Angiogenic potential and wound healing efficacy of chitosan derived hydrogels at varied concentrations of APTES in chick and mouse models

Author(s):  
Chaman Ara ◽  
Sehrish Jabeen ◽  
Gul Afshan ◽  
Ariba Farooq ◽  
Muhammad Sarfraz Akram ◽  
...  
2020 ◽  
Author(s):  
Meredith J. Crane ◽  
Yun Xu ◽  
Sean F. Monaghan ◽  
Benjamin M. Hall ◽  
Jorge E. Albina ◽  
...  

SummaryStudies of the immune response typically focus on single-insult systems, with little known about how multi-insult encounters are managed. Pneumonia in patients recovering from surgery is a clinical situation that exemplifies the need for the patient to mount two distinct immune responses. Examining this, we have determined that poor wound healing is an unreported complication of pneumonia in laparotomy patients. Using mouse models, we found that lung infection suppressed the trafficking of innate leukocytes to wounded skin, while pulmonary resistance to the bacterial infection was maintained. The dual insults caused distinct systemic and local changes to the inflammatory response, the most striking being a rapid and sustained decrease in chemokine levels at the wound site of mice with pneumonia. Remarkably, replenishing wound chemokine levels completely rescued the wound-healing rate in mice with a pulmonary infection. These findings have broad implications for understanding the mechanisms guiding the innate immune system to prioritize inflammatory sites.One Sentence SummaryChemokine-mediated signaling drives the prioritization of innate immune responses to bacterial pulmonary infection over cutaneous wound healing.HighlightsHuman laparotomy patients with pneumonia have an increased rate of incision dehiscence, and this observation can be recapitulated in mouse models of bacterial lung infections and skin wounds.Lung infection causes rapid and sustained suppression of skin wound chemokine and inflammatory cytokine production as well as leukocyte recruitment.Unique systemic shifts in the immune compartment occur with two inflammatory insults, including the cytokine/chemokine signature and the mobilization, recruitment, and phenotype of innate leukocytes.Restoration of chemokine signaling in the wounds of mice that have a lung infection results in increased neutrophil trafficking to the wound site and rescues the rate of healing.Graphical Abstract


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 321-321
Author(s):  
James Dunleavey ◽  
St Brad Croix ◽  
Nancy Emenaker ◽  
Jessica Dunleavey

Abstract Objectives We sought to develop a workflow to evaluate the anti-angiogenic potential of dietary agents in a stringent, systemic manner: 1) in vitro inhibition of angiogenesis, 2) in vivo testing of normal angiogenesis inhibition, and 3) in vivo testing of tumor prevention. Methods We used a tiered workflow for assessment of anti-angiogenic potential of dietary compounds, beginning with cell culture methods, moving to high-throughput D. rerio angiogenesis modeling and finally mouse models of angiogenesis and tumor development to identify potent dietary agents which block tumor angiogenesis. Results We identified quercetin dihydrate as an orally available inhibitor of angiogenesis and our lead candidate for further evaluation for chemoprevention of angiogenesis. Quercetin blocked in vitro sprouting angiogenesis, and displayed a dose-dependent reduction in sprouting angiogenesis in the tail regeneration model in zebrafish. Finally, quercetin implanted at reported physiologic levels blocked blood vessel growth in mouse models of angiogenesis. Conclusions We describe a workflow for systematic evaluation of dietary compounds in increasing complexity models for stringent, systematic evaluation of angiogenesis inhibition. These multi-model approaches allow for filtering of pan-assay interference compounds (PAINS) prior to in vivo screening. This workflow identified quercetin as a potent inhibitor of angiogenesis which warrants further study for chemoprevention through diet. Funding Sources National Cancer Institute Division of Cancer Prevention, National Cancer Institute Center for Cancer Research.


2021 ◽  
Vol 12 ◽  
Author(s):  
Amr Hassan ◽  
Ahmed I. Abd El Maksoud ◽  
Dalia Elebeedy ◽  
Mohammad A. Zoair ◽  
Emadeldin R. Matar

The angiogenesis process is an essential issue in tissue engineering. Zinc oxide nanorods are biocompatible metals capable of generating reactive oxygen species (ROS) that respond to induced angiogenesis through various mechanisms; however, released Zn (II) ions suppress the angiogenesis process. In this study, we fabricated green ZnO nanorods using albumin eggshell as a bio-template and investigate its angiogenic potential through chorioallantoic membrane assay and excision wound healing assay. This study demonstrated that angiogenesis and wound healing processes depend on pro-angiogenic factors as VEGF expression due to ZnO nanorods' exiting. Angiogenesis induced via zinc oxide nanorods may develop sophisticated materials to apply in the wound healing field.


2016 ◽  
Vol 48 (12) ◽  
pp. 889-896 ◽  
Author(s):  
Aksone Nouvong ◽  
Aaron M. Ambrus ◽  
Ellen R. Zhang ◽  
Lucas Hultman ◽  
Hilary A. Coller

Chronic wounds are a common and debilitating complication for the diabetic population. It is challenging to study the development of chronic wounds in human patients; by the time it is clear that a wound is chronic, the early phases of wound healing have passed and can no longer be studied. Because of this limitation, mouse models have been employed to better understand the early phases of chronic wound formation. In the past few years, a series of reports have highlighted the importance of reactive oxygen species and bacterial biofilms in the development of chronic wounds in diabetics. We review these recent findings and discuss mouse models that are being utilized to enhance our understanding of these potentially important contributors to chronic wound formation in diabetic patients.


2012 ◽  
Vol 26 (7) ◽  
pp. 1856-1864 ◽  
Author(s):  
Xiaohong Yan ◽  
Thomas R. Gardner ◽  
Michael Grieco ◽  
Sonali A. C. Herath ◽  
Joon Ho Jang ◽  
...  

2015 ◽  
Vol 130 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Dorinne Desposito ◽  
Catherine Chollet ◽  
Christopher Taveau ◽  
Vincent Descamps ◽  
François Alhenc-Gelas ◽  
...  

Kinin B2 receptor activation impairs skin wound healing in mice, in part through imbalance of keratinocyte/fibroblast proliferation. Such activation occurs in diabetes and contributes to delaying wound healing. B2 receptor blockade restores the normal wound healing pattern in mouse models of diabetes.


Science ◽  
2021 ◽  
Vol 372 (6540) ◽  
pp. eaba2374 ◽  
Author(s):  
Shamik Mascharak ◽  
Heather E. desJardins-Park ◽  
Michael F. Davitt ◽  
Michelle Griffin ◽  
Mimi R. Borrelli ◽  
...  

Skin scarring, the end result of adult wound healing, is detrimental to tissue form and function. Engrailed-1 lineage–positive fibroblasts (EPFs) are known to function in scarring, but Engrailed-1 lineage–negative fibroblasts (ENFs) remain poorly characterized. Using cell transplantation and transgenic mouse models, we identified a dermal ENF subpopulation that gives rise to postnatally derived EPFs by activating Engrailed-1 expression during adult wound healing. By studying ENF responses to substrate mechanics, we found that mechanical tension drives Engrailed-1 activation via canonical mechanotransduction signaling. Finally, we showed that blocking mechanotransduction signaling with either verteporfin, an inhibitor of Yes-associated protein (YAP), or fibroblast-specific transgenic YAP knockout prevents Engrailed-1 activation and promotes wound regeneration by ENFs, with recovery of skin appendages, ultrastructure, and mechanical strength. This finding suggests that there are two possible outcomes to postnatal wound healing: a fibrotic response (EPF-mediated) and a regenerative response (ENF-mediated).


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