Zachariah G Schonberger, Sophie J Y Huang, Radhika N Thakkar, Amar A Mamone, Daniyal I Khan, Natalie L Y Chow, Moeiz Ahmed, Namashi Sivaram, Yuki Bao, Vihirthan Kesavan, Jordan Côté, Clara Sun, Jashnoor Chhina, Brayden D Halvorson, Gabrielle H Alimorad, Nithin J Menon, Daniel Goldman, Stephanie J Frisbee
{"title":"Assessments of Perfusion, Blood Flow, and Vascular Structure in Ambulatory Subjects: Guidance for Translational Research Scientists.","authors":"Zachariah G Schonberger, Sophie J Y Huang, Radhika N Thakkar, Amar A Mamone, Daniyal I Khan, Natalie L Y Chow, Moeiz Ahmed, Namashi Sivaram, Yuki Bao, Vihirthan Kesavan, Jordan Côté, Clara Sun, Jashnoor Chhina, Brayden D Halvorson, Gabrielle H Alimorad, Nithin J Menon, Daniel Goldman, Stephanie J Frisbee","doi":"10.1159/000527765","DOIUrl":"https://doi.org/10.1159/000527765","url":null,"abstract":"<p><p>Research involving human subjects in ambulatory settings is a critical link in the chain comprising translational research, spanning preclinical research to human subject and patient cohort studies. There are presently a wide array of techniques and approaches available to investigators wishing to study blood flow, perfusion, and vascular structure and function in human subjects. In this multi-sectioned review, we discuss capillaroscopy, carotid intima-media thickness, flow-mediated dilation, laser Doppler flowmetry, near-infrared spectroscopy, peripheral arterial tonometry, pulse wave velocity, retinal fundus imaging, and vascular plethysmography. Each section contains a general overview and the physical basis of the technique followed by a discussion of the procedures involved and the necessary equipment, with attention paid to specific requirements or limitations. Subsequently, we detail which aspects of vascular function can be studied with a given technique, the analytical approach to the collected data, and the appropriate application and limitation(s) to the interpretation of the data collected. Finally, a modified scoping review provides a summary of how each assessment technique has been applied in previous studies. It is anticipated that this review will provide an efficient source of information and insight for preclinical investigators seeking to add translational aspects to their research programs.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"60 1","pages":"12-68"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9233588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"What Is Next for Connexin and Pannexin?","authors":"Timothy M Sveeggen, Anna Kosmach, Pooneh Bagher","doi":"10.1159/000533281","DOIUrl":"10.1159/000533281","url":null,"abstract":"Signaling across membranes is vital for tissue and organ function throughout the body. This is achieved through careful regulation of transmembrane channels allowing for passage of ions and second messengers to and from the cytosol and intracellular compartments, which can generate electrical impulses and trigger signaling cascades. Connexins and pannexins are among the most versatile transmembrane channel proteins, which shape cell behavior and tissue function with extraordinary finesse. In this volume, pannexins and connexins 37, 40, and 43 are reviewed [1–4], with special consideration for tissue specificity of expression, cell type-specific functions, and their roles in development and disease.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"60 2","pages":"69-72"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10570909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10149218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chun-Kai Hsu, Shang-Jen Chang, Li-Yi Lim, Hsi-Hsien Chang, Stephen Shei-Dei Yang
{"title":"Methyl Palmitate Modulated NMDA-Induced Cerebral Hyperemia in Hypertensive Rats.","authors":"Chun-Kai Hsu, Shang-Jen Chang, Li-Yi Lim, Hsi-Hsien Chang, Stephen Shei-Dei Yang","doi":"10.1159/000529916","DOIUrl":"10.1159/000529916","url":null,"abstract":"<p><p>N-methyl-D-aspartate (NMDA) receptors were found to be dysfunctional in hypertensive rats. Methyl palmitate (MP) has been shown to diminish the nicotine-induced increase in blood flow in the brainstem. The aim of this study was to determine how MP modulated NMDA-induced increased regional cerebral blood flow (rCBF) in normotensive (WKY), spontaneously hypertensive (SHR), and renovascular hypertensive (RHR) rats. The increase in rCBF after the topical application of experimental drugs was measured using laser Doppler flowmetry. Topical NMDA application induced an MK-801-sensitive increase in rCBF in anesthetized WKY rats, which was inhibited by MP pretreatments. This inhibition was prevented by pretreatment with chelerythrine (a PKC inhibitor). The NMDA-induced increase in rCBF was also inhibited by the PKC activator in a concentration-dependent manner. Neither MP nor MK-801 affected the increase in rCBF induced by the topical application of acetylcholine or sodium nitroprusside. Topical application of MP to the parietal cortex of SHRs, on the other hand, increased basal rCBF slightly but significantly. MP enhanced the NMDA-induced increase in rCBF in SHRs and RHRs. These results suggested that MP had a dual effect on the modulation of rCBF. MP appears to play a significant physiological role in CBF regulation.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"137-147"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9583634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Potential Implications of Exercise Training on Pannexin Expression and Function.","authors":"Brent Wakefield, Silvia Penuela","doi":"10.1159/000527240","DOIUrl":"10.1159/000527240","url":null,"abstract":"<p><p>Pannexins (PANX1, 2, 3) are channel-forming glycoproteins that are expressed throughout the cardiovascular and musculoskeletal system. The canonical function of these proteins is to release nucleotides that act as purinergic signalling at the cell membrane or Ca2+ channels at the endoplasmic reticulum membrane. These two forms of signalling are essential for autocrine and paracrine signalling in health, and alterations in this signalling have been implicated in the pathogenesis of many diseases. Many musculoskeletal and cardiovascular diseases are largely the result of a lack of physical activity which causes altered gene expression. Considering exercise training has been shown to alter a wide array of gene expression in musculoskeletal tissues, understanding the interaction between exercise training, gene function and expression in relevant diseases is warranted. With regards to pannexins, multiple publications have shown that exercise training can influence pannexin expression and may influence the significance of its function in certain diseases. This review further discusses the potential interaction between exercise training and pannexin biology in relevant tissues and disease models. We propose that exercise training in relevant animal and human models will provide a more comprehensive understanding of the implications of pannexin biology in disease.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"60 2","pages":"114-124"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10138452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Melissa R Dennis, Paulo W Pires, Christopher T Banek
{"title":"Vascular Dysfunction in Polycystic Kidney Disease: A Mini-Review.","authors":"Melissa R Dennis, Paulo W Pires, Christopher T Banek","doi":"10.1159/000531647","DOIUrl":"10.1159/000531647","url":null,"abstract":"<p><p>Polycystic kidney disease (PKD) is one of the most common hereditary kidney diseases, which is characterized by progressive cyst growth and secondary hypertension. In addition to cystogenesis and renal abnormalities, patients with PKD can develop vascular abnormalities and cardiovascular complications. Progressive cyst growth substantially alters renal structure and culminates into end-stage renal disease. There remains no cure beyond renal transplantation, and treatment options remain largely limited to chronic renal replacement therapy. In addition to end-stage renal disease, patients with PKD also present with hypertension and cardiovascular disease, yet the timing and interactions between the cardiovascular and renal effects of PKD progression are understudied. Here, we review the vascular dysfunction found in clinical and preclinical models of PKD, including the clinical manifestations and relationship to hypertension, stroke, and related cardiovascular diseases. Finally, our discussion also highlights the critical questions and emerging areas in vascular research in PKD.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"125-136"},"PeriodicalIF":1.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10947982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9936445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"European Society for Microcirculation Conference 2023.","authors":"","doi":"10.1159/000533846","DOIUrl":"https://doi.org/10.1159/000533846","url":null,"abstract":"","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"60 Suppl 1 ","pages":"1-63"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71483036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Raúl Devia Rodriguez, Eline Huizing, Çağdaş Ünlü, Frank F J Simonis, Reinoud P H Bokkers, Jean-Paul P M de Vries, Richte C L Schuurmann, Dalibor Nakladal, Hendrik Buikema, Jan-Luuk Hillebrands, Henri G D Leuvenink
{"title":"Validation of an ex vivo Flow Model Including Magnetic Resonance Imaging to Study the Effects of Endovascular Treatments on the Arterial Wall.","authors":"Raúl Devia Rodriguez, Eline Huizing, Çağdaş Ünlü, Frank F J Simonis, Reinoud P H Bokkers, Jean-Paul P M de Vries, Richte C L Schuurmann, Dalibor Nakladal, Hendrik Buikema, Jan-Luuk Hillebrands, Henri G D Leuvenink","doi":"10.1159/000529115","DOIUrl":"https://doi.org/10.1159/000529115","url":null,"abstract":"<p><p>Endovascular revascularization is the preferred treatment for peripheral arterial disease. Restenosis often occurs as a response to procedure-induced arterial damage. Reducing vascular injury during endovascular revascularization may improve its success rate. This study developed and validated an ex vivo flow model using porcine iliac arteries, obtained from a local abattoir. Twenty arteries (of 10 pigs) were equally allocated to two groups: a mock-treated control group and an endovascular intervention group. Arteries of both groups were perfused with porcine blood for 9 min, including 3 min of balloon angioplasty in the intervention group. Vessel injury was assessed by calculating the presence of endothelial cell denudation, vasomotor function, and histopathological analysis. MR imaging displayed balloon positioning and inflation. Endothelial cell staining showed 76% of denudation after ballooning compared to 6% in the control group (p < 0.001). This was confirmed by histopathological analysis, showing a significantly reduced endothelial nuclei count after ballooning compared to the controls (median: 22 vs. 37 nuclei/mm, p = 0.022). In the intervention group, vasoconstriction and endothelium-dependent relaxation were significantly reduced (p < 0.05).We present an ex vivo flow model to test the effects of endovascular therapy on the vessel's wall morphology, endothelial denudation, and endothelial-dependent vasomotor function under physiological conditions. Additionally, it allows the future testing of human arterial tissue.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"60 1","pages":"1-11"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9287238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Isolation and Cultivation of Vascular Smooth Muscle Cells from the Mouse Circle of Willis.","authors":"Wei Chang, Yajuan Li, Fengzhou Liu, Kehai Zang, Peiran Zhang, Shuai Qu, Jingyu Zhao, Junhui Xue","doi":"10.1159/000532033","DOIUrl":"10.1159/000532033","url":null,"abstract":"<p><strong>Introduction: </strong>Culturing cerebrovascular smooth muscle cells (CVSMCs) in vitro can provide a model for studying many cerebrovascular diseases. This study describes a convenient and efficient method to obtain mouse CVSMCs by enzyme digestion.</p><p><strong>Methods: </strong>Mouse circle of Willis was isolated, digested, and cultured with platelet-derived growth factor-BB (PDGF-BB) to promote CVSMC growth, and CVSMCs were identified by morphology, immunofluorescence analysis, and flow cytometry. The effect of PDGF-BB on vascular smooth muscle cell (VSMC) proliferation was evaluated by cell counting kit (CCK)-8 assay, morphological observations, Western blotting, and flow cytometry.</p><p><strong>Results: </strong>CVSMCs cultured in a PDGF-BB-free culture medium had a typical peak-to-valley growth pattern after approximately 14 days. Immunofluorescence staining and flow cytometry detected strong positive expression of the cell type-specific markers alpha-smooth muscle actin (α-SMA), smooth muscle myosin heavy chain 11 (SMMHC), smooth muscle protein 22 (SM22), calponin, and desmin. In the CCK-8 assay and Western blotting, cells incubated with PDGF-BB had significantly enhanced proliferation compared to those without PDGF-BB.</p><p><strong>Conclusion: </strong>We obtained highly purified VSMCs from the mouse circle of Willis using simple methods, providing experimental materials for studying the pathogenesis and treatment of neurovascular diseases in vitro. Moreover, the experimental efficiency improved with PDGF-BB, shortening the cell cultivation period.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"234-244"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614493/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10109932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A Preliminary Discussion on the Safety of Mild Therapeutic Hypothermia in Target Vessels after Endovascular Intervention in Acute Large Vessel Occlusion Cerebral Infarction.","authors":"Jiang Li, Shaonian Tang, Juanli Liu, Wenlin He, Jinjin Yan, Zhiyong Huang, Xuesong Li","doi":"10.1159/000532030","DOIUrl":"10.1159/000532030","url":null,"abstract":"<p><strong>Introduction: </strong>The aim of this study was to discuss the safety of rapid administration of 4°C hypothermic normal saline into the occluded vessels using an intra-arterial catheter to induce mild hypothermia following endovascular thrombectomy in patients with acute large vessel occlusion cerebral infarction.</p><p><strong>Methods: </strong>We selected 78 patients with acute large vessel occlusion cerebral infarction who underwent endovascular thrombectomy in the Department of Neurology of our hospital from January 2020 to July 2022 and achieved TICI 2b recanalization.</p><p><strong>Result: </strong>Twenty-five patients were administered 500 mL of 4°C hypothermic normal saline in the occluded vessels at a rate of 25 mL/min to induce mild hypothermia. Twenty pairs of subjects conformed to strict matching and were finally included in the statistical analysis. The two groups of patients differed significantly in white blood cell count and percentage of neutrophils (p < 0.05); however, there were no significant differences in D-dimer, procalcitonin, and BNP levels. The two groups of patients did not differ significantly with respect to the incidence of the following indicators: upper gastrointestinal bleeding; pulmonary infection; venous thrombosis; vasospasms; seizures; and chills (p > 0.05).</p><p><strong>Conclusion: </strong>Mild therapeutic hypothermia in target vessels plus endovascular thrombectomy was shown to be safe in patients with acute large vessel occlusion cerebral infarction.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"227-233"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10110364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cx43 Facilitates Mesenchymal Transition of Endothelial Cells Induced by Shear Stress.","authors":"En Zhou, Jing Zhou, Changlong Bi, Zongqi Zhang","doi":"10.1159/000533320","DOIUrl":"10.1159/000533320","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to determine the function of Cx43 in the endothelial-to-mesenchymal transition (EndMT) process of endothelial cells (ECs) and to explore the potential signaling pathways underlying these functions.</p><p><strong>Methods: </strong>ECs were extracted from rat aorta. ECs were transfected with Cx43 cDNA and Cx43 siRNA and then exposed to 5 or 12 dyne/cm2. Immunofluorescence staining was used to detect the expression of SM22α, Cx43, and acetylated α-tubulin in ECs. Western blotting was used to detect the protein expression of α-SMA, CD31, Cx43, H1-calponin, Ift88, and p-smad3 in ECs.</p><p><strong>Results: </strong>The expression of αSMA, SM22α, and Cx43 was significantly increased, and CD31 was markedly decreased in ECs treated with laminar shear stress at 5 dyn/cm2. The Cx43 cDNA transfection could induce the expression of SM22α or H1-calponin and attenuate CD31 expression in ECs. Also, Cx43 overexpression harms cilia formation in ECs exposed to 5 dyn/cm2, accompanied with the regulated Ift88 and smad signaling.</p><p><strong>Conclusions: </strong>This study found that laminar shear stress at 5 dyn/cm2 would increase the expression of Cx43 to facilitate the EndMT process of ECs, associated with morphological changes in primary cilia and the decreased expression of Ift88 in ECs.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"204-212"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10226346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}