Stimulation of the chemotactic migration of human fibroblasts by transforming growth factor beta.

Postlethwaite, Arnold E.; Keski‐Oja, Jorma; Moses, Harold L.; Kang, Andrew H.

doi:10.1084/jem.165.1.251

Cited by 727 publications

(317 citation statements)

References 14 publications

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“…Furthermore, it has been demonstrated that there is ongoing proteolytic enzyme activity in prolapsed discs [19]. PDGF stimulates collagenase production in fibroblasts [29] and has a chemotactic effect on them [22]. Our results may suggest a possible role for PDGF in regulation of proteolysis including in DHT.…”

Section: Discussionsupporting

confidence: 51%

“…DHT contains vascular ingrowth promoting granulation tissue formation [14,17], PDGF is a potent chemotactic agent for fibroblasts [22] and it induces cellular growth of fibroblasts and stimulates their collagenase production [29]. PDGF is liberated from alpha-granules of platelets and macrophages [26,29].…”

Section: Discussionmentioning

confidence: 99%

“…It stimulates the growth of vascular endothelial cells [26] and fibroblasts [29]. It also acts as a chemotactic signal for fibroblasts, even at very low concentrations [22]. In cartilage it has been demonstrated to increase the level of intracellular free calcium ions in chondrocytes [9].…”

Section: Introductionmentioning

confidence: 99%

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Platelet-derived growth factor and vascular endothelial growth factor expression in disc herniation tissue: an immunohistochemical study

et al. 1997

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Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

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Platelet-derived growth factor and vascular endothelial growth factor expression in disc herniation tissue: an immunohistochemical study

et al. 1997

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“…We have recently shown that TGF-,B1 administered over a protracted period of time can significantly suppress the proliferative activity in the small intestinal crypts, the effect being particularly pronounced in the stem cell region . In addition, TGF-ps can have the opposite effect on some cell types and act as indirect mitogens, particularly for mesenchymal cell types, and exert effects on chemotaxis and on the synthesis and degradation of extracellular matrix proteins (Ignotz and Massague 1986;Posthlethwaite et al, 1987;Wahl et al, 1987;Roberts and Sporn, 1991).…”

Section: Discussionmentioning

confidence: 99%

Pretreatment with transforming growth factor beta-3 protects small intestinal stem cells against radiation damage in vivo

Potten

Booth²,

Haley³

1997

Br J Cancer

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Summary The gastrointestinal tract, with its rapid cell replacement, is sensitive to cytotoxic damage and can be a site of dose-limiting toxicity in cancer therapy. Here, we have investigated the use of one growth modulator to manipulate the cell cycle status of gastrointestinal stem cells before cytotoxic exposure to minimize damage to this normal tissue. Transforming growth factor beta-3 (TGF-,3), a known inhibitor of cell cycle progression through G,, was used to alter intestinal crypt stem cell sensitivity before 12-16 Gy of gamma irradiation, which was used as a model cytotoxic agent. Using a crypt microcolony assay as a measure of functional competence of gastrointestinal stem cells, it was shown that the administration of TGF-P3 over a 24-h period before irradiation increased the number of surviving crypts by four-to six-fold.To test whether changes in crypt survival are reflected in the well-being of the animal, survival time analyses were performed. After 14.5 Gy of radiation, only 35% of the animals survived within a period of about 12 days, while prior treatment with TGF-,B3 provided significant protection against this early gastrointestinal animal death, with 95% of the treated animals surviving for greater than 30 days.

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“…TGF-β1 enhances the synthesis of collagens and fibronectin and the formation of the extracellular matrix in vivo [22]. TGF-β1 is also a chemoattractant for fibroblasts and monocytes, and may thus stimulate the migration of cells to the injured area [20]. Its relationship to endothelial cells seems to be contradictory, as it inhibits endothelial cell proliferation [7] and migration [2] in vitro, but it has been reported to stimulate microvessel formation in vivo [21].…”

Section: Transforming Growth Factor-β1mentioning

confidence: 99%

Cytokines and growth factors in the protruded intervertebral disc of the lumbar spine

et al. 2002

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IntroductionThe pathogenetic mechanism of low back pain and nerve root damage in lumbar disc herniation is the subject of ongoing debate. In particular, given that the mechanicalischaemic hypothesis alone cannot explain the cause-effect relationship between disc degeneration and neurological impairment, a biochemical mechanism is likely to be involved. It has recently been demonstrated that the autologous nucleus pulposus can induce histological and functional changes in spinal nerve roots when applied epidurally [17]. Cells of the nucleus pulposus can produce prostaglandin E2, interleukin-1 and interleukin-6 (IL-6) [31], phospholipase A2 [26], and growth factors like fibroblast-like growth factor (FGF) [32] and insulin-like growth factor-1 (IGF-1) [18]. These factors are known to control cell metabolism and to promote inflammatory processes. Moreover, recent studies suggest a critical role for IL-6 and its receptor in the modulation of pain [8]. The mechanisms of action underlying the possible effect of these factors on spinal nerve root structure and function are, however, still unknown. In addition, the fact that nerve roots differ from peripheral nerves in their anatomical, biomechanical, and physiological properties prevents extrapolation from the extensive literature and the numerous experimental models of peripheral nerve compression to the pathophysiology of root injury [5,23,25]. The working hypothesis of the present study is that transforming growth factor-β1 (TGF-β1), IGF-1, IL-6 and IL-6-receptor (IL-6R) can be produced at the site of herniation. This hypothesis was immunohistochemically explored by analysing normal and protruded intervertebral disc tissue for these factors.Abstract Nerve root irritation induced by factors produced by the intervertebral disc may play a crucial role in the pathophysiology of sciatic pain production. In this study we used immunohistochemistry to investigate the presence of transforming growth factor-β1 (TGF-β1), insulinlike growth factor-1 (IGF-1), interleukin-6 (IL-6), IL-6-receptor (IL-6R) and fibronectin in lumbar disc bioptic specimens from 30 patients with disc herniation (protrusion type). Chondrocytes of herniated discs stained positive for TGF-β1, IGF-1, IL-6 and fibronectin. We demonstrated for the first time the presence of IL-6-R in the chondrocytes of herniated tissue. Specimens from autoptic healthy tissue were used as controls. In these sections no immunoreaction for TGF-β1, IL-6, or IL-6R was found, while they expressed IGF-1 and fibronectin, but in lower quantities than herniated discs. These results demonstrated the production of factors such as TGF-β1, IGF-1, IL-6, IL-6R and fibronectin at the site of lumbar disc herniation.

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Stimulation of the chemotactic migration of human fibroblasts by transforming growth factor beta.

Cited by 727 publications

References 14 publications

Platelet-derived growth factor and vascular endothelial growth factor expression in disc herniation tissue: an immunohistochemical study

Platelet-derived growth factor and vascular endothelial growth factor expression in disc herniation tissue: an immunohistochemical study

Pretreatment with transforming growth factor beta-3 protects small intestinal stem cells against radiation damage in vivo

Cytokines and growth factors in the protruded intervertebral disc of the lumbar spine

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