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[PMID]: 29388466
[Au] Autor:Suresh K; Servinsky L; Jiang H; Bigham Z; Yun X; Kliment C; Huetsch JC; Damarla M; Shimoda LA
[Ad] Address:Pulmonary / Critical Care, Johns Hopkins University, United States.
[Ti] Title:Reactive oxygen species induced Ca2+ influx via TRPV4 and microvascular endothelial dysfunction in the SU5416/Hypoxia model of pulmonary arterial hypertension.
[So] Source:Am J Physiol Lung Cell Mol Physiol;, 2018 Feb 01.
[Is] ISSN:1522-1504
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pulmonary arterial hypertension (PAH) is a lethal disease characterized by elevations in pulmonary arterial pressure, in part due to formation of occlusive lesions in the distal arterioles of the lung. These complex lesions may comprise multiple cell types, including endothelial cells (ECs). To better understand the molecular mechanisms underlying EC dysfunction in PAH, lung microvascular endothelial cells (MVECs) were isolated from normoxic rats (N-MVEC) and rats subjected to SU5416 plus hypoxia (SuHx), an experimental model of PAH. Compared to N-MVEC, MVEC isolated from SuHx rats (SuHx-MVEC) appeared larger and more spindle-shaped morphologically, and expressed canonical smooth muscle cell markers smooth muscle-specific -actin (SMA) and myosin heavy chain (MHC) in addition to endothelial markers such as Griffonia simplicifolia and von willebrand factor (VWF). SuHx-MVEC mitochondria were dysfunctional, as evidenced by increased fragmentation/fission, decreased oxidative phosphorylation and increased reactive oxygen species (ROS) production. Functionally, SuHx-MVEC exhibited increased basal levels of intracellular calcium concentration ([Ca2+]i), and enhanced migratory and proliferative capacity. Treatment with global (TEMPOL) or mitochondria-specific (MitoQ) antioxidants decreased ROS levels and basal [Ca2]i in SuHx-MVEC. TEMPOL and MitoQ also decreased migration and proliferation in SuHx-MVEC. Additionally, inhibition of ROS-induced Ca2+ entry via pharmacologic blockade of TRPV4 attenuated [Ca2]i, migration and proliferation. These findings suggest a role for mitochondrial ROS-induced Ca2+ influx via TRPV4 in promoting abnormal migration and proliferation in MVECs in this PAH model.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:Publisher
[do] DOI:10.1152/ajplung.00430.2017

  2 / 977 MEDLINE  
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[PMID]: 29286398
[Au] Autor:Lukaszewicz KM; Durand MJ; Priestley JRC; Schmidt JR; Allen LA; Geurts AM; Lombard JH
[Ad] Address:Department of Physical Therapy, Marquette University.
[Ti] Title:Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats.
[So] Source:J Vis Exp;(130), 2017 Dec 05.
[Is] ISSN:1940-087X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:This protocol describes the use of in vitro television microscopy to evaluate vascular function in isolated cerebral resistance arteries (and other vessels), and describes techniques for evaluating tissue perfusion using Laser Doppler Flowmetry (LDF) and microvessel density utilizing fluorescently labeled Griffonia simplicifolia (GS1) lectin. Current methods for studying isolated resistance arteries at transmural pressures encountered in vivo and in the absence of parenchymal cell influences provide a critical link between in vivo studies and information gained from molecular reductionist approaches that provide limited insight into integrative responses at the whole animal level. LDF and techniques to selectively identify arterioles and capillaries with fluorescently-labeled GS1 lectin provide practical solutions to enable investigators to extend the knowledge gained from studies of isolated resistance arteries. This paper describes the application of these techniques to gain fundamental knowledge of vascular physiology and pathology in the rat as a general experimental model, and in a variety of specialized genetically engineered "designer" rat strains that can provide important insight into the influence of specific genes on important vascular phenotypes. Utilizing these valuable experimental approaches in rat strains developed by selective breeding strategies and new technologies for producing gene knockout models in the rat, will expand the rigor of scientific premises developed in knockout mouse models and extend that knowledge to a more relevant animal model, with a well understood physiological background and suitability for physiological studies because of its larger size.
[Pt] Publication type:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Em] Entry month:1712
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[St] Status:In-Data-Review
[do] DOI:10.3791/56133

  3 / 977 MEDLINE  
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[PMID]: 29175484
[Au] Autor:Nikel KE; Shanishchara NK; Ivy CM; Dawson NJ; Scott GR
[Ad] Address:Department of Biology, McMaster University, Hamilton, ON, Canada.
[Ti] Title:Effects of hypoxia at different life stages on locomotory muscle phenotype in deer mice native to high altitudes.
[So] Source:Comp Biochem Physiol B Biochem Mol Biol;, 2017 Nov 22.
[Is] ISSN:1879-1107
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Animals native to high altitude must overcome the constraining effects of hypoxia on tissue O supply to support routine metabolism, thermoregulation in the cold, and exercise. Deer mice (Peromyscus maniculatus) native to high altitude have evolved an enhanced aerobic capacity in hypoxia, along with increased capillarity and oxidative capacity of locomotory muscle. Here, we examined whether exposure to chronic hypoxia during development or adulthood affects muscle phenotype. Deer mice from a highland population were bred in captivity at sea level, and exposed to normoxia or one of four treatments of hypobaric hypoxia (12kPa O , simulating hypoxia at ~4300m): adult hypoxia (6-8weeks), post-natal hypoxia (birth to adulthood), pre-natal hypoxia (before conception to adulthood), and parental hypoxia (in which mice were conceived and raised in normoxia, but their parents were previously exposed to hypoxia). Litter size was similar across treatments, and pups survived the hypoxia exposures and grew to similar body masses at ~6-8months of age. Hypoxia had no effect on the masses of gastrocnemius and soleus muscles. There was a strong concordance between two distinct histological methods for staining capillaries in the gastrocnemius - alkaline phosphatase activity and binding of Griffonia simplicifolia lectin I - each of which showed that capillarity and muscle fibre size were largely unaffected by hypoxia. Maximal activities of several metabolic enzymes (cytochrome c oxidase, citrate synthase, isocitrate dehydrogenase, and lactate dehydrogenase) in the gastrocnemius were also largely unaffected by hypoxia. Therefore, the evolved muscle phenotype of high-altitude deer mice is relatively insensitive to hypoxia across life stages.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171204
[Lr] Last revision date:171204
[St] Status:Publisher

  4 / 977 MEDLINE  
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[PMID]: 29169841
[Au] Autor:Kozlowska A; Mikolajczyk A; Majewski M
[Ad] Address:Department of Human Physiology, Faculty of Medical Sciences, University of Warmia and Mazury Olsztyn, Poland. Electronic address: kozlowska.anna@uwm.edu.pl.
[Ti] Title:Distribution and neurochemistry of porcine urinary bladder-projecting sensory neurons in subdomains of the dorsal root ganglia: a quantitative analysis.
[So] Source:Ann Anat;, 2017 Nov 20.
[Is] ISSN:1618-0402
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:The aim of the present study has been to verify the inter- and intraganglionic distribution pattern of porcine urinary bladder-projecting (UBP) neurons localized in the sacral dorsal root ganglia (DRGs). The morphology and chemical phenotype of these cells have also been investigated. These neurons were visualized using the fluorescent tracer Fast Blue (FB) which was injected bilaterally into the urinary bladder wall of five juvenile female pigs. The intraganglionic distribution showed that small- and medium-sized FB+ perikarya were mainly located in the central (S -S ) and periphero-central (S ) region of the ganglia, while large cells were heterogeneously distributed. Immunohistochemistry revealed that the most frequently observed markers in small and medium-sized UBP perikarya were: neurofilament 200, lectin from Bandeiraea simplicifolia (Griffonia simplicifolia) isolectin B4, substance P, calcitonin gene-related peptide, pituitary adenylate cyclase-activating polypeptide and transient receptor potential vanilloid 1. Moreover, UBP neurons containing these substances were also mainly observed in the central and periphero-central region of the ganglion. Differences in the percentage of traced cells and their neuropeptide content were observed between the S , S and S DRGs. In conclusion, the present study, for the first time, describes the arrangement of UBP DRGs neurons within particular subdomains of sacral ganglia, taking into account their size and chemical phenotype.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171124
[Lr] Last revision date:171124
[St] Status:Publisher

  5 / 977 MEDLINE  
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[PMID]: 29136334
[Au] Autor:Park Y; Yeom J; Kim Y; Lee HJ; Han KC; Lee S; Lee C; Lee JE
[Ad] Address:Center for Theragnosis, Biomedical Research Institute, Korea Institute of Science and Technology, Seoul, Republic of Korea.
[Ti] Title:Identification of plasma membrane glycoproteins specific to human glioblastoma multiforme cells using lectin arrays and LC-MS/MS.
[So] Source:Proteomics;, 2017 Nov 14.
[Is] ISSN:1615-9861
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Glioblastoma, also known as glioblastoma multiforme (GBM), is the most malignant type of brain cancer and has poor prognosis with a median survival of less than one year. While the structural changes of tumor cell surface carbohydrates are known to be associated with invasive behavior of tumor cells, the cell surface glycoproteins to differentiate the low- and high-grade glioma cells can be potential diagnostic markers and therapeutic targets for GBMs. In the present study, lectin arrays consisting of eight lectins were employed to explore cell surface carbohydrate expression patterns on low-grade oligodendroglioma cells (Hs683) and GBM cells (T98G). Griffonia simplicifolia I (GS I) was found to selectively bind to T98G cells and not to Hs683 cells. For identification of the glioblastoma-specific cell surface markers, the glycoproteins from each cell type were captured by a GS I lectin column and analyzed by LC-MS/MS. The identified proteins from the two cell types were quantified using label-free quantitative analysis based on spectral counting. Of cell surface glycoproteins showing significant increases in T98G cells, five proteins were selected for verification of both protein and glycosylation level changes using western blot and GSI lectin-based immunosorbent assay. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171114
[Lr] Last revision date:171114
[St] Status:Publisher
[do] DOI:10.1002/pmic.201700302

  6 / 977 MEDLINE  
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[PMID]: 29049716
[Au] Autor:Caballero S; Kent DL; Sengupta N; Li Calzi S; Shaw L; Beli E; Moldovan L; Dominguez JM; Moorthy RS; Grant MB
[Ad] Address:Pharmacology and Therapeutics, University of Florida, Gainesville, Florida, United States.
[Ti] Title:Bone Marrow-Derived Cell Recruitment to the Neurosensory Retina and Retinal Pigment Epithelial Cell Layer Following Subthreshold Retinal Phototherapy.
[So] Source:Invest Ophthalmol Vis Sci;58(12):5164-5176, 2017 Oct 01.
[Is] ISSN:1552-5783
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Purpose: We investigated whether subthreshold retinal phototherapy (SRPT) was associated with recruitment of bone marrow (BM)-derived cells to the neurosensory retina (NSR) and RPE layer. Methods: GFP chimeric mice and wild-type (WT) mice were subjected to SRPT using a slit-lamp infrared laser. Duty cycles of 5%, 10%, 15%, and 20% (0.1 seconds, 250 mW, spot size 50 µm) with 30 applications were placed 50 to 100 µm from the optic disc. In adoptive transfer studies, GFP+ cells were given intravenously immediately after WT mice received SRPT. Immunohistochemistry was done for ionized calcium-binding adapter molecule-1 (IBA-1+), CD45, Griffonia simplicifolia lectin isolectin B4, GFP or cytokeratin). Expression of Ccl2, Il1b, Il6, Hspa1a, Hsp90aa1, Cryab, Hif1a, Cxcl12, and Cxcr4 mRNA and flow cytometry of the NSR and RPE-choroid were performed. Results: Within 12 to 24 hours of SRPT, monocytes were detected in the NSR and RPE-choroid. Detection of reparative progenitors in the RPE occurred at 2 weeks using flow cytometry. Recruitment of GFP+ cells to the RPE layer occurred in a duty cycle-dependent manner in chimeric mice and in mice undergoing adoptive transfer. Hspa1a, Hsp90aa1, and Cryab mRNAs increased in the NSR at 2 hours post laser; Hif1a, Cxcl12, Hspa1a increased at 4 hours in the RPE-choroid; and Ccl2, Il1b, Ifng, and Il6 increased at 12 to 24 hours in the RPE-choroid. Conclusions: SRPT induces monocyte recruitment to the RPE followed by hematopoietic progenitor cell homing at 2 weeks. Recruitment occurs in a duty cycle-dependent manner and potentially could contribute to the therapeutic efficacy of SRPT.
[Mh] MeSH terms primary: Bone Marrow Cells/physiology
Cell Movement/physiology
Phototherapy
Retina/cytology
Retinal Pigment Epithelium/cytology
[Mh] MeSH terms secundary: Adoptive Transfer
Animals
Biomarkers/metabolism
Cells, Cultured
Chemokine CXCL12/metabolism
Choroid/cytology
Choroid/metabolism
Female
Flow Cytometry
Green Fluorescent Proteins/metabolism
Heat-Shock Proteins/metabolism
Hematopoietic Stem Cell Transplantation
Immunohistochemistry
Laser Therapy
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Monocytes/physiology
Receptors, CXCR4/metabolism
Retina/metabolism
Retina/surgery
Retinal Pigment Epithelium/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Biomarkers); 0 (CXCR4 protein, mouse); 0 (Chemokine CXCL12); 0 (Cxcl12 protein, mouse); 0 (Heat-Shock Proteins); 0 (Receptors, CXCR4); 147336-22-9 (Green Fluorescent Proteins)
[Em] Entry month:1710
[Cu] Class update date: 171027
[Lr] Last revision date:171027
[Js] Journal subset:IM
[Da] Date of entry for processing:171020
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-20736

  7 / 977 MEDLINE  
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[PMID]: 28534963
[Au] Autor:Nishino K; Yamamoto E; Niimi K; Sekiya Y; Yamashita Y; Kikkawa F
[Ad] Address:Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
[Ti] Title:N-acetylglucosaminyltransferase IVa promotes invasion of choriocarcinoma.
[So] Source:Oncol Rep;38(1):440-448, 2017 Jul.
[Is] ISSN:1791-2431
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Gestational trophoblastic neoplasia (GTN) results from the malignant transformation of placental trophoblasts which secrete human chorionic gonadotropin (hCG) as do normal placenta or hydatidiform mole. N-acetylglucosaminyltransferase IV (GnT-IV) is a glycosyltransferase which catalyses the formation of ß1,4GlcNAc branches on the mannose core of N-glycans. Previous studies reported that ß1,4GlcNAc branches on hCG were detected in GTN but not in normal pregnancy or hydatidiform mole. The aim of the present study was to understand the role of GnT-IVa in choriocarcinoma and find the target proteins for GnT-IVa glycosylation which contribute to the malignancy of choriocarcinoma. Immunohistochemistry showed that Griffonia simplicifolia lectin-II staining and GnT-IVa staining were intense in trophoblastic cells of invasive mole and choriocarcinoma. We established a choriocarcinoma cell line with GnT-IVa overexpression (Jar-GnT4a), and examined its malignant potential and target proteins for GnT-IVa glycosylation. GnT-IVa overexpression increased the cell migration and invasion (2.5- and 1.4-fold) as well as the ability to adhere to the extracellular matrix (ECM) components, including fibronectin and collagen type I and IV. The tumour formation potential of Jar-GnT4a in mice was significantly higher than that of control (P=0.0407), and the cumulative survival rate of mice with Jar-GnT4a was relatively lower than those with control. Immunoprecipitation studies showed that ß1,4GlcNAc branches of N-glycans on integrin ß1 in choriocarcinoma cells were increased by GnT-IVa overexpression. Nano-LC/MS/MS analysis suggested that lysosome-associated membrane glycoprotein 2 (LAMP-2) was a target protein for glycosylation by GnT-IVa. The increase in ß1,4GlcNAc branches on LAMP-2 by GnT-IVa overexpression was confirmed by lectin blot analysis using whole cell lysate and conditioned medium. Our results suggest that highly branched N-glycans generated by the action of GnT-IVa are present in trophoblastic cells of GTN in proportion to GnT-IVa expression level, and that GnT-IVa may contribute to the malignancy of choriocarcinoma by promoting cell adhesion, migration and invasion through glycosylation of integrin ß1 and LAMP-2.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1705
[Cu] Class update date: 170619
[Lr] Last revision date:170619
[St] Status:In-Process
[do] DOI:10.3892/or.2017.5661

  8 / 977 MEDLINE  
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[PMID]: 27932312
[Au] Autor:Burclaff J; Osaki LH; Liu D; Goldenring JR; Mills JC
[Ad] Address:Division of Gastroenterology, Department of Medicine, Department of Pathology and Immunology, Department of Developmental Biology, Washington University, St. Louis, Missouri.
[Ti] Title:Targeted Apoptosis of Parietal Cells Is Insufficient to Induce Metaplasia in Stomach.
[So] Source:Gastroenterology;152(4):762-766.e7, 2017 Mar.
[Is] ISSN:1528-0012
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Parietal cell atrophy is considered to cause metaplasia in the stomach. We developed mice that express the diphtheria toxin receptor specifically in parietal cells to induce their death, and found this to increase proliferation in the normal stem cell zone and neck but not to cause metaplastic reprogramming of chief cells. Furthermore, the metaplasia-inducing agents tamoxifen or DMP-777 still induced metaplasia even after previous destruction of parietal cells by diphtheria toxin. Atrophy of parietal cells alone therefore is not sufficient to induce metaplasia: completion of metaplastic reprogramming of chief cells requires mechanisms beyond parietal cell injury or death.
[Mh] MeSH terms primary: Apoptosis
Chief Cells, Gastric/pathology
Parietal Cells, Gastric/pathology
Parietal Cells, Gastric/physiology
Stomach/pathology
[Mh] MeSH terms secundary: Animals
Apoptosis/drug effects
Apoptosis/genetics
Atrophy/chemically induced
Azetidines
Cell Proliferation
Cellular Reprogramming
Chief Cells, Gastric/metabolism
Diphtheria Toxin/pharmacology
Heparin-binding EGF-like Growth Factor/genetics
Intrinsic Factor/metabolism
Metaplasia/chemically induced
Metaplasia/genetics
Metaplasia/metabolism
Mice
Parietal Cells, Gastric/drug effects
Peptides/metabolism
Piperazines
Plant Lectins/metabolism
Tamoxifen
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Azetidines); 0 (Diphtheria Toxin); 0 (Griffonia simplicifolia lectins); 0 (Heparin-binding EGF-like Growth Factor); 0 (Peptides); 0 (Piperazines); 0 (Plant Lectins); 0 (spasmolytic polypeptide); 094ZI81Y45 (Tamoxifen); 3Q0469283P (DMP 777); 9008-12-2 (Intrinsic Factor)
[Em] Entry month:1706
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:161210
[St] Status:MEDLINE

  9 / 977 MEDLINE  
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[PMID]: 27872404
[Au] Autor:O'Neil A; Petersen CP; Choi E; Engevik AC; Goldenring JR
[Ad] Address:Department of Surgery (AO, EC, ACE, JRG), Vanderbilt University Medical Center, Nashville, Tennessee.
[Ti] Title:Unique Cellular Lineage Composition of the First Gland of the Mouse Gastric Corpus.
[So] Source:J Histochem Cytochem;65(1):47-58, 2017 01.
[Is] ISSN:1551-5044
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The glandular stomach has two major zones: the acid secreting corpus and the gastrin cell-containing antrum. Nevertheless, a single gland lies at the transition between the forestomach and corpus in the mouse stomach. We have sought to define the lineages that make up this gland unit at the squamocolumnar junction. The first gland in mice showed a notable absence of characteristic corpus lineages, including parietal cells and chief cells. In contrast, the gland showed strong staining of Griffonia simplicifolia-II (GSII)-lectin-positive mucous cells at the bases of glands, which were also positive for CD44 variant 9 and Clusterin. Prominent numbers of doublecortin-like kinase 1 (DCLK1) positive tuft cells were present in the first gland. The first gland contained Lgr5-expressing putative progenitor cells, and a large proportion of the cells were positive for Sox2. The cells of the first gland stained strongly for MUC4 and EpCAM, but both were absent in the normal corpus mucosa. The present studies indicate that the first gland in the corpus represents a unique anatomic entity. The presence of a concentration of progenitor cells and sensory tuft cells in this gland suggests that it may represent a source of reserve reparative cells for adapting to severe mucosal damage.
[Mh] MeSH terms primary: Gastric Mucosa/cytology
Stem Cells/cytology
Stomach/cytology
[Mh] MeSH terms secundary: Animals
Clusterin/analysis
Gastric Mucosa/ultrastructure
Male
Mice
Mice, Inbred C57BL
Mucin-4/analysis
Parietal Cells, Gastric/cytology
Plant Lectins/analysis
Protein-Serine-Threonine Kinases/analysis
Receptors, G-Protein-Coupled/analysis
SOXB1 Transcription Factors/analysis
Stem Cells/ultrastructure
Stomach/ultrastructure
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Clusterin); 0 (Griffonia simplicifolia lectins); 0 (Lgr5 protein, mouse); 0 (Muc4 protein, mouse); 0 (Mucin-4); 0 (Plant Lectins); 0 (Receptors, G-Protein-Coupled); 0 (SOXB1 Transcription Factors); 0 (Sox2 protein, mouse); EC 2.7.1.- (Dcamkl1 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Entry month:1705
[Cu] Class update date: 170922
[Lr] Last revision date:170922
[Js] Journal subset:IM
[Da] Date of entry for processing:161123
[St] Status:MEDLINE
[do] DOI:10.1369/0022155416678182

  10 / 977 MEDLINE  
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[PMID]: 28293502
[Au] Autor:Stone R; Rathbone CR
[Ad] Address:Extremity Trauma and Regenerative Medicine, US Army Institute of Surgical Research, Fort Sam Houston, Tex.
[Ti] Title:Microvascular Fragment Transplantation Improves Rat Dorsal Skin Flap Survival.
[So] Source:Plast Reconstr Surg Glob Open;4(12):e1140, 2016 Dec.
[Is] ISSN:2169-7574
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: The development of flap necrosis distally remains a concern during microsurgical flap transfers because, at least in part, of decreased perfusion. Microvascular fragments (MVFs) are microvessels isolated from adipose tissue that are capable of improving tissue perfusion in a variety of tissue defects. The aim of this study was to determine whether the transplantation of MVFs in a dorsal rat skin flap model can improve flap survival. METHODS: A 10 × 3 cm flap was raised in a cranial to caudal fashion on the dorsal side of 16 Lewis rats, with the caudal side remaining intact. The rats were equally divided into a treatment group (MVFs) and a control group (sterile saline). At the time of surgery, sterile saline with or without MVFs was injected directly into the flap. Microvessel density was determined after harvesting flap tissue by counting vessels that positively stained for Griffonia simplicifolia lectin I-isolectin B . Laser Doppler was used to measure blood flow before and after surgery and 7 and 14 days later. Flap survival was evaluated 7 and 14 days after surgery by evaluating the percentage of viable tissue of the flap with photodigital planimetry. RESULTS: Despite the lack of a significant difference in microvessel density and tissue perfusion, flap survival increased 6.4% ( < 0.05) in MVF-treated animals compared with controls. CONCLUSIONS: The use of MVFs may be a means to improve flap survival. Future studies are required to delineate mechanisms whereby this occurs and to further optimize their application.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1703
[Cu] Class update date: 170816
[Lr] Last revision date:170816
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1097/GOX.0000000000001140


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