Regulation of matrix metalloproteinases in a model of colonic wound healing in a rabbit

2001 ◽  
Vol 44 (12) ◽  
pp. 1857-1866 ◽  
Author(s):  
Katherine R. L. Shaper ◽  
Felicity J. Savage ◽  
Rosalind M. Hembry ◽  
Paul B. Boulos

2001 ◽  
Vol 12 (5) ◽  
pp. 373-398 ◽  
Author(s):  
Bjorn Steffensen ◽  
Lari Häkkinen ◽  
Hannu Larjava

During wound-healing, cells are required to migrate rapidly into the wound site via a proteolytically generated pathway in the provisional matrix, to produce new extracellular matrix, and, subsequently, to remodel the newly formed tissue matrix during the maturation phase. Two classes of molecules cooperate closely to achieve this goal, namely, the matrix adhesion and signaling receptors, the integrins, and matrix-degrading and -processing enzymes, the matrix metalloproteinases (MMPs). There is now substantial experimental evidence that blocking key molecules of either group will prevent or seriously delay wound-healing. It has been known for some time now that cell adhesion by means of the integrins regulates the expression of MMPs. In addition, certain MMPs can bind to integrins or other receptors on the cell surface involved in enzyme activation, thereby providing a mechanism for localized matrix degradation. By proteolytically modifying the existing matrix molecules, the MMPs can then induce changes in cell behavior and function from a state of rest to migration. During wound repair, the expression of integrins and MMPs is simultaneously up-regulated. This review will focus on those aspects of the extensive knowledge of fibroblast and keratinocyte MMPs and integrins in biological processes that relate to wound-healing.



2021 ◽  
Vol 17 (6) ◽  
pp. 1160-1169
Author(s):  
Zhiyong Zhang ◽  
Xin Zhang

Despite the antibacterial, and anti-inflammatory properties of curcumin (C), its effect on wound healing, especially in the colorectal, is ambiguous. Moreover, due to the hydrophobic properties of C, its use is limited. Therefore, to reduce the bioavailability challenge and improve the transfer to colon area, we designed a C-alginate-based nano-micelle (C-A-NM). After fabrication of C-A-NM (55.5 nm) and physicochemical studies with the TEM, DLS and XRD, the C release rate based on gastrointestinal state was evaluated. Furthermore, the effects of C-A-NM on the survival of HCT-8 cells at 24 and 48 hours by MTT method and its antibacterial effects were also evaluated. To explain the effects of wound healing in rats, in addition to colonoscopy on the 14th-day, the repaired tissue on the 7th and 14th days were examined by Hematoxylin and Eosin method. Also, for evaluating wound healing in the colon, the protein/collagen concentration, and TGFβ1/NFκB gene expression were determined. The results of C cumulative release showed that the NM allows the drug to be loaded in the colon in a favourable manner. Also, the toxicity outputs revealed that C-A-NM at a concentration of 7.5 mg had no negative effects on cell viability. While the activity of Staphylococcus aureus, Pseudomonas aeruginosa and Escherichia coli, bacteria decreased based on the minimum inhibitory concentration value with 153, 245 and 319 (μg/mL). The use of C-A-NM not only increases protein and collagen in damaged sites, but also increases TGFβ1 expression in contrast to NFκB. Based on these results, and the results of histopathology and colonoscopy, it was found that C-A-NM accelerates the healing of damaged areas. Overall, the results show that the use of C-A-NM can significantly accelerate the healing of wounds in the gastrointestinal tract based on collagen induction and reduced bacterial activity.



1992 ◽  
Vol 24 (5) ◽  
pp. 283-290 ◽  
Author(s):  
F. Vaxman ◽  
S. Olender ◽  
H. Maldonado ◽  
S. Randriamananjo ◽  
G. Chalkiadakis ◽  
...  


2003 ◽  
Vol 77 (6) ◽  
pp. 653-664 ◽  
Author(s):  
Julie T Daniels ◽  
Gerd Geerling ◽  
Robert A Alexander ◽  
Gillian Murphy ◽  
Peng T Khaw ◽  
...  


2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Sandra Matabi Ayuk ◽  
Heidi Abrahamse ◽  
Nicolette Nadene Houreld

The integration of several cellular responses initiates the process of wound healing. Matrix Metalloproteinases (MMPs) play an integral role in wound healing. Their main function is degradation, by removal of damaged extracellular matrix (ECM) during the inflammatory phase, breakdown of the capillary basement membrane for angiogenesis and cell migration during the proliferation phase, and contraction and remodelling of tissue in the remodelling phase. For effective healing to occur, all wounds require a certain amount of these enzymes, which on the contrary could be very damaging at high concentrations causing excessive degradation and impaired wound healing. The imbalance in MMPs may increase the chronicity of a wound, a familiar problem seen in diabetic patients. The association of diabetes with impaired wound healing and other vascular complications is a serious public health issue. These may eventually lead to chronic foot ulcers and amputation. Low intensity laser irradiation (LILI) or photobiomodulation (PBM) is known to stimulate several wound healing processes; however, its role in matrix proteins and diabetic wound healing has not been fully investigated. This review focuses on the role of MMPs in diabetic wound healing and their interaction in PBM.



2002 ◽  
Vol 110 (3) ◽  
pp. 801-811 ◽  
Author(s):  
Ziv M. Peled ◽  
Eric D. Phelps ◽  
Dawn L. Updike ◽  
James Chang ◽  
Thomas M. Krummel ◽  
...  






2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e24074-e24074
Author(s):  
Nikola Besic ◽  
Katja Goricar ◽  
Petra Piber ◽  
Neza Vavpetic ◽  
Vita Dolzan ◽  
...  

e24074 Background: Matrix metalloproteinases (MMPs) are zinc-containing endopeptidases that are involved in tissue remodeling. They can regulate interactions of cells with extracellular matrix and can play a role in wound healing. High levels of metalloproteinases have been correlated with significantly delayed wound healing in wounds of a variety of etiologies. The aim of our present study was to evaluate the association of MMP9 and MMP14 genetic polymorphisms with long-term complications of surgical treatment in breast cancer patients. Methods: The study included 99 breast cancer patients treated with either 75 or 37.5 mg of tramadol for pain relief after axillary breast cancer surgery as part of a randomized clinical trial KCT 04/2015-DORETAonko/si at Institute of Oncology Ljubljana. All patients were genotyped for MMP9 polymorphisms rs2250889, rs17577, rs17576, and rs20544 as well as MMP14 rs1042703, rs1042704, and rs743257. The association of genetic factors with long-term complications was evaluated using logistic regression. Results: One year after surgery, 24 (24.2%) patients had lymphedema, 25 (25.3%) experienced neuropathic pain and 21 (21.1%) experienced chronic pain. Carriers of polymorphic MMP9 rs2250889 allele experienced significantly more lymphedema compared to carriers of two wild-type alleles (OR = 3.45, 95% CI = 1.10-10.84, P = 0.034), even after adjustment for tramadol dose (OR = 3.76, 95% CI = 1.16-12.18, P = 0.027). Carriers of polymorphic MMP14 rs1042704 allele experienced more neuropathic pain compared to carriers of two wild-type alleles (OR = 3.21, 95% CI = 1.26-8.20, P = 0.015), even after adjustment for tramadol dose (OR = 3.80, 95% CI = 1.42-10.17, P = 0.008). Conclusions: MMP genetic variability was associated with long-term complications after axillary surgery in breast cancer patients, suggesting that MMPs may have an important role as modulators of wound healing.



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