Expression patterns of β1-related α integrin subunits in murine lens during embryonic development and wound healing

Barbour, Walid; Saika, Shizuya; Miyamoto, Takeshi; Ohkawa, Kousaku; Utsunomiya, Hirotoshi; Ohnishi, Yoshitaka

doi:10.1080/02713680490513137

Cited by 16 publications

(11 citation statements)

References 27 publications

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“…There are reports showing that integrin expression patterns are modulated during wound healing and those molecules are critical for re-epithelialization (Barbour et al, 2004;Reynolds et al, 2008). Thus, the involvement of integrins in galvanotaxis of fish keratocytes may provide new information for studies on wound healing.…”

Section: Journal Of Cellular Physiology C a 2 + A N D I N T E G R I Nmentioning

confidence: 99%

The involvement of Ca²⁺ and integrins in directional responses of zebrafish keratocytes to electric fields

Huang

Cormie

Messerli

et al. 2008

Journal Cellular Physiology

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Many cells respond directionally to small DC electrical fields (EFs) by an unknown mechanism, but changes in intracellular Ca(2+) are widely assumed to be involved. We have used zebrafish (Danio rerio) keratocytes in an effort to understand the nature of the EF-cell interaction. We find that the adult zebrafish integument drives substantial currents outward through wounds produced by scale removal, establishing that keratocytes near the wound will experience endogenous EFs. Isolated keratocytes in culture turn toward the cathode in fields as small as 7 mV mm(-1), and the response is independent of cell size. Epidermal sheets are similarly sensitive. The frequency of intracellular Ca(2+) spikes and basal Ca(2+) levels were increased by EFs, but the spikes were not a necessary aspect of migration or EF response. Two-photon imaging failed to detect a pattern of gradients of Ca(2+) across the lamellipodia during normal or EF-induced turning but did detect a sharp, stable Ca(2+) gradient at the junction of the lamellipodium and the cell body. We conclude that gradients of Ca(2+) within the lamellipodium are not required for the EF response. Immunostaining revealed an anode to cathode gradient of integrin beta1 during EF-induced turning, and interference with integrin function attenuated the EF response. Neither electrophoretic redistribution of membrane proteins nor asymmetric perturbations of the membrane potential appear to be involved in the EF response, and we propose a new model in which hydrodynamic forces generated by electro-osmotic water flow mediate EF-cell interactions via effects on focal adhesions.

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Section: Journal Of Cellular Physiology C a 2 + A N D I N T E G R I Nmentioning

confidence: 99%

The involvement of Ca²⁺ and integrins in directional responses of zebrafish keratocytes to electric fields

Huang

Cormie

Messerli

et al. 2008

Journal Cellular Physiology

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“…This study emphasizes that β1 integrins function both in the protection of the epithelial phenotype and in the emergence of a mesenchymal phenotype. While the identity of the individual β1 integrins in these opposing processes is unknown, there is evidence for upregulation of α2β1 and α5β1 integrins in lens disease (Barbour et al, 2004; Zuk and Hay, 1994). Misexpression of α5 integrin also is correlated with cataract formation and fiber cell dysmorphogenesis.…”

Section: Integrins and Lens Diseasementioning

confidence: 99%

Integrins in lens development and disease

Walker

Menko

2009

Experimental Eye Research

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Integrins are the major cell surface receptors for proteins in the extracellular matrix. These receptors form major cell signaling centers that are bidirectional, communicating messages between the cell and its environment. They are a large receptor family, with members well-known to regulate cellular processes essential to both development and disease. In this review we examine the literature regarding integrins in the lens. Here we cover integrin function in lens cell differentiation, in the development of the lens and in protection of the lens epithelial cell phenotype. In addition, we analyze the role of integrins in the progression of lens fibrotic diseases, focusing particularly on integrin regulation of TGFβ signaling pathways in Posterior Capsule Opacification (PCO) and Anterior Subcapsular Cataract (ASC).

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“…34,35 Specifically, beta1-integrins are localized at the basal surface of the anterior epithelium and in the basal membrane complex, 36 which all are areas where the lens cells contact the capsule, and mediate the attachment of fiber cells to the capsule. 33 Beta1-integrins also are detected at the apicalapical interaction between the epithelium and the fibers, where their role is unclear in the absence of matrix.…”

mentioning

confidence: 99%

Integrin-Linked Kinase Deletion in the Developing Lens Leads to Capsule Rupture, Impaired Fiber Migration and Non-Apoptotic Epithelial Cell Death

Cammas

Wolfe

Choi

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. The lens is a powerful model system to study integrinmediated cell-matrix interaction in an in vivo context, as it is surrounded by a true basement membrane, the lens capsule. To characterize better the function of integrin-linked kinase (ILK), we examined the phenotypic consequences of its deletion in the developing mouse lens.METHODS. ILK was deleted from the embryonic lens either at the time of placode invagination using the Le-Cre line or after initial lens formation using the Nestin-Cre line.RESULTS. Early deletion of ILK leads to defects in extracellular matrix deposition that result in lens capsule rupture at the lens vesicle stage (E13.5). If ILK was deleted at a later time-point after initial establishment of the lens capsule, rupture was prevented. Instead, ILK deletion resulted in secondary fiber migration defects and, most notably, in cell death of the anterior epithelium (E18.5 -P0). Remarkably, dying cells did not stain positively for terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) or activated-caspase 3, suggesting that they were dying from a non-apoptotic mechanism. Moreover, cross to a Bax fl/fl /Bak -/-mouse line that is resistant to most forms of apoptosis failed to promote cell survival in the ILKdeleted lens epithelium. Electron microscopy revealed the presence of numerous membranous vacuoles containing degrading cellular material.CONCLUSIONS. Our study reveals a role for ILK in extracellular matrix organization, fiber migration, and cell survival. Furthermore, to our knowledge we show for the first time that ILK disruption results in non-apoptotic cell death in vivo. (Invest Ophthalmol Vis Sci. 2012;53:3067-3081)

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Expression patterns of β1-related α integrin subunits in murine lens during embryonic development and wound healing

Cited by 16 publications

References 27 publications

The involvement of Ca²⁺ and integrins in directional responses of zebrafish keratocytes to electric fields

The involvement of Ca²⁺ and integrins in directional responses of zebrafish keratocytes to electric fields

Integrins in lens development and disease

Integrin-Linked Kinase Deletion in the Developing Lens Leads to Capsule Rupture, Impaired Fiber Migration and Non-Apoptotic Epithelial Cell Death

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Expression patterns of β1-related α integrin subunits in murine lens during embryonic development and wound healing

Cited by 16 publications

References 27 publications

The involvement of Ca2+ and integrins in directional responses of zebrafish keratocytes to electric fields

The involvement of Ca2+ and integrins in directional responses of zebrafish keratocytes to electric fields

Integrins in lens development and disease

Integrin-Linked Kinase Deletion in the Developing Lens Leads to Capsule Rupture, Impaired Fiber Migration and Non-Apoptotic Epithelial Cell Death

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The involvement of Ca²⁺ and integrins in directional responses of zebrafish keratocytes to electric fields

The involvement of Ca²⁺ and integrins in directional responses of zebrafish keratocytes to electric fields