A novel mechanism in wound healing: Laminin 332 drives MMP9/14 activity by recruiting syndecan-1 and CD44

Michopoulou, Anna; Montmasson, Marine; Garnier, Cécile; Lambert, Elise; Dayan, Guila; Rousselle, Patricia

doi:10.1016/j.matbio.2020.06.004

Cited by 29 publications

(31 citation statements)

References 80 publications

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“…Additionally, knockout α3 or β4 integrin both lead to changes to LM332 organisation, clearly indicating a direct role for FAs and HD in defining LM332 patterning (deHart et al, 2003;Sehgal et al, 2006). This model also supports the MMP activity increase: although we observed a large overall increase in MMP activity, this could be achieved through a modest initial effect as feedback from MMP-induced release of LMα3 LG4/5 has been shown to drive further MMP activation (Momota et al, 2005;Michopoulou et al, 2020).…”

Section: Discussionsupporting

confidence: 78%

Laminin N-terminus α31 regulates keratinocyte adhesion and migration through modifying the organisation and proteolytic processing of laminin 332

Troughton

Iorio

Shaw

et al. 2019

Preprint

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Highlights LaNt 31 is a new mediator of laminin-dependent processes. LaNt 31 codistributes and is deposited with laminin 332 in the extracellular matrix of epithelial cells. Increased LaNt 31 expression leads to changes in laminin 332 organisation into tight clusters compared with broad tracks.  Epithelial cells expressing increased LaNt 31 exhibit early hemidesmosome maturation and mislocalization of focal adhesion complexes.  LaNt 31 overexpression decreases scratch wound closure rates and single cell migration rates of epithelial keratinocytes which is rescues through the provision of a preformed matrix. This manuscript identifies a new way in which laminin deposition and organisation is controlled, via LaNt α31. Specifically, these data demonstrate that this relatively unstudied laminin-gene splice isoform, induces the formation of laminin 332 clusters during times of new matrix synthesis, leading to changes in cell-matrix adhesion and behaviour. Abbreviations LM, laminin, hTCEpi, human telomerase reverse transcriptase immortalised corneal epithelial cells, LN, laminin N-terminal domain, LaNt, laminin N-terminus protein, HD, hemidesmosome, FA, focal adhesion, HaCaT, human adult low calcium high temperature epidermal keratinocytes, ECM, extracellular matrix, BM, basement membrane, eGFP, enhanced green fluorescent protein, IP, immunoprecipitation, IB, immunoblot, LE, laminin-type epidermal growth factor-like domain, LG, laminin globular domain, TIRF, total internal reflection microscopy.

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Section: Discussionsupporting

confidence: 78%

Laminin N-terminus α31 regulates keratinocyte adhesion and migration through modifying the organisation and proteolytic processing of laminin 332

Troughton

Iorio

Shaw

et al. 2019

Preprint

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“…Both cell lines were grown in Dulbecco's modified Eagle medium (DMEM) supplemented with 1% L-glutamine and 10% of fetal calf serum at 37°C with 5% CO2 atmosphere. Normal human keratinocytes (NHK) cultures were established from foreskin after dermal-epidermal dissociation with 0.05% trypsin and 0.01% ethylenediaminetetraacetic acid (EDTA) in phosphate-buffered saline (PBS), pH 7.4 and grown in supplemented keratinocyte growth medium containing 0.15 mM CaCl2 (KBM-2 BulletKit, Lonza Biosciences, Basel, Switzerland) as previously described (38). NHK were used between passages 1-3.…”

Section: Methodsmentioning

confidence: 99%

Incidence of an intracellular multiplication niche amongstAcinetobacter baumanniiclinical isolates

Rubio

Gagné

Debruyne

et al. 2021

Preprint

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The spread of antibiotic resistant Acinetobacter baumannii poses a significant threat to public health worldwide. This nosocomial bacterial pathogen can be associated with life-threatening infections, particularly in intensive care units. A. baumannii is mainly described as an extracellular pathogen with restricted survival within cells. This study shows that a subset of A. baumannii clinical isolates extensively multiply within non-phagocytic immortalized and primary cells, without the induction of apoptosis, and with bacterial clusters visible up to 48 hours after infection. This phenotype was observed for the A. baumannii C4 strain associated with high mortality in a hospital outbreak, and the A. baumannii ABC141 strain which wasn't isolated from an infection site but was found to be hyperinvasive. Intracellular multiplication of these A. baumannii strains occurred within spacious single membrane-bound vacuoles, labeled with the lysosomal associate membrane protein (LAMP1). However, these compartments excluded lysotracker, an indicator of acidic pH, suggesting that A. baumannii can divert its trafficking away from the lysosomal degradative pathway. These compartments were also devoid of autophagy features. A high-content microscopy screen of 43 additional A. baumannii clinical strains highlighted various phenotypes: (1) the majority of strains remained extracellular, (2) a significant proportion was capable of invasion and limited persistence, and (3) two strains efficiently multiplied within LAMP1-positive vacuoles, one of which was also hyperinvasive. These data identify an intracellular niche for specific A. baumannii clinical strains that enables extensive multiplication in an environment protected from host immune responses and out of reach from many antibiotics.

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“…In addition, the DEJ provides a highly dynamic microenvironment to the keratinocytes by participating in epidermal renewal under physiological conditions and taking part in repair processes during skin healing [13][14][15][16]. In both scenarios, the DEJ serves as an adhesive scaffold, and its constituents may be part of signaling events that vary depending on maturation processes driven by ECM-modifying enzymes [17,18].…”

Section: Introductionmentioning

confidence: 99%

The Human Epidermal Basement Membrane: A Shaped and Cell Instructive Platform That Aging Slowly Alters

Roig-Rosello

Rousselle

2020

Biomolecules

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One of the most important functions of skin is to act as a protective barrier. To fulfill this role, the structural integrity of the skin depends on the dermal-epidermal junction—a complex network of extracellular matrix macromolecules that connect the outer epidermal layer to the underlying dermis. This junction provides both a structural support to keratinocytes and a specific niche that mediates signals influencing their behavior. It displays a distinctive microarchitecture characterized by an undulating pattern, strengthening dermal-epidermal connectivity and crosstalk. The optimal stiffness arising from the overall molecular organization, together with characteristic anchoring complexes, keeps the dermis and epidermis layers extremely well connected and capable of proper epidermal renewal and regeneration. Due to intrinsic and extrinsic factors, a large number of structural and biological changes accompany skin aging. These changes progressively weaken the dermal–epidermal junction substructure and affect its functions, contributing to the gradual decline in overall skin physiology. Most changes involve reduced turnover or altered enzymatic or non-enzymatic post-translational modifications, compromising the mechanical properties of matrix components and cells. This review combines recent and older data on organization of the dermal-epidermal junction, its mechanical properties and role in mechanotransduction, its involvement in regeneration, and its fate during the aging process.

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A novel mechanism in wound healing: Laminin 332 drives MMP9/14 activity by recruiting syndecan-1 and CD44

Cited by 29 publications

References 80 publications

Laminin N-terminus α31 regulates keratinocyte adhesion and migration through modifying the organisation and proteolytic processing of laminin 332

Laminin N-terminus α31 regulates keratinocyte adhesion and migration through modifying the organisation and proteolytic processing of laminin 332

Incidence of an intracellular multiplication niche amongstAcinetobacter baumanniiclinical isolates

The Human Epidermal Basement Membrane: A Shaped and Cell Instructive Platform That Aging Slowly Alters

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