Transforming growth factor-beta (TGFβ) is chemotactic for human monocytes and induces their expression of angiogenic activity

Wiseman, David M.; Polverini, Peter J.; Kamp, David W.; Leibovich, Samuel

doi:10.1016/s0006-291x(88)80319-x

Cited by 215 publications

(94 citation statements)

References 20 publications

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“…Some, but not all, of the events can be ascribed to the direct activities of TGF0. For example, TGFS has been shown to be approximately three orders of magnitude more potent than C5a as a chemoattractant for human monocytes (35,36), and as shown in the present study, TGFal, TGF02, and rTGF-(31 are also chemotactic for rat monocytes. Thus, it appears likely that the mononuclear cell infiltration seen in the synovium after i.a.…”

Section: Resultssupporting

confidence: 81%

“…Our next series of experiments, therefore, focused on delineating in vitro the mechanisms whereby TGF0 might be mediating these tissue responses. Natural TGFf31, recently shown to be a potent chemoattractant for human peripheral blood monocytes (35,36) was assayed for its ability to induce rat monocyte-macrophage chemotaxis in an in vitro assay in parallel with TGFfl2 and the recombinant form ofTGFf31. TGFfl1, whether natural or recombinant, induced peripheral blood monocyte (Fig.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Rapid onset synovial inflammation and hyperplasia induced by transforming growth factor beta.

Allen

Manthey

Hand

et al. 1990

The Journal of Experimental Medicine

241

131

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Transforming growth factor /3 (TGF (3),t originally isolated from platelets as a 25-kD peptide (1, 2), has been shown to be a product of other inflammatory cells, including lymphocytes (3, 4) and macrophages (5, 6), and to have potent immunomodulatory effects (7). Although five different forms of TGFJ3 have now been characterized (1), only TGF01 and its homologue, TGF02 (8, 9), have thus far been identified in hemopoietic cells (6). Each ofthese peptides has been cloned, demonstrating that TGF01 is encoded as a 390 amino acid precursor (10), TGFs2 as a 412 amino acid precursor (11,12), and that both have a signal peptide of 20-23 amino acids at the NH2 terminus . The processed 112 amino acid chains of the two peptides share 72% sequence homology and appear to bind equally well to TGFS class III receptors (13), although TGFS1 binds with greater affinity than TGF02 to class I and II receptors (14, 15). Interestingly, lymphoid cells appear to possess only class I and II TGF,6 receptors (16), although in vitro, lymphocyte and monocyte responses to TGF01 and 02 appear comparable (6,17,18). The secretion of TGFa peptides by lymphocytes and monocytes only after activation (3-6) implicates these polypeptides in the evolution of immunologic processes, and in recent studies TGFR has been identified in chronic inflammatory tissues (19)(20)(21)(22), including the synovium of rheumatoid arthritis patients (7,22) and in experimentally induced arthritis in rodents (22). To define the role of TGFS in such lesions, we injected natural or recombinant TGF0 directly into the joint cavity of Lewis rats and monitored its effect on cellular recruitment and activation, and on its potential modulation of pathogenic effects. TGF01 and TGF02 were both found to induce synovial erythema, swelling, and leukocyte infiltration . The infiltrating mononuclear cells, activated to express growth factors, likely regulated the pronounced synovial hyperplasia that was apparent within 2-3 d. Based on these observations, it appears that TGF0, released by platelets and inflammatory cells in the arthritic synovium, may directly contribute to the events associated with inflammatory arthropathies.

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Section: Resultssupporting

confidence: 81%

Section: Resultsmentioning

confidence: 99%

Rapid onset synovial inflammation and hyperplasia induced by transforming growth factor beta.

Allen

Manthey

Hand

et al. 1990

The Journal of Experimental Medicine

241

131

View full text Add to dashboard Cite

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“…Several studies have shown that bFGF 19,24,26,31) and PDGF 5,8,9) significantly enhanced wound healing. Other studies have shown that TGF-b 6,8,32,33) enhanced wound healing and stimulated migration of neutrophiles and monocytes and that EGF 34) enhanced keratinocyte growth and fibronectin secretion. The present study suggested that the amount of platelets, macrophages, neutrophiles and lymphocytes adhered onto and the amount of bFGF, EGF, PDGF and TGF-b adsorbed onto the poly(CMBr-BMA) film are smaller than the amounts adhered and adsorbed onto the PBMA and PET films.…”

Section: Discussionmentioning

confidence: 90%

Effect of Zwitterionic Polymers on Wound Healing

Fujishita

Inaba

Tada

et al. 2008

Biological & Pharmaceutical Bulletin

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The effect of a thin film of a zwitterionic random copolymer composed of carboxybetaine [1-carboxy-N,Ndimethyl-N-(2 -methacryloyloxyethyl)methanaminium inner salt] (CMB) and n-butyl methacrylate (BMA), poly(CMB-r-BMA) (CMB, 30 mol%), on the healing of a full-thickness excisional and incisional wound in hairless rats was examined. The poly(CMB-r-BMA) film significantly enhanced wound closure and complete healing of a full-thickness excisional wound compared with the effect of the poly(n-butyl methacrylate) (PBMA) and the poly(ethylene terephthalate) (PET) films. However, the poly(CMB-r-BMA) film did not enhance healing of a fullthickness incisional wound in hairless rats. The amount of proteins adsorbed and that of neutrophiles adhered onto the poly(CMB-r-BMA) film were significantly smaller than those onto the PBMA and PET films. The results suggested that various cells and growth factors in the wound exudate are utilized effectively by covering an excisional wound with the poly(CMB-r-BMA) film, resulting in acceleration of healing. In addition, the poly(CMB-r-BMA) film significantly enhanced healing of a full-thickness excisional wound in hairless rats compared with the effect of Tegaderm ® as wound dressings. The poly(CMB-r-BMA) film has potential as a new wound dressing.

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“…On the other hand, angioinhibition may affect endothelial cells directly or indirectly via stimulation/inhibition of cytokines such as thrombospondin, TNF-␣, IFN-␣2, FGF, TGF-␣, and TGF-␤, or of several angiogenic factors (Folkman and Klagsbrun, 1987;FraterSchroder et al, 1987;Heinmark et al, 1986;Sidky and Borden, 1987;Wiseman et al, 1988). TNP-470 alone or in combination with cyclosporin suppressed VEGF production in CIA (Oliver et al, 1995) and the level of VEGF in the culture supernatant of a TNP-470 -treated cell line derived from a carcinosarcoma of the human uterus was significantly lower than that of the control (Emoto et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Study of the Mechanism Involved in Angiogenesis and Synovial Cell Proliferation in Human Synovial Tissues of Patients with Rheumatoid Arthritis Using SCID Mice

Nagashima

Tanaka

Takahashi

et al. 2002

Laboratory Investigation

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SUMMARY:To examine whether synovial cell proliferation is due to angiogenesis, we studied the relationship between the inhibition of synovial cell proliferation and an angiogenesis inhibitor, TNP-470, in human synovial tissues. Human synovial tissues were implanted into the back of SCID mice (SCID-HuAg mice). Sixteen mice were divided into two groups of eight mice each: the untreated group (vehicle group) and the TNP-470-treated group that received a dose of 10 mg/kg body weight by subcutaneous injection. The number of blood vessels and synovial lining cells clearly increased in the vehicle group, but the number of synovial lining cells clearly decreased and the blood vessels were hardly detected in the TNP-470 group. Immunohistochemically, cells that stained positively for the anti-proliferating cell nuclear antigen (PCNA) mAb were abundant in synovial lining cells and endothelial cells in synovial tissues. Cells that stained positively for the anti-CD34 polyclonal antibody were abundant in the endothelial cells in the vehicle group, but these positively stained cells were hardly detected in the TNP-470 group. The PCNA positivity ratio in the vehicle group was 0.64 Ϯ 0.019, whereas that in the TNP-470 group was 0.199 Ϯ 0.007. The numbers of cells that stained positively for anti-CD34 polyclonal antibody were 242 Ϯ 13.4 in the vehicle group and 153 Ϯ 6.73 in the TNP-470 group per 10 microscopic fields. Cells that stained positively for anti-mouse CD31 mAb were mainly localized in the synovial lining, but invaded the subsynovial lining layer in human synovial tissues. On the other hand, cells that stained positively for anti-human CD31 mAb were mainly localized in the subsynovial lining layer. We found that endothelial cell proliferation is dependent on angiogenesis based on the result that angiogenesis and synovial cell proliferation were inhibited by treatment with TNP-470. (Lab Invest 2002, 82:981-988).

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Transforming growth factor-beta (TGFβ) is chemotactic for human monocytes and induces their expression of angiogenic activity

Cited by 215 publications

References 20 publications

Rapid onset synovial inflammation and hyperplasia induced by transforming growth factor beta.

Rapid onset synovial inflammation and hyperplasia induced by transforming growth factor beta.

Effect of Zwitterionic Polymers on Wound Healing

Study of the Mechanism Involved in Angiogenesis and Synovial Cell Proliferation in Human Synovial Tissues of Patients with Rheumatoid Arthritis Using SCID Mice

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