Conserved mechanisms of repair: from damaged single cells to wounds in multicellular tissues

Woolley, Katie; Martin, Paul

doi:10.1002/1521-1878(200010)22:10<911::aid-bies6>3.3.co;2-m

Cited by 10 publications

(16 citation statements)

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“…Upon injury, the first response of an epithelial layer is to move forward to cover the denuded area. Epithelia display two main mechanisms of motility during the wound healing response: the so-called purse-string closure and cell migration by lamellipodial crawling (18,45,48). In the first mechanism, an actomyosin cable develops at the free border of the leading cells (2).…”

mentioning

confidence: 78%

“…Thus, for the case of small circular wounds, the contraction of this ring can rapidly close the gap, similarly to the pulling of a purse string. This type of wound closure is typical of embryonic tissues (36,48), although it has also been observed in several adult tissues both in vivo and in culture (5,46). The second mechanism, observed in adult epithelia in vivo (16 -18), consists of the emission of lamellipodia by the cells at the wound border followed by the migration of the cell towards the center of the wound, utilizing similar cellular and molecular mechanisms to those of single migrating cells.…”

mentioning

confidence: 99%

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Roles of wound geometry, wound size, and extracellular matrix in the healing response of bovine corneal endothelial cells in culture

Grasso¹,

Hernández²,

Chifflet³

2007

American Journal of Physiology-Cell Physiology

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It has classically been accepted that the healing of narrow wounds in epithelia occurs by the formation of a contractile actin cable, while wide wounds are resurfaced by lamellipodia-dependent migration of border cells into the denuded area. To further investigate the general validity of this idea, we performed systematic experiments of the roles of wound geometry, wound size, and extracellular matrix (ECM) in wound healing in monolayers of bovine corneal endothelial cells, a system shown here to predominantly display any of the two healing mechanisms according to the experimental conditions. We found that, in this system, it is the absence or presence of the ECM on the wound surface that determines the specific healing mode. Our observations demonstrate that, independent of their size and geometry, wounds created maintaining the ECM heal by migration of cells into the wound area, while ECM removal from the wound surface determines the predominant formation of an actin cable. While the latter mechanism is slower, the actin cable permits the maintainance of the epithelial phenotype to a larger extent during the healing process, as also confirmed by our finding of a more conserved localization of cadherin and vinculin. We also introduce a model that simulates experimental findings about the dynamics of healing mechanisms, both for the maintenance or removal of the ECM on the wound surface. The findings of this study may contribute to the understanding of physiological and pathological aspects of epithelial wound healing and to the design of therapeutic strategies.

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confidence: 78%

mentioning

confidence: 99%

Roles of wound geometry, wound size, and extracellular matrix in the healing response of bovine corneal endothelial cells in culture

Grasso¹,

Hernández²,

Chifflet³

2007

American Journal of Physiology-Cell Physiology

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“…Another possibility is that ENaC proteins may participate in the transduction of mechanical signaling cues involved in migration (59). Evidence suggests that cell migration requires integration of multiple signaling cues, including chemical and mechanical signals, and mechanosensory elements, such as integrins, growth factor receptors, G proteins, and ion channels, have been under consideration (13,30,51).…”

Section: Discussionmentioning

confidence: 99%

ENaC proteins contribute to VSMC migration

Grifoni¹,

Gannon²,

Stec³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Vascular smooth muscle cell (VSMC) migration plays a key role in tissue repair after arterial wall injury. VSMC migration requires integration of chemical and mechanical signaling mechanisms. Recently, we showed that epithelial Na(+) channel (ENaC) proteins are expressed in VSMCs and that ENaC inhibition abolishes pressure-induced constriction in isolated artery segments. However, whether ENaC proteins play a role in VSMC migration is unknown. The goal of this study was to determine whether ENaC molecules are required for VSMC migration. Using RT-PCR, immunoblotting, and immunolabeling, we detected expression of alpha-, beta-, and gammaENaC transcripts and proteins in cultured VSMCs (SV40-LT and A10 cells). Of the three proteins, betaENaC was the most readily detected in both cell lines by immunolocalization and Western blotting. Inhibition of ENaC activity with 1 microM benzamil blunted VSMC migration associated with wound healing (40.3% at 8 h and 26.2% at 24 h) and in response to the chemotactic stimulant platelet-derived growth factor-BB (38.1%). Furthermore, silencing ENaC gene expression with small interfering RNA blunted VSMC migration. These data indicate that expression of ENaC proteins is required for normal VSMC migration and suggest a potential new role for ENaC proteins in vascular tissue repair.

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“…Intermediate filaments may be important for repair as well as for the normal development and differentiation of organs. Wounding leads to a dramatic re-organization of the cytoskeleton, since a dense cytoskeletal network is rapidly localized to the region of the cell membrane adjacent to the wound site (Woolley and Martin, 2000).…”

Section: Mechanisms Contributing To Tertiary Dentin Deposition In Patmentioning

confidence: 99%

Parallels between Tooth Development and Repair: Conserved Molecular Mechanisms following Carious and Dental Injury

Mitsiadis

Rahiotis²

2004

J Dent Res

115

108

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The reparative mechanisms that operate following carious and traumatic dental injury are critical for pulp survival and involve a series of highly conserved processes. It appears that these processes share genetic programs-linked to cytoskeletal organization, cell movement, and differentiation-that occur throughout embryogenesis. Reactionary dentin is secreted by surviving odontoblasts in response to moderate stimuli, leading to an increase in metabolic activity. In severe injury, necrotic odontoblasts are replaced by other pulp cells, which are able to differentiate into odontoblast-like cells and produce a reparative dentin. This complex process requires the collaborative efforts of cells of different lineage. The behavior of each of the contributing cell types during the phases of proliferation, migration, and matrix synthesis as well as details of how growth factors control wound cell activities are beginning to emerge. In this review, we discuss what is known about the molecular mechanisms involved in dental repair.

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Conserved mechanisms of repair: from damaged single cells to wounds in multicellular tissues

Cited by 10 publications

References 0 publications

Roles of wound geometry, wound size, and extracellular matrix in the healing response of bovine corneal endothelial cells in culture

Roles of wound geometry, wound size, and extracellular matrix in the healing response of bovine corneal endothelial cells in culture

ENaC proteins contribute to VSMC migration

Parallels between Tooth Development and Repair: Conserved Molecular Mechanisms following Carious and Dental Injury

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