bluuebunny/crossref_metadata_2025_split huggingface dataset:
Epiligulyl oxide from Saussurea lappa inhibited allergic asthma using in vivo and in vitro experiments
Authors: Huang Jin , Lee Bo‐Kyung , Park Soo‐Jin , Kang Saeromi , Im Dong‐Soon 
Published: June 2021

BackgroundThe root of Saussurea lappa is used in Asian traditional medicine to treat asthma, rheumatism, and other conditions. Extracts of Saussurea lappa were reported to alleviate house dust mite‐induced atopic‐like dermatitis in Nc/Nga mice, and sesquiterpene lactones were isolated. To elucidate whether epiligulyl oxide, a sesquiterpene lactone has beneficial effects on allergic asthma, anti‐asthma effects were studied using female Balb/c mice and rat RBL‐2H3 mast cellsMETHODSAntigen‐induced degranulation was measured in vitro by measuring β‐hexosaminidase activity. A murine ovalbumin‐induced allergic asthma model was used to test the in vivo efficacy of epiligulyl oxide.RESULTSAntigen‐induced degranulation was inhibited by epiligulyl oxide. Potency Sensitization and challenge of ovalbumin induced allergic asthma responses. Administration of epiligulyl oxide decreased numbers of inflammatory cells, especially eosinophils, and reduced the expression and secretion of Th2 cytokines, including IL‐4 and IL‐13, in lung tissues and bronchoalveolar lavage fluid. Histologic studies showed administration of epiligulyl oxide reduced inflammatory signs and mucin production in lungs.CONCLUSIONThese findings provide evidence that the epiligulyl oxide has potential use as anti‐asthma therapeutics.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The comparative study of anti‐oxidative and anti‐melanogenic effects by Angelica tenuissima extract and its biotransformed
Authors: Sohn Eunsoo , Park Yuna , Lee Jin Woo , Lim Hyosun , Kim Youn Kyu , Koo Hyun Jung , Namkoong Seung , Jang Seon‐A , Sohn Eun‐Hwa 
Published: June 2021

Angelica tenuissimae Nakai (Umbelliferae) has been used as a traditional medicine in Asia because of its various pharmaceutical efficacies. Fermentation produces different compounds from the original one and is secondary trial to augment the contents or compositions of beneficial components. Here, we retrieved 56 articles regarding to A. tenuissima from the SCOPUS database and analyzed recent R&D status and the biological activities of principal ingredients by bibliometric methods, and then investigated the anti‐oxidative and anti‐melanogenic activities of A. tenuissimae ethanol extract (ATE) and fermented ATE (FATE). HPLC was used to evaluate changes in the levels of biogenic amines in ATE and FATE. Depigmenting effects of ATE and FATE were also examined with B16F10 melanocytes. As a result, FATE had no cytotoxicity until 2000 ug/ml, and was superior to ATE in regulating melanin production and tyrosinase activity in α‐MSH‐stimulated B16F10 cells in dose‐dependent manners. Both of ATE and FATE showed a similar degree of anti‐oxidant activities. Therefore, our results suggest that FATE could be used as an ingredient in cosmeceutical agent with whitening and anti‐oxidative effects.Support or Funding InformationThis research was supported by the Ministry of Trade, Industry and Energy (MOTIE), Korea Institute for Advancement of Technology (KIAT) through the Encouragement Program for The Industries of Economic Cooperation Region, and Korea Institute of Science and Technology Information (KISTI).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Troponin Subunits are Expressed in the Rat Afferent Arteriole
Authors: Walsh Michael Patrick , Kathol Iris , Sutherland Cindy , Wang Xuemei , Loutzenhiser Rodger , Takeya Kosuke 
Published: June 2021

Vascular smooth muscle cells of the renal afferent arteriole are unusual: they must be able to contract very rapidly in response to a sudden increase in systemic blood pressure, thereby protecting the downstream glomerular capillaries from catastrophic damage. We showed that this could be accounted for in part by exclusive expression, at the protein level, of the “fast” (B) isoforms of smooth muscle myosin II heavy chains in the afferent arteriole, in contrast to other vascular smooth muscle cells such as the rat aorta and efferent arteriole, which express exclusively the “slow” (A) isoforms (Shiraishi M et al (2003) FASEB J 17: 2284–2286). Since contraction of the more rapidly‐contracting striated (skeletal and cardiac) muscles is regulated by the thin filament‐associated troponin (Tn) system, we hypothesized that Tn or a Tn‐like system may exist in afferent arteriolar cells and contribute to the unusually rapid contraction of this tissue in response to increased intraluminal pressure. We examined the expression of TnC (Ca2+‐binding subunit), TnI (inhibitory subunit) and TnT (tropomyosin‐binding subunit) in vascular smooth muscle cells of the rat renal afferent arteriole at the mRNA level. Fast skeletal muscle and slow skeletal muscle/cardiac TnC isoforms and slow skeletal muscle and cardiac TnI isoforms were detected by RT‐PCR and confirmed by cDNA sequencing. Furthermore, cardiac and slow skeletal muscle TnI isoforms, but not fast skeletal muscle TnI were detected in isolated afferent arterioles at the protein level by proximity ligation assay. We conclude that, in addition to Ca2+‐mediated phosphorylation of myosin regulatory light chains, contraction of the afferent arteriole may be regulated by a mechanism normally associated with the much more rapidly contracting cardiac and skeletal muscles, which involves Ca2+ binding to TnC, leading to alleviation of inhibition of the actomyosin MgATPase by TnI and tropomyosin and rapid contraction of the vessel.Support or Funding InformationSupported by the Canadian Institutes of Health ResearchThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Novel non‐canonical regulation of soluble VEGF/VEGFR2 signaling by mechanosensitive ion channel TRPV4 in endothelial cells
Authors: Kanugula Anantha Koteswararao , Adapala Ravi K. , Midha Priya , Cappelli Holly C. , Meszaros Gary j. , Paruchuri Sailaja , Chilian William M. , Thodeti Charles K. 
Published: June 2021

VEGF and VEGFR2 signaling is the major regulator of endothelial functions such as proliferation, migration, and angiogenesis. While many studies on the modulation of angiogenesis focus on targeting VEGF signaling, mechanical forces also play critical role. We have recently shown that the mechanosensitive ion channel transient receptor potential vanilloid 4 (TRPV4) negatively regulates angiogenesis via modulation of Rho/Rho kinase‐dependent endothelial mechanosensing. Nevertheless, it is not known if a cross‐talk exists between TRPV4 and VEGF signaling. To explore this nexus, we silenced TRPV4 in endothelial cells (EC) and measured VEGFR2 expression, localization, and phosphorylation. Immunofluorescence analysis revealed significant localization of total‐VEGFR2 around the perinuclear (Golgi) compartment in control EC. Small interfering RNA (siRNA) knockdown of TRPV4 significantly decreased perinuclear localization of VEGFR2. Interestingly, we found increased phosphorylation of VEGFR2 at Y1175 and its localization to the plasma membrane in TRPV4 knocked‐down cells. We also found increased plasma membrane localization of phospho‐VEGFR2 Y1175 in TRPV4 null EC. Western blot analysis further revealed a significant increase in phospho‐VEGFR2 at Y1175 in whole cell lysates and membrane fractions of TRPV4 knocked‐down cells compared to control siRNA‐treated cells. Finally, TRPV4 deletion/knockdown also increased VEGF‐mediated migration with localization of phospho‐VEGFR2 at the leading edge of migrating EC. Taken together, our results suggest that TRPV4 channels regulate VEGFR2 localization and activation to identify novel cross‐talk between mechanical (TRPV4) and soluble (VEGF) signaling in EC.Support or Funding InformationThis work was supported by National Institutes of Health (NIH) R01HL119705 and National Cancer Institute (NCI) R15CA202847This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Microvascular Lattice: An Updated Paradigm of Flow Distribution Through Capillary Networks
Authors: Mendelson Asher , Ho Edward , Milkovich Stephanie , Goldman Daniel , Ellis Christopher 
Published: June 2021

BackgroundCapillaries, as the smallest vessels in the microcirculation, represent the most essential site for oxygen delivery; yet, given their overwhelming density and complicated geometry, understanding how they integrate within the broader microvascular network has been challenging.Classical microvascular flow modelling has used linear branching networks such that each capillary bundle (CB) corresponds to a unique arteriolar‐venular pair with one‐directional pathway of flow. However, it has long been observed in vivo that terminal arterioles supply multiple CBs and similarly, post‐capillary venules collect from multiple CBs. Such a network forms a lattice‐like structure with an alternating pattern of arterioles, CBs, and venules.ObjectiveWe aim to develop a mathematical model for the microvascular lattice that can be applied to study blood flow properties through capillary networks in skeletal muscle.Methods/ResultsMicrovascular lattice networks are generated from our own rodent intravital videomicroscopy data and compared to data reported in the literature. Distinct CBs are selected and their anatomical features are delineated with 3‐D reconstruction software. Capillary hemodynamics (RBC velocity, RBC supply rate, hematocrit) are extracted from video data and used to characterize the flow within and between multiple CBs. The generalized architecture of a microvascular lattice is then extrapolated from our experimental data and applied to a dual‐phase steady‐state blood flow model. Flow properties of the lattice are compared to those of a classical linear branching network ‐ both containing the same number of CBs.Conclusions/ImpactThe microvascular lattice represents an updated paradigm for describing blood flow through capillary networks. This lattice structure raises important questions regarding how flow can be regulated to support local oxygen demand and how larger microvessels interact with capillaries within the microcirculation. Furthermore, CB functional data for a variety of microvascular conditions can be inputted into this lattice model to determine how alterations to capillary architecture affect overall flow through the microvascular network.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Role of Myocardial Endothelin‐Converting Enzyme in Promoting Coronary Arteriolar Constriction during Diabetes
Authors: Tsai Shu‐Huai , Hein Travis W. , Kuo Lih 
Published: June 2021

Coronary blood flow is regulated, by adjusting the diameters of coronary arterioles, to meet the oxygen demand of the myocardium. The release of local metabolites by the myocardium upon metabolic activation can trigger nitric oxide (NO)‐dependent coronary arteriolar dilation. In diabetes, coronary blood flow regulation is compromised by impairing endothelium‐dependent NO‐mediated vasodilation. However, it is unclear whether the myocardium plays a role in altering coronary arteriolar constriction to endothelin‐1 (ET‐1), which has been shown to contribute to the development of diabetic cardiomyopathy. To address this issue, pig coronary arterioles were isolated with the surrounding myocardial tissue, cannulated and pressurized for functional study. The vasomotor function was analyzed using the videomicroscopic technique and compared with isolated arterioles without myocardium. Streptozocin‐injected pigs (2 wk of hyperglycemia; 524 ± 48 mg/dl; n = 7) or age‐matched control pigs (euglycemia; 91 ± 7 mg/dl; n = 7) were used to study the influence of myocardium on coronary vasomotor function under diabetes. Coronary arterioles with and without myocardial tissue from control pigs constricted to ET‐1 (0.1 nM) in a comparable manner. Without myocardium, incubating the arterioles with ET‐1 precursor big ET‐1 (0.1 μM) for 40 minutes caused a 32% constriction of the vessels. The vasoconstriction reached 53% in the presence of myocardial tissue. The enhanced big ET‐1‐induced vasoconstriction was inhibited 74% by ETA receptor antagonist BQ123, 24% by ETB receptor antagonist BQ788, and 87% by endothelin‐converting enzyme (ECE) inhibitor CGS35066. In diabetic pigs, coronary arteriolar constriction in response to big ET‐1 was enhanced by 26% compared with that from the euglycemic pigs, and the vasoconstriction was further increased in the presence of myocardial tissue. However, ET‐1‐induced coronary arteriolar constriction without surrounding myocardium was not altered by diabetes. The ECE1 protein expression was increased in the myocardium in diabetic pigs. In conclusion, myocardial ECE is capable of converting big ET‐1 to ET‐1 for coronary arteriolar constriction. Under diabetic condition, upregulated myocardial ECE1 expression appears to promote ET‐1 synthesis for coronary arteriolar constriction, and may contribute to coronary blood flow dysregulation and lead to insufficient blood supply to the heart.Support or Funding InformationSupported by Baylor Scott & White Kruse Chair Endowment Fund, and NIH Grants R01EY023335 and R01EY024624This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Cerebral Vascular KIR2.x Channels are Distinctly Regulated by Membrane Lipids and Hemodynamic Forces.
Authors: Sancho Maria , Welsh Donald G. 
Published: June 2021

This study examined membrane lipid (phosphatidylinositol‐bis‐phosphate (PIP2) and cholesterol) regulation of cerebral arterial KIR and whether these signaling molecules enable distinct channel pools to uniquely sense hemodynamic forces. Endothelial and smooth muscle cells were freshly isolated from rat cerebral arteries; patch‐clamp electrophysiology, Q‐PCR and immunohistochemistry delineated KIR channel activity and expression. Electrophysiology revealed a Ba2+‐sensitive KIR current in smooth muscle and endothelial cells, while Q‐PCR and immunohistochemistry confirmed KIR2.x mRNA and protein expression respectively. Each cellular pool of KIR channels was sensitive to particular membrane lipids and hemodynamic forces. Endothelial KIR responded dynamically to PIP2 manipulations, and laminar flow activated this channel pool in a PIP2 dependent manner. In contrast, smooth muscle KIR reacted to cholesterol perturbations, and pressure stimuli (e.g. hyposmotic challenge or negative pressure application) modulated this channel pool in a cholesterol dependent manner. The flow and pressure sensitivity of KIR channels was confirmed in intact cerebral arteries using vessel myography. In summary, while both vascular cell types express KIR2.x channels, each pool is distinctly regulated by membrane lipids and hemodynamic stimuli. This emerging picture of KIR regulation advances our mechanistic understanding of how hemodynamic forces interact to control arterial tone development.Support or Funding InformationThis research was supported by an operating grant from the Canadian Institute of Health Research. DG Welsh is Rorabeck Chair of Molecular Neuroscience and Vascular Biology at the University of Western Ontario.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effects of Heated versus Thermoneutral Bikram Yoga Interventions on Endothelial Function and Arterial Stiffness
Authors: Hunter Stacy D. , Laosiripisan Jitanan , Elmenshawy Ahmed , Tanaka Hirofumi 
Published: June 2021

Bikram (hot) yoga is a style of hatha yoga practiced at 40.5° C with 40–60% relative humidity. We have previously documented improvements in endothelium‐dependent vasodilation but not arterial stiffness in healthy, middle‐aged adults with an 8‐week Bikram yoga intervention. Currently, it is unknown whether the effect of hot yoga on endothelial function might be attributed to the hatha yoga asanas or the high temperature/humidity. It is also unknown whether a longer intervention might produce significant alterations in arterial stiffness.PURPOSEThe purpose of this investigation was to determine the effects of a 12‐week Bikram yoga intervention performed in standard heated conditions and in a thermoneutral environment on endothelium‐dependent vasodilation and arterial stiffness.METHODSFifty‐two sedentary but apparently healthy adults aged 40–60 years were randomly assigned to one of three groups: Bikram yoga practiced at 40.5°C (n=19); Bikram yoga practiced at 23°C (n=14); or sedentary time‐control (n=19). The 12‐week yoga intervention consisted of 3 weekly 90‐minute Bikram yoga classes. The time control group was instructed to maintain current lifestyle patterns for the study duration. Body composition was determined via dual energy x‐ray absorptiometry (DXA). Endothelium‐dependent vasodilation was measured noninvasively using brachial artery flow‐mediated dilation (FMD) after 5 minutes of blood flow occlusion. Arterial stiffness was measured via brachial‐ankle pulse wave velocity (PWV).RESULTSAge, anthropometric variables, plasma lipid, glucose, and triglyceride concentrations, brachial artery FMD and brachial‐ankle PWV were not different among the three groups at baseline. Body fat percentage declined (p<0.01) and total‐ (p=0.051) and LDL‐cholesterol (p =0.09) concentrations tended to decline only in the hot (40.5°C) yoga group. Brachial artery FMD increased (P<0.05) in both yoga groups but brachial‐ankle PWV was not significantly altered in any group. There were no changes in any outcome variables in the time control group.CONCLUSIONSBikram yoga practiced in hot/humid and thermoneutral conditions produced similar improvements in endothelium‐dependent vasodilation in healthy, middle‐aged adults. The addition of the heat led to reductions in body fat percentage. Bikram yoga does not appear to modulate arterial stiffness in middle‐aged adults.Support or Funding InformationThis study was funded by Pure Action, Inc. Austin, TX, USAThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Myoblasts enhance collateral capillary arteriogenesis during chronic ischemia
Authors: Hamzeinejad Vahid , Banuelos Leo , Cardinal Trevor Ryan 
Published: June 2021

Peripheral arterial occlusive disease (PAOD) involves peripheral artery occlusion, which causes ischemia (i.e. insufficient blood flow) and is the leading cause of amputation. Natural bypass vessels known as collaterals can preserve downstream tissue viability by creating an alternative route for blood flow. Increased blood flow through preexisting collateral increases shear stress and triggers arteriogenesis, the outward remodeling of arterial vessels. The presence of collaterals improves prognosis in patients with ischemic disease, but many patients never develop identifiable collaterals to relieve peripheral ischemia. Animal models that lack preexisting collaterals are capable of forming collaterals from capillaries that undergo arteriogenesis to become arterialized capillary collaterals (ACC). A treatment to induce the formation of ACCs, particularly in diseased or aged tissues that lack the propensity to form new collateral vessels, could be highly effective in giving protection against ischemia. Exercise is a great therapy for PAOD, since following exercise, resident muscle stem cells known as satellite cells (SCs) activate and regulate local angiogenesis. SCs and their progeny myoblasts secrete factors known to be involved in arteriogenesis (many of these compounds involved in angiogenesis are also involved in arteriogenesis) and the recruitment of other cells involved in remodeling. Therefore, transplanting these putative arteriogenic cells is a potential therapy to recapitulate some of the beneficial effects of exercise therapy. In this study, the lateral feed artery in the spinotrapezius muscle of Balb/C mice was ligated to induce chronic ischemia; myoblasts were transplanted during surgery to enhance arteriogenesis of collateral capillaries. Implanted mice exhibited increased arteriogenesis, ACC diameter increased to 28.11 ± 0.85 μm vs 16.25 ± 0.62 μm in a no transplant control. As corollary, we evaluated the process for cell construct preparation and discovered that cells cultured on scaffold overnight (20.86 ± 1.6 μm) before transplant did not stimulate arteriogenesis as significantly as those who were cultured for 6‐hours only. Limited nutrient supply and gas exchange while incubating on scaffolds could induce stress on myoblast and cause limited reactivity/apoptosis post implant. In summary, myoblast transplantation increases ACC arteriogenesis; however, they need to be transplanted as early as possible post‐harvest from culture flask.Support or Funding InformationFunding: CIRM ( California Institute for Regenerative Medicine)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Selectively Impaired Vasodilation of Human White Matter Penetrating Cerebral Arterioles in Microvascular Brain Injury and Alzheimer's disease
Authors: Bagi Zsolt , Brander Dieter D. , Le Phuong D. , McNeal David D. , Gong Xi D. , Dou Huijuan , Fulton David , Beller Allison , Ngyuen Thuan D. , Larson Eric , Montine Thomas , Keene Dirk , Back Stephen D. 
Published: June 2021

Microvascular brain injury (mVBI) is a common pathologic correlate of vascular contributions to cognitive impairment and dementia (VCID) that leads to white matter (WM) injury. VCID appears to arise from chronic recurrent WM ischemia. We hypothesized that in mVBI WM injury is specifically attributed to vasodilator dysfunction of WM penetrating arterioles. We analyzed 38 cases of mVBI with low and high Alzheimer's disease (AD) neuropathologic changes in prefrontal cortex WM from rapid autopsies in a population‐based cohort where VCID and AD frequently occur. Arteriolar vasodilator function was quantified by videomicroscopy. Acetylcholine‐mediated arteriolar dilation in mVBI with low AD pathology was significantly reduced in WM penetrators relative to pial arterioles. Astrogliosis‐defined WM injury was associated with impaired vasodilator function of WM penetrating arterioles. In mVBI with high AD pathology vasodilator function of WM penetrating arterioles was further diminished. Presence of moderate/frequent neuritic plaques and cerebral amyloid angiopathy were associated with impaired dilation in WM penetrating, but not in pial arterioles. In conclusion, we successfully assessed vasodilator function of human WM penetrating arterioles in postmortem rapid autopsy samples. We found that selectively impaired vasodilator function of WM penetrating arterioles in mVBI occurs in association with WM injury and AD neuropathologic change.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.