Matrilysin-1 (MMP7) cleaves galectin-3 and inhibits wound healing in intestinal epithelial cells

Puthenedam, Manjula; Wu, Feng; Shetye, Alysha; Michaels, Alex D.; Rhee, Ki Jong; Kwon, John H.

doi:10.1002/ibd.21443

Cited by 61 publications

(53 citation statements)

References 39 publications

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“…Galectins in oysters, such as Crassostrea virginica [9], Crassostrea gigas [10] and scallop Argopectens irradians [11], have been reported to play roles in immune response. Besides, galectins are implicated in epithelial cell adhesion and wound repair [6,12,13]. In the case of P. fucata, the cDNAs of a galectin with multiple carbohydrate-recognition domains, and a tandem-repeat galectin contained two tandem carbohydrate recognition domains have been cloned, and the mRNA expression levels were up-regulated after bacterial invasion [4,5].…”

Section: Introductionmentioning

confidence: 99%

DNA methylation is associated with expression level changes of galectin gene in mantle wound healing process of pearl oyster, Pinctada fucata

Huang

Guan

et al. 2015

Fish & Shellfish Immunology

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Section: Introductionmentioning

confidence: 99%

DNA methylation is associated with expression level changes of galectin gene in mantle wound healing process of pearl oyster, Pinctada fucata

Huang

Guan

et al. 2015

Fish & Shellfish Immunology

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“…Neutrophil activation by galectin-3, enhanced after extravasation of the cells into tissue, may contribute to tissue destruction by the production of toxic oxygen radicals and cytokines and the release of neutrophil proteases (15,22,25). Another mechanism could involve the cleavage of galectin-3 by SspB (as shown here) and by neutrophil-released metalloproteases and serine proteases (25,27,28), impairing the production of immunomodulatory ROS, as well as galectin-3-dependent opsonophagocytic processes, possibly resulting in impaired infection control and aggravated tissue destruction (14,15,24). Furthermore, protease-cleaved galectin-3 (CRD) may possibly have proinflammatory effects per se, contributing to inflammatory tissue damage, as seen in other disease models (51)(52)(53)(54).…”

Section: Discussionmentioning

confidence: 70%

“…This N-domain is essential for oligomerization of galectin-3 and for many of the galectin-3-induced effects in inflammation (14,22,26). There are proteases known to cleave galectin-3; human neutrophil elastase and matrix metalloproteinases-2, -7, and -9 can proteolytically process the lectin (25,27,28), a feature shared by proteases from protozoa (29) and bacteria (26,30,31). Hence, N-terminal cleavage of galectin-3 could be suggested as a regulatory mechanism in infection and inflammation.…”

mentioning

confidence: 99%

Galectin-3 Is a Target for Proteases Involved in the Virulence of Staphylococcus aureus

Elmwall

Kwieciński

et al. 2017

Infect Immun

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Staphylococcus aureus is a major cause of skin and soft tissue infection. The bacterium expresses four major proteases that are emerging as virulence factors: aureolysin (Aur), V8 protease (SspA), staphopain A (ScpA), and staphopain B (SspB). We hypothesized that human galectin-3, a ␤-galactoside-binding lectin involved in immune regulation and antimicrobial defense, is a target for these proteases and that proteolysis of galectin-3 is a novel immune evasion mechanism. Indeed, supernatants from laboratory strains and clinical isolates of S. aureus caused galectin-3 degradation. Similar proteolytic capacities were found in Staphylococcus epidermidis isolates but not in Staphylococcus saprophyticus. Galectin-3-induced activation of the neutrophil NADPH oxidase was abrogated by bacterium-derived proteolysis of galectin-3, and SspB was identified as the major protease responsible. The impact of galectin-3 and protease expression on S. aureus virulence was studied in a murine skin infection model. In galectin-3 ϩ/ϩ mice, SspB-expressing S. aureus caused larger lesions and resulted in higher bacterial loads than protease-lacking bacteria. No such difference in bacterial load or lesion size was detected in galectin-3 Ϫ/Ϫ mice, which overall showed smaller lesion sizes than the galectin-3 ϩ/ϩ animals. In conclusion, the staphylococcal protease SspB inactivates galectin-3, abrogating its stimulation of oxygen radical production in human neutrophils and increasing tissue damage during skin infection.

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“…MMP7 levels are high in the blood of patients with pancreatic adenocarcinoma. In mice STAT3 dictates the pace of pancreas adenocarcinoma cell divisions and MMP7 expression (208,209). The ZIP4 protein (zink transporter protein; Zrt/Irtlike protein: zink/iron responsive transporter) works with IL6 and STAT in stimulating pancreatic cancer cell growth; silencing it with shRNAs inhibits cancer cell growth (210,211).…”

Section: Papillary Carcinoma Cells Of the Thyroid Release Inflammatormentioning

confidence: 99%

Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review)

Sinkovics

2011

Int J Oncol

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Abstract. In some inflammasomes tumor cells are generated. The internal environment of the inflammasome is conducive to the induction of malignant transformation. Epigenetic changes initiate this process. The subverted stromal connective tissue cells act to promote and sustain the process of malignant trans formation. In its early stages, the premalignant cells depend on paracrine circuitries for the reception of growth factors. The ligands are derived from the connective tissue, and the receptors are expressed on the recipient premalignant cells. The initial events are not a direct attack on the protooncogenes, and thus it may be entirely reversible. Epigenetic processes of hypermethylation of the genes at the promoters of tumor suppressor genes (to silence them), and deacetylation of the histones aimed at the promoters of protooncogenes (to activate them) are ongoing. A large number of short RNA sequences (interfering, micro, short hairpin, noncoding RNAs) silence tumor suppressor genes, by neutralizing their mRNAs. In a serial sequence oncogenes undergo amplifications, pointmutations, translocations and fusions. In its earliest stage, the process is reversible by demethylation of the silenced suppressor gene promoters (to reactivate them), or reacetylation of the histones of the oncogene promoters, thus deactivating them. The external administration of histone deacetylase inhibitors usually leads to the restoration of histone acetylation. In time, the uncorrected processes solidify into constitutive and irreversible gene mutations. Some of the pathogens inducing inflammations with consquential malignant transformation contain oncogenic gene sequences (papilloma viruses, EpsteinBarr virus, Kaposi's sarcomaassociated herpesvirus, hepatitis B and C viruses, Merkel cell polyoma virus, Helicobacter pylori, enterotoxigenic Bacteroides fragilis). These induced malignancies may be multifocal. Other pathogens are devoid of any known oncogenic genomic sequences (mycoplasma vavcarcinogenesis, chlamydia MALTlymphoma genesis). In these cases the host's inflammatory reactions induce the malignant transformation in serial sequences of gene alterations initiated by hypoxia and reactive oxygen and nitrogen species generation. Carcinogenic intrinsic inflammatory processes endogenously initiated without a pathogen are recognized. Chronic inflammatory processes signal the RNA/DNA complex. In response, the DNA may revert into its ancient primordial 'immortal' format, which the clinics recognize as 'oncogenesis'. The DNA remains the ultimate master of bioengineering in order to sustain life. A discussion on the most versatile and resistant primordial RNA/ DNA complex and the pre, proto, and unicellular world in which they coexisted is included. Contents1. Pathogens without oncogenic genomic sequences activating cellular oncogenes 2. The inflammasome 3. Tumor cell colonies generated in the inflammasomes 4. Pathogens with potentially oncogenic genomic sequences 5. Mechanisms of inflammatory carcinogenesis Pathogens without oncogenic...

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Matrilysin-1 (MMP7) cleaves galectin-3 and inhibits wound healing in intestinal epithelial cells

Cited by 61 publications

References 39 publications

DNA methylation is associated with expression level changes of galectin gene in mantle wound healing process of pearl oyster, Pinctada fucata

DNA methylation is associated with expression level changes of galectin gene in mantle wound healing process of pearl oyster, Pinctada fucata

Galectin-3 Is a Target for Proteases Involved in the Virulence of Staphylococcus aureus

Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review)

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