimized N gene constructs and by CTG & CTC in canine CUB optimized N gene constructs. For CUB suboptimized N gene constructs only CTT coded for leucine. The purpose of this experiment was to determine the effects of synonymous leucine codon changes. Protein expression from human & canine CUB optimized constructs in which CTG was replaced with CTT was compared using flow cytometry to that from WT, human & canine CUB optimized versions. Protein expression from CUB suboptimized versions with CTT changed to CTG was also compared to that from unmodified constructs. Human & canine CUB optimized CTT versions of the HMV N gene had significantly decreased protein production, with expression from the CTT canine CUB optimized construct the most suppressed. Replacing CTG with CTT in the human optimized CDV N gene constructs decreased the level of protein expression, while changing CTG to CTT in the canine optimized CDV N gene construct did not significantly change the level of protein expression. Protein expression from the CTT modified suboptimized CDV N gene construct was significantly increased compared to that from the unmodified suboptimized version. These results indicate that synonymous changes in specific leucine codons can significantly impact morbilliviral protein production in ways that vary with the virus and the context in which they occur.Support or Funding InformationThe project depicted was sponsored by the Department of Defense Threat Reduction Agency. The content of the information does not necessarily reflect the position or the policy of the federal government, and no official endorsement should be inferredThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Pathogenicity of Mycoplasma hyopneumoniae strain in Naturally Infected Slaughtered Pigs in Nigeria: Immunohistochemical and Ultrastructural Studies
Authors: Olaniyi Moshood , Omotainse Samuel , Ajayi Lawrence , Ojo O , Brown Corrie , Shields John , Ard Mary , Nagy Tamas , Alaka O 
Published: June 2021

Enzootic pneumonia caused by Mycoplasma hyopneumoniae (MHYO) remains a serious concern to swine industry in many countries including Nigeria. MHYO strains isolated from different countries and geographical locations are known to vary in pathogenicity in pigs. There is paucity of information on the pathogenicity of MHYO strain affecting pigs in Nigeria. This study investigated the pathogenicity of MHYO strain in naturally infected slaughtered pigs in Nigeria using immunohistochemistry and electron microscopy. Two hundred and sixty four lungs were randomly collected from abattoirs at Abeokuta, Ibadan and Lagos, Southwest Nigeria. A sub‐sample of 104 pneumonic lungs was selected, processed for routine histopathological examination and immunohistochemistry, while 3 lung tissues were selected for ultrastructural studies. The most significant microscopic changes were suppurative broncho‐interstitial pneumonia associated with varying degrees of lymphoid hyperplasia of the bronchus‐associated lymphoid tissue (BALT) and thickening of alveolar septa due to cellular infiltration. Immunohistochemically, MHYO antigens were detected in 86/104 (82.7%) lungs. Bronchial and bronchiolar epithelial cells typically exhibited a granular brown reaction on the surface, in the BALT and luminal cellular exudates of MHYO‐infected lung tissues. Transmission electron microscopy revealed numerous Mycoplasmas in the lumina of respiratory tract, in between degenerated cilia, while a few Mycoplasmas were located within the alveoli. It is concluded that the MHYO strain detected in this study is pathogenic to pigs and capable of inducing pneumonic lesions, and therefore implicated in the pathogenesis. This is the first investigative study on pathogenicity of MYHO strain in slaughtered pigs in Nigeria.Support or Funding InformationSupport from the Federal University of Agriculture, AbeokutaThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Dietary Sugars and bacteria interactions affect cariogenic properties of cavity‐causing bacteria
Authors: Wu Janina , Yang Chan 
Published: June 2021

Cavity is becoming more prevalent in our society. One major contributor is the modern diet, specifically the large amounts of sugars in diet. Another key factor is bacteria in our mouth that eat these sugars. Streptococcus mutans is one of the leading bacteria that initiate and promote cavity. They metabolize sugars to build up plaque over time and simultaneously produce acid that erodes tooth surface and causes cavity. We were interested in studying how different sugars interact with S. mutans: how different sugars influence pH changes and affect S. mutans colonization, which would help us recognize what sugar is beneficial or harmful to your teeth.We used a fruit fly model because fruit flies like sugars and mixing S. mutans with sugars can facilitate S. mutans colonize fruit flies. To make sugary food I mixed 8 different sugar solutions with S. mutans (labeled with green fluorescent protein) and soaked them to small filters. Then we grew fruit flies and separated them into 8 different tubes that were prepared with the sugar‐bacteria soaked filters on top. We then waited for 6 days to let flies eat the food and grow at room temperature. After the incubation, we took 1–2 flies every 2 days and frozen them to image the green color under Fluorescent Microscope, which indicates S. mutans colonization. On the final day, we harvested all of the remaining flies, ground them up, made different solutions, and then streaked various dilutions onto agar plates and incubated them for 2 days to count bacterial colonies, which represents bacterial colonization of flies. Flies fed with five sugars including sucrose showed bacterial colonization by direct imaging and calculating bacterial colony forming units. Flies fed with sucrose exhibited the best colonization, while flies fed with xylitol did not show any colonization. Overall the data indicated that S. mutans utilizes some dietary sugars more efficiently and as a result, can colonize more by eating some sugar than others.To evaluate the effects of different sugars on the pH of S. mutans cultured in bacterial medium Todd Hewitt Broth, with pH adjusted to 7.5, we added various sugars to the medium and incubated for 30 minutes to monitor the pH changes using a pH meter. With all 8 sugars, the pH dropped significantly after five minutes. The pH did not drop below 4.5 with 6 sugars. But the pH dropped even below 4.5 with two sugars, glucose and sucrose. The pH dropped at an average of 2.91 during the 30 minutes testing period, suggesting sugars and bacteria fuel acid production. These studies reveal different sugars ate by S. mutans can produce different amounts of acid that drives the pH drop of S. mutant culture media, thus interactions between bacteria and sugars are important for the development of cavity.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.