Wound repair in a spider, Geolycosa pikei

1981 ◽  
Vol 59 (8) ◽  
pp. 1488-1492 ◽  
Author(s):  
Charles Bursey
Keyword(s):  
Wound Repair ◽  
Wolf Spider ◽  
Repair Process ◽  
Tissue Structure ◽  
Lateral Aspect ◽  
Wound Site ◽  
Made In

Observations are presented on the wound repair process of a burrowing wolf spider, Geolycosa pikei. Awound,0.3 × 1.0 × 0.5 mm, was made in the superior lateral aspect of the abdomen and observations on tissue from the wound site were made at 2, 6, 12, 24 h, 4, 8, 16, 32, 60, 90, 120 days. The wound was plugged immediately by a hemolymph coagulum. With time, the external portion of the coagulum was reduced to a scale which bridged the hole in the exoskeleton; the internal portion of the coagulum was replaced by a fibrous mass which was gradually lost through a series of changes that eventually restored the original tissue structure.

Histological response to injury in the horseshoe crab, Limulus polyphemus

1977 ◽  
Vol 55 (7) ◽  
pp. 1158-1165 ◽  
Author(s):  
Charles R. Bursey
Keyword(s):  
Epithelial Cells ◽  
Wound Repair ◽  
Horseshoe Crab ◽  
Thick Layer ◽  
Repair Process ◽  
Limulus Polyphemus ◽  
Tissue Structure ◽  
Histological Response ◽  
Wound Site

Observations are presented on the wound repair process of the horseshoe crab, Limulus polyphemus. A cut, 1 × 40 × 3 mm, was made through the dorsal abdominal carapace and observations of the tissue at the wound site were made at 6, 24, 48, 96 h and 5, 10, 15, 30, 60, 90, 120, and 180 days. The wound was immediately plugged by a hemolymph coagulum and there was heavy infiltration of hemocytes into the area. Infiltrating hemocytes undergo a series of changes. The outermost cells hyalinize and form a thick layer between the cut ends of the exoskeleton. Pigmented epithelial cells migrate into the scar and produce a layer of cuticle under the cut exoskeleton. During the remaining period of observation, the cuticular scab enlarged and the cellular mass that filled the wound channel was lost through a series of changes that eventually restored the original tissue structure.

scholarly journals Membrane dynamics during cellular wound repair

2016 ◽  
Vol 27 (14) ◽  
pp. 2272-2285 ◽  
Author(s):  
Nicholas R. Davenport ◽  
Kevin J. Sonnemann ◽  
Kevin W. Eliceiri ◽  
William M. Bement
Keyword(s):  
Wound Repair ◽  
Repair Process ◽  
Membrane Dynamics ◽  
Xenopus Laevis Oocytes ◽  
Spatial Patterning ◽  
Membrane Repair ◽  
Spatiotemporal Resolution ◽  
Wound Site ◽  
Compound Exocytosis ◽  
Intracellular Compartments

Cells rapidly reseal after damage, but how they do so is unknown. It has been hypothesized that resealing occurs due to formation of a patch derived from rapid fusion of intracellular compartments at the wound site. However, patching has never been directly visualized. Here we study membrane dynamics in wounded Xenopus laevis oocytes at high spatiotemporal resolution. Consistent with the patch hypothesis, we find that damage triggers rampant fusion of intracellular compartments, generating a barrier that limits influx of extracellular dextrans. Patch formation is accompanied by compound exocytosis, local accumulation and aggregation of vesicles, and rupture of compartments facing the external environment. Subcellular patterning is evident as annexin A1, dysferlin, diacylglycerol, active Rho, and active Cdc42 are recruited to compartments confined to different regions around the wound. We also find that a ring of elevated intracellular calcium overlaps the region where membrane dynamics are most evident and persists for several minutes. The results provide the first direct visualization of membrane patching during membrane repair, reveal novel features of the repair process, and show that a remarkable degree of spatial patterning accompanies damage-induced membrane dynamics.

Tu1734 Inhibition of MRP4 Enhances the Wound Repair Process:

2013 ◽  
Vol 144 (5) ◽  
pp. S-833
Author(s):  
Chandrima Sinha ◽  
Anjaparavanda P. Naren
Keyword(s):  
Wound Repair ◽  
Repair Process

scholarly journals Microfluidic guillotine for single-cell wound repair studies

2017 ◽  
Vol 114 (28) ◽  
pp. 7283-7288 ◽  
Author(s):  
Lucas R. Blauch ◽  
Ya Gai ◽  
Jian Wei Khor ◽  
Pranidhi Sood ◽  
Wallace F. Marshall ◽  
...  
Keyword(s):  
Single Cell ◽  
High Throughput ◽  
Wound Repair ◽  
Time Course ◽  
Single Cells ◽  
Repair Process ◽  
Gene Knockdown ◽  
Viscous Stress ◽  
Repair Capacity ◽  
Stentor Coeruleus

Wound repair is a key feature distinguishing living from nonliving matter. Single cells are increasingly recognized to be capable of healing wounds. The lack of reproducible, high-throughput wounding methods has hindered single-cell wound repair studies. This work describes a microfluidic guillotine for bisecting single Stentor coeruleus cells in a continuous-flow manner. Stentor is used as a model due to its robust repair capacity and the ability to perform gene knockdown in a high-throughput manner. Local cutting dynamics reveals two regimes under which cells are bisected, one at low viscous stress where cells are cut with small membrane ruptures and high viability and one at high viscous stress where cells are cut with extended membrane ruptures and decreased viability. A cutting throughput up to 64 cells per minute—more than 200 times faster than current methods—is achieved. The method allows the generation of more than 100 cells in a synchronized stage of their repair process. This capacity, combined with high-throughput gene knockdown in Stentor, enables time-course mechanistic studies impossible with current wounding methods.

scholarly journals Cell wound repair in Drosophila occurs through three distinct phases of membrane and cytoskeletal remodeling

2011 ◽  
Vol 193 (3) ◽  
pp. 455-464 ◽  
Author(s):  
Maria Teresa Abreu-Blanco ◽  
Jeffrey M. Verboon ◽  
Susan M. Parkhurst
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Single Cell ◽  
Wound Repair ◽  
Single Cells ◽  
Repair Process ◽  
Wound Edge ◽  
Cytoskeletal Remodeling ◽  
Tissue Integrity ◽  
E Cadherin

When single cells or tissues are injured, the wound must be repaired quickly in order to prevent cell death, loss of tissue integrity, and invasion by microorganisms. We describe Drosophila as a genetically tractable model to dissect the mechanisms of single-cell wound repair. By analyzing the expression and the effects of perturbations of actin, myosin, microtubules, E-cadherin, and the plasma membrane, we define three distinct phases in the repair process—expansion, contraction, and closure—and identify specific components required during each phase. Specifically, plasma membrane mobilization and assembly of a contractile actomyosin ring are required for this process. In addition, E-cadherin accumulates at the wound edge, and wound expansion is excessive in E-cadherin mutants, suggesting a role for E-cadherin in anchoring the actomyosin ring to the plasma membrane. Our results show that single-cell wound repair requires specific spatial and temporal cytoskeleton responses with distinct components and mechanisms required at different stages of the process.

scholarly journals Overcoming stromal barriers to immuno-oncological responses via fibroblast activation protein-targeted therapy

Immunotherapy ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 155-175
Author(s):  
W Nathaniel Brennen ◽  
Daniel L J Thorek ◽  
Wen Jiang ◽  
Timothy E Krueger ◽  
Lizamma Antony ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Targeted Therapy ◽  
Immune Suppression ◽  
Feedback Loop ◽  
Wound Repair ◽  
Repair Process ◽  
Fibroblast Activation Protein ◽  
Primary Data ◽  
Positive Feedback Loop ◽  
Fibroblast Activation

The tumor microenvironment contributes to disease progression through multiple mechanisms, including immune suppression mediated in part by fibroblast activation protein (FAP)-expressing cells. Herein, a review of FAP biology is presented, supplemented with primary data. This includes FAP expression in prostate cancer and activation of latent reservoirs of TGF-β and VEGF to produce a positive feedback loop. This collectively suggests a normal wound repair process subverted during cancer pathophysiology. There has been immense interest in targeting FAP for diagnostic, monitoring and therapeutic purposes. Until recently, this development has outpaced an understanding of the biology; impeding optimal translation into the clinic. A summary of these applications is provided with an emphasis on eliminating tumor-infiltrating FAP-positive cells to overcome stromal barriers to immuno-oncological responses.

scholarly journals ECRG4 regulates neutrophil recruitment and CD44 expression during the inflammatory response to injury

2020 ◽  
Vol 6 (11) ◽  
pp. eaay0518 ◽  
Author(s):  
Robert A. Dorschner ◽  
Jisook Lee ◽  
Olga Cohen ◽  
Todd Costantini ◽  
Andrew Baird ◽  
...  
Keyword(s):  
Wound Repair ◽  
Repair Process ◽  
Neutrophil Recruitment ◽  
Related Gene ◽  
Cd44 Expression ◽  
Cancer Related Gene ◽  
Inflammation Resolution ◽  
Inflammatory Response To Injury ◽  
Gene 4

The complex molecular microenvironment of the wound bed regulates the duration and degree of inflammation in the wound repair process, while its dysregulation leads to impaired healing. Understanding factors controlling this response provides therapeutic targets for inflammatory disease. Esophageal cancer–related gene 4 (ECRG4) is a candidate chemokine that is highly expressed on leukocytes. We used ECRG4 knockout (KO) mice to establish that the absence of ECRG4 leads to defective neutrophil recruitment with a delay in wound healing. An in vitro human promyelocyte model identified an ECRG4-mediated suppression of the hyaluronic acid receptor, CD44, a key receptor mediating inflammation resolution. In ECRG4 KO mouse leukocytes, there was an increase in CD44 expression, consistent with a model in which ECRG4 negatively regulates CD44 levels. Therefore, we propose a previously unidentified mechanism in which ECRG4 regulates early neutrophil recruitment and subsequent CD44-mediated resolution of inflammation.

scholarly journals Wound wood formation in Eucalyptus globulus and Eucalyptus nitens: anatomy and chemistry

2003 ◽  
Vol 33 (12) ◽  
pp. 2331-2339 ◽  
Author(s):  
Alieta Eyles ◽  
Noel W Davies ◽  
Caroline Mohammed
Keyword(s):  
Eucalyptus Globulus ◽  
Wound Repair ◽  
Wood Formation ◽  
Negative Ion ◽  
Eucalyptus Nitens ◽  
Diverse Range ◽  
Wound Site ◽  
Formylated Phloroglucinol Compounds ◽  
Wood Extracts ◽  
Volatile Terpenes

The wound-associated wood that developed 17 months following artificial xylem injury in Eucalyptus globulus (Labill) and Eucalyptus nitens (Maiden) was examined anatomically and chemically. This new tissue located immediately adjacent to the wound site and termed "wound wood" was highly variable consisting of callus, altered wood of increased parenchyma density, and dark extractives, visible to the naked eye. Subsequent chemical analysis of crude wound wood extracts by HPLC coupled to negative ion electrospray mass spectrometry revealed the presence of a diverse range of polyphenolic compounds including hydrolysable tannins, proanthocyanidins, flavanone glycosides, and formylated phloroglucinol compounds. A number of polyphenols were unequivocally identified including engelitin, pedunculagin, and tellimagrandin I. Other compounds present in wound wood include various hydroxystilbene glycosides and volatile terpenes. The importance of the diverse range of secondary metabolites detected in wound wood is discussed in relation to tree wound repair responses.

scholarly journals Senescence of IPF Lung Fibroblasts Disrupt Alveolar Epithelial Cell Proliferation and Promote Migration in Wound Healing

Pharmaceutics ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 389 ◽  
Author(s):  
Kaj E. C. Blokland ◽  
David W. Waters ◽  
Michael Schuliga ◽  
Jane Read ◽  
Simon D. Pouwels ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Wound Repair ◽  
Alveolar Epithelial Cell ◽  
Lung Parenchyma ◽  
Repair Process ◽  
Lung Fibroblasts ◽  
Epithelial Cell Proliferation ◽  
Alveolar Epithelial ◽  
M Phase

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease marked by excessive accumulation of lung fibroblasts (LFs) and collagen in the lung parenchyma. The mechanisms that underlie IPF pathophysiology are thought to reflect repeated alveolar epithelial injury leading to an aberrant wound repair response. Recent work has shown that IPF-LFs display increased characteristics of senescence including growth arrest and a senescence-associated secretory phenotype (SASP) suggesting that senescent LFs contribute to dysfunctional wound repair process. Here, we investigated the influence of senescent LFs on alveolar epithelial cell repair responses in a co-culture system. Alveolar epithelial cell proliferation was attenuated when in co-culture with cells or conditioned media from, senescence-induced control LFs or IPF-LFs. Cell-cycle analyses showed that a larger number of epithelial cells were arrested in G2/M phase when co-cultured with IPF-LFs, than in monoculture. Paradoxically, the presence of LFs resulted in increased A549 migration after mechanical injury. Our data suggest that senescent LFs may contribute to aberrant re-epithelialization by inhibiting proliferation in IPF.

scholarly journals The reorganization of microfilaments, centrosomes, and microtubules during in vitro small wound reendothelialization.

1988 ◽  
Vol 107 (5) ◽  
pp. 1777-1783 ◽  
Author(s):  
M K Wong ◽  
A I Gotlieb
Keyword(s):  
Cell Spreading ◽  
Time Lapse ◽  
Repair Process ◽  
Specific Sequence ◽  
Actin Microfilament ◽  
Wound Model ◽  
Microfilament Bundles ◽  
Endothelial Integrity ◽  
Made In

The repair of small endothelial wounds is an important process by which endothelial cells maintain endothelial integrity. An in vitro wound model system was used in which precise wounds were made in a confluent endothelial monolayer. The repair process was observed by time-lapse cinemicrophotography. Using fluorescence and immunofluorescence microscopy, the cellular morphological events were correlated with the localization and distribution of actin microfilament bundles and vinculin plaques, and centrosomes and their associated microtubules. Single to four-cell wounds underwent closure by cell spreading while wounds seven to nine cells in size closed by initially spreading which was then followed at approximately 1 h after wounding by cell migration. These two processes showed different cytoskeletal patterns. Cell spreading occurred independent of centrosome location. However, centrosome redistribution to the front of the cell occurred as the cells began to elongate and migrate. While the peripheral actin microfilament bundles (i.e., the dense peripheral band) remained intact during cell spreading, they broke down during migration and were associated with a reduction in peripheral vinculin plaque staining. Thus, the major events characterizing the closure of endothelial wounds were precise in nature, followed a specific sequence, and were associated with specific cytoskeletal patterns which most likely were important in maintaining directionality of migration and reducing the adhesion of the cells to their neighbors within the monolayer.

Sign in / Sign up

Export Citation Format

Share Document