β8 integrin and band 4.1B cooperatively regulate morphogenesis of the embryonic heart

Jung, Youn-Sang; Kissil, Joseph L.; McCarty, Joseph H.

doi:10.1002/dvdy.22513

Cited by 20 publications

(16 citation statements)

References 52 publications

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“…FITC-conjugated phalloidin was purchased from Sigma. The anti-αv integrin and anti-β8 integrin rabbit polyclonal antibodies used for immunoblotting have been described elsewhere (24, 25). Secondary antibodies were goat anti-rabbit, goat anti-chicken, goat anti-rat and goat anti-mouse, all conjugated to Alexa488 or Alexa594 (Molecular Probes).…”

Section: Methodsmentioning

confidence: 99%

Glioblastoma Angiogenesis and Tumor Cell Invasiveness Are Differentially Regulated by β8 Integrin

et al. 2011

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Glioblastoma multiforme (GBM) is a highly invasive brain tumor that develops florid microvascular proliferation and hemorrhage. However, mechanisms that favor invasion versus angiogenesis in this setting remain largely uncharacterized. Here we show that integrin β8 is an essential regulator of both GBM-induced angiogenesis and tumor cell invasiveness. Highly angiogenic and poorly invasive tumors expressed low levels of β8 integrin, whereas highly invasive tumors with limited neovascularization expressed high levels of β8 integrin. Manipulating β8 integrin protein levels altered the angiogenic and invasive growth properties of GBMs, in part reflected by a diminished activation of latent transforming growth factor βs (TGFβs), which are extracellular matrix (ECM) protein ligands for β8 integrin. Taken together, these results establish a role for β8 integrin in differential control of angiogenesis versus tumor cell invasion in GBM. Our findings suggest that inhibiting β8 integrin or TGFβ signaling may diminish tumor cell invasiveness during malignant progression and following anti-vascular therapies.

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Section: Methodsmentioning

confidence: 99%

Glioblastoma Angiogenesis and Tumor Cell Invasiveness Are Differentially Regulated by β8 Integrin

et al. 2011

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“…Integrins have been shown to regulate morphogenesis, angiogenesis, heart remodeling, and neuritogenesis. [125][126][127] For example, integrin a5 and aV were not required in endothelial cells for initial vasculogenesis and angiogenesis but they were significantly involved in the remodeling of the heart and great vessels. 126 It was also shown that b1 integrin played a critical role in skeletal myoblast response to stretch by activating the downstream effector FAK.…”

Section: Stretch Signaling Pathwaysmentioning

confidence: 99%

Mechanical Stretching for Tissue Engineering: Two-Dimensional and Three-Dimensional Constructs

Riehl

Park

Kwon

et al. 2012

Tissue Engineering Part B: Reviews

176

175

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Mechanical cell stretching may be an attractive strategy for the tissue engineering of mechanically functional tissues. It has been demonstrated that cell growth and differentiation can be guided by cell stretch with minimal help from soluble factors and engineered tissues that are mechanically stretched in bioreactors may have superior organization, functionality, and strength compared with unstretched counterparts. This review explores recent studies on cell stretching in both two-dimensional (2D) and three-dimensional (3D) setups focusing on the applications of stretch stimulation as a tool for controlling cell orientation, growth, gene expression, lineage commitment, and differentiation and for achieving successful tissue engineering of mechanically functional tissues, including cardiac, muscle, vasculature, ligament, tendon, bone, and so on. Custom stretching devices and lab-specific mechanical bioreactors are described with a discussion on capabilities and limitations. While stretch mechanotransduction pathways have been examined using 2D stretch, studying such pathways in physiologically relevant 3D environments may be required to understand how cells direct tissue development under stretch. Cell stretch study using 3D milieus may also help to develop tissue-specific stretch regimens optimized with biochemical feedback, which once developed will provide optimal tissue engineering protocols.

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“…There is increasing evidence for a role for interactions between the 4.1 proteins and integrins (22,(51)(52)(53)(54). Data in Fig.…”

Section: Discussionmentioning

confidence: 98%

A 130-kDa Protein 4.1B Regulates Cell Adhesion, Spreading, and Migration of Mouse Embryo Fibroblasts by Influencing Actin Cytoskeleton Organization

Wang

Song

et al. 2014

Journal of Biological Chemistry

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Background:The function of protein 4.1B in behaviors of motile cells remains poorly understood. Results: Deficiency of 130-kDa 4.1B resulted in impaired cell adhesion, spreading, migration, and stress fiber formation. Conclusion: Protein 4.1B plays an important role in modulating cell adhesion and motility. Significance: Our results identify a novel function for protein 4.1B and have implications for understanding the mechanisms of 4.1 function.

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β8 integrin and band 4.1B cooperatively regulate morphogenesis of the embryonic heart

Cited by 20 publications

References 52 publications

Glioblastoma Angiogenesis and Tumor Cell Invasiveness Are Differentially Regulated by β8 Integrin

Glioblastoma Angiogenesis and Tumor Cell Invasiveness Are Differentially Regulated by β8 Integrin

Mechanical Stretching for Tissue Engineering: Two-Dimensional and Three-Dimensional Constructs

A 130-kDa Protein 4.1B Regulates Cell Adhesion, Spreading, and Migration of Mouse Embryo Fibroblasts by Influencing Actin Cytoskeleton Organization

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