Fibroblast subpopulations as accelerators of tumor progression: The role of migration stimulating factor

Schor, Seth L.

doi:10.1007/978-3-0348-9070-0_14

Cited by 14 publications

(16 citation statements)

References 60 publications

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“…The differences between paired skin and gingival fibroblasts indicated in the preceding section are consistent with a considerable literature documenting inter-site heterogeneity in fibroblast phenotype (Schor and Schor, 1987;Schor 1995). Such studies have demonstrated differences between gingival and skin fibroblasts with respect to glycosaminoglycan synthesis (Bronson et al, 1988).…”

Section: Fibroblast Heterogeneity: Implications For Connective Tissuesupporting

confidence: 84%

Subpopulations of fetal‐like gingival fibroblasts: characterisation and potential significance for wound healing and the progression of periodontal disease

et al. 1996

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Wound healing in the adult is commonly compromised by excessive scar formation. In contrast, fetal wound healing is a regenerative process characterised by the conspicuous absence of scarring. Available evidence suggests that phenotypic differences between fetal and adult fibroblasts are important determinants of these distinct modes of tissue repair. In this context, a number of groups (including our own) have documented differences between fetal and adult fibroblasts with respect to such potentially relevant characteristics as migratory activity, motogenic response to cytokines and the synthesis of motility factors, cytokines and matrix macromolecules. The oral mucosa appears to be a privileged site in the adult in that it continues to display a fetal‐like mode of wound healing. Data are presented in this review indicating that a subpopulation of gingival fibroblasts expresses several ‘fetal‐like’ phenotypic characteristics. These observations are discussed in terms of both the continued expression of a fetal‐like mode of wound healing in the oral mucosa and the possible differential involvement of distinct fibroblast subpopulations in the progression of periodontal disease.

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Section: Fibroblast Heterogeneity: Implications For Connective Tissuesupporting

confidence: 84%

Subpopulations of fetal‐like gingival fibroblasts: characterisation and potential significance for wound healing and the progression of periodontal disease

et al. 1996

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“…This phenotype was different from the invasive phenotype seen at the invasion front in SCCs. It seems reasonable to assume that the regulatory mechanisms for cell-cell, cell-ECM adhesion, and cell migration are different in non-premalignant inflammatory tissue, premalignant lesions, and carcinomas (24,31). In vitro studies might shed light on the functional significance of the alterations.…”

Section: Discussionmentioning

confidence: 99%

Can alterations in integrin and laminin‐5 expression be used as markers of malignancy?

Thorup

Reibel

Schiødt

et al. 1998

APMIS

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Development of squamous cell carcinomas (SCCs) involves alterations in the adhesive interactions in the epithelium and invasion through the basement membrane. Therefore, changes in the expression of receptors and ligands involved in cell‐cell and cell‐matrix adhesion may be essential for the transformation of a premalignant into a malignant lesion. The aim of this study was to examine if expression of specific cell adhesion molecules can be used as markers of malignant development. By immunohistochemistry, we examined the expression pattern of integrins α2β1, α3β1, α6β4 and laminin‐5 in biopsies from SCCs (n=18), premalignant lesions (leukoplakias, n=21) and non‐premalignant tissue with chronic inflammation (n=11). In poorly differentiated SCCs, patchy loss of α3β1, α6β4 and laminin‐5 expression was pronounced at the invasion front, whereas there was a tendency to increased expression of α2β1. Analogous to the SCCs, biopsies from the leukoplakias and the non‐premalignant inflammatory tissue showed alterations of the expression of α3β1 and α6β4 in the basal cell layers and of laminin‐5. However, a characteristic finding in biopsies from leukoplakias was loss of α2β1 and α3β1 in the suprabasal cells. There was no unequivocal expression of the adhesion molecules distinguishing between inflammatory tissue, premalignant, and malignant lesions.

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“…Injured epithelial cells are a major source of both cytokines and activating integrin receptors. TGF-β acts as an important factor in vascular development through the signaling of endothelial cells to pericytes (85, 86). In fact, TGF-β mutant mice and TGF-β-activated kinase mutant mice die during fetal development due to vascular defects (87–89).…”

Section: Epithelial-to-mesenchymal Transition Versus Epithelial Signamentioning

confidence: 99%

Host Responses in Tissue Repair and Fibrosis

Duffield

Lupher

Thannickal

et al. 2013

Annu. Rev. Pathol. Mech. Dis.

532

500

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Myofibroblasts accumulate in the spaces between organ structures and produce extracellular matrix (ECM) proteins, including collagen I. They are the primary “effector” cells in tissue remodeling and fibrosis. Previously, leukocyte progenitors termed fibrocytes and myofibroblasts generated from epithelial cells through epithelial-to-mesenchymal transition (EMT) were considered the primary sources of ECM-producing myofibroblasts in injured tissues. However, genetic fate mapping experiments suggest that mesenchyme-derived cells, known as resident fibroblasts, and pericytes are the primary precursors of scar-forming myofibroblasts, whereas epithelial cells, endothelial cells, and myeloid leukocytes contribute to fibrogenesis predominantly by producing key fibrogenic cytokines and by promoting cell-to-cell communication. Numerous cytokines derived from T cells, macrophages, and other myeloid cell populations are important drivers of myofibroblast differentiation. Monocyte-derived cell populations are key regulators of the fibrotic process: They act as a brake on the processes driving fibrogenesis, and they dismantle and degrade established fibrosis. We discuss the origins, modes of activation, and fate of myofibroblasts in various important fibrotic diseases and describe how manipulation of macrophage activation could help ameliorate fibrosis.

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Fibroblast subpopulations as accelerators of tumor progression: The role of migration stimulating factor

Cited by 14 publications

References 60 publications

Subpopulations of fetal‐like gingival fibroblasts: characterisation and potential significance for wound healing and the progression of periodontal disease

Subpopulations of fetal‐like gingival fibroblasts: characterisation and potential significance for wound healing and the progression of periodontal disease

Can alterations in integrin and laminin‐5 expression be used as markers of malignancy?

Host Responses in Tissue Repair and Fibrosis

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