scholarly journals Detection of Differentially Expressed Wound-Healing–Related Glycogenes in Galectin-3–Deficient Mice

2009 ◽  
Vol 50 (12) ◽  
pp. 5690 ◽  
Author(s):  
Chandrassegar Saravanan ◽  
Zhiyi Cao ◽  
Steven R. Head ◽  
Noorjahan Panjwani
Keyword(s):  
Wound Healing ◽  
Differentially Expressed ◽  
Galectin 3 ◽  
Deficient Mice

Impaired intestinal wound healing in Fhl2-deficient mice is due to disturbed collagen metabolism

2008 ◽  
Vol 314 (20) ◽  
pp. 3684-3691 ◽  
Author(s):  
Jutta Kirfel ◽  
Dimitrios Pantelis ◽  
Mustapha Kabba ◽  
Philip Kahl ◽  
Anke Röper ◽  
...  
Keyword(s):  
Wound Healing ◽  
Collagen Metabolism ◽  
Deficient Mice

Spontaneous skin damage and delayed wound healing in SOD1-deficient mice

2010 ◽  
Vol 341 (1-2) ◽  
pp. 181-194 ◽  
Author(s):  
Yoshihito Iuchi ◽  
Dipa Roy ◽  
Futoshi Okada ◽  
Noriko Kibe ◽  
Satoshi Tsunoda ◽  
...  
Keyword(s):  
Wound Healing ◽  
Skin Damage ◽  
Delayed Wound Healing ◽  
Deficient Mice

scholarly journals Differentially expressed genes in cotyledon of ewes fed mycotoxins

BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
J. L. Britt ◽  
R. E. Noorai ◽  
S. K. Duckett
Keyword(s):  
Wound Healing ◽  
Differentially Expressed Genes ◽  
Ergot Alkaloid ◽  
Ergot Alkaloids ◽  
Late Gestation ◽  
Fetal Weight ◽  
Differentially Expressed ◽  
Coagulation Cascade ◽  
Peroxisome Proliferator ◽  
Metabolism Regulation

Abstract Background Ergot alkaloids (E+) are mycotoxins produced by the endophytic fungus, Epichloë coenophiala, in tall fescue that are associated with ergotism in animals. Exposure to ergot alkaloids during gestation reduces fetal weight and placental mass in sheep. These reductions are related to vasoconstrictive effects of ergot alkaloids and potential alterations in nutrient transport to the fetus. Cotyledon samples were obtained from eight ewes that were fed E+ (n = 4; E+/E+) or E- (endophyte-free without ergot alkaloids; n = 4; E−/E-) seed during both mid (d 35 to 85) and late (d 85–133) gestation to assess differentially expressed genes associated with ergot alkaloid induced reductions in placental mass and fetal weight, and discover potential adaptive mechanisms to alter nutrient supply to fetus. Results Ewes fed E+/E+ fescue seed during both mid and late gestation had 20% reduction in fetal body weight and 33% reduction in cotyledon mass compared to controls (E−/E-). Over 13,000 genes were identified with 110 upregulated and 33 downregulated. Four genes had a |log2FC| > 5 for ewes consuming E+/E+ treatment compared to controls: LECT2, SLC22A9, APOC3, and MBL2. REViGO revealed clusters of upregulated genes associated glucose, carbohydrates, lipid, protein, macromolecular and cellular metabolism, regulation of wound healing and response to starvation. For downregulated genes, no clusters were present, but all enriched GO terms were associated with anion and monocarboxylic acid transport. The complement and coagulation cascade and the peroxisome proliferator-activated receptor signaling pathway were found to be enriched for ewes consuming E+/E+ treatment. Conclusions Consumption of ergot alkaloids during gestation altered the cotyledonary transcriptome specifically related to macronutrient metabolism, wound healing and starvation. These results show that ergot alkaloid exposure upregulates genes involved in nutrient metabolism to supply the fetus with additional substrates in attempts to rescue fetal growth.

scholarly journals Chanzyme TRPM7 protects against cardiovascular inflammation and fibrosis

2019 ◽  
Vol 116 (3) ◽  
pp. 721-735 ◽  
Author(s):  
Francisco J Rios ◽  
Zhi-Guo Zou ◽  
Adam P Harvey ◽  
Katie Y Harvey ◽  
Ryszard Nosalski ◽  
...  
Keyword(s):  
Cardiovascular System ◽  
Molecular Mechanisms ◽  
Transient Receptor Potential ◽  
Inflammatory Responses ◽  
Cardiac Fibroblasts ◽  
Nuclear Antigen ◽  
Culture Systems ◽  
Transient Receptor Potential Melastatin ◽  
Galectin 3 ◽  
Deficient Mice

Abstract Aims Transient Receptor Potential Melastatin 7 (TRPM7) cation channel is a chanzyme (channel + kinase) that influences cellular Mg2+ homeostasis and vascular signalling. However, the pathophysiological significance of TRPM7 in the cardiovascular system is unclear. The aim of this study was to investigate the role of this chanzyme in the cardiovascular system focusing on inflammation and fibrosis. Methods and results TRPM7-deficient mice with deletion of the kinase domain (TRPM7+/Δkinase) were studied and molecular mechanisms investigated in TRPM7+/Δkinase bone marrow-derived macrophages (BMDM) and co-culture systems with cardiac fibroblasts. TRPM7-deficient mice had significant cardiac hypertrophy, fibrosis, and inflammation. Cardiac collagen and fibronectin content, expression of pro-inflammatory mediators (SMAD3, TGFβ) and cytokines [interleukin (IL)-6, IL-10, IL-12, tumour necrosis factor-α] and phosphorylation of the pro-inflammatory signalling molecule Stat1, were increased in TRPM7+/Δkinase mice. These processes were associated with infiltration of inflammatory cells (F4/80+CD206+ cardiac macrophages) and increased galectin-3 expression. Cardiac [Mg2+]i, but not [Ca2+]i, was reduced in TRPM7+/Δkinase mice. Calpain, a downstream TRPM7 target, was upregulated (increased expression and activation) in TRPM7+/Δkinase hearts. Vascular functional and inflammatory responses, assessed in vivo by intra-vital microscopy, demonstrated impaired neutrophil rolling, increased neutrophil: endothelial attachment and transmigration of leucocytes in TRPM7+/Δkinase mice. TRPM7+/Δkinase BMDMs had increased levels of galectin-3, IL-10, and IL-6. In co-culture systems, TRPM7+/Δkinase macrophages increased expression of fibronectin, proliferating cell nuclear antigen, and TGFβ in cardiac fibroblasts from wild-type mice, effects ameliorated by MgCl2 treatment. Conclusions We identify a novel anti-inflammatory and anti-fibrotic role for TRPM7 and suggest that its protective effects are mediated, in part, through Mg2+-sensitive processes.

scholarly journals CNS Wound Healing Is Severely Depressed in Metallothionein I- and II-Deficient Mice

1999 ◽  
Vol 19 (7) ◽  
pp. 2535-2545 ◽  
Author(s):  
Milena Penkowa ◽  
Javier Carrasco ◽  
Mercedes Giralt ◽  
Torben Moos ◽  
Juan Hidalgo
Keyword(s):  
Wound Healing ◽  
Deficient Mice

Wound healing delays in α-Klotho -deficient mice that have skin appearance similar to that in aged humans – Study of delayed wound healing mechanism

2016 ◽  
Vol 473 (4) ◽  
pp. 845-852 ◽  
Author(s):  
Makoto Yamauchi ◽  
Yoshihiko Hirohashi ◽  
Toshihiko Torigoe ◽  
Yoshitaka Matsumoto ◽  
Ken Yamashita ◽  
...  
Keyword(s):  
Wound Healing ◽  
Delayed Wound Healing ◽  
Deficient Mice

scholarly journals Plasminogen activation independent of uPA and tPA maintains wound healing in gene-deficient mice

2006 ◽  
Vol 25 (12) ◽  
pp. 2686-2697 ◽  
Author(s):  
Leif R Lund ◽  
Kirsty A Green ◽  
Allart A Stoop ◽  
Michael Ploug ◽  
Kasper Almholt ◽  
...  
Keyword(s):  
Wound Healing ◽  
Plasminogen Activation ◽  
Deficient Mice

Delayed wound healing in Mac-1?deficient mice is associated with normal monocyte recruitment

2007 ◽  
Vol 15 (4) ◽  
pp. 566-571 ◽  
Author(s):  
Mark Sisco ◽  
Jerome D. Chao ◽  
Injoong Kim ◽  
Jon E. Mogford ◽  
Tanya N. Mayadas ◽  
...  
Keyword(s):  
Wound Healing ◽  
Delayed Wound Healing ◽  
Monocyte Recruitment ◽  
Normal Monocyte ◽  
Deficient Mice
Sign in / Sign up

Export Citation Format

Share Document