High molecular weight type-α transforming growth factor in the urine of patients with surgical bone wound involved in mandibular osteotomy

Aladib, Walid; Yoshida, Hideo; Sato, Mitsunobu

doi:10.1016/0169-6009(90)90100-t

Cited by 3 publications

(3 citation statements)

References 21 publications

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“…These forms of a-TGF ranged in size from 10 kDa to 70 kDa and have been found in extracts of human placenta (Stromberg et al,I982) and mouse tumours (Popik, 1987), in medium conditioned by various cell lines (Yamada & Serrero, 1989;McGeady et al, 1989;Kanno el al., 1989), including human breast cancer cell lines (Salomon et al, 1984), in the urine of patients with surgical bone wounds (Aladib et al, 1990), and in human milk (Okada et al, 1991). The presence of these high-molecular-weight forms of 0t-TGF has been suggested to be due to either differential cleavage of the precursor molecule or to N-and O-glycosylation of the larger forms (Teixido & Massagu6, 1988;Luetteke et aI., 1988).…”

Section: Discussionmentioning

confidence: 99%

“…The mature form of ~-TGF was found to be a 50-amino acid protein of molecular weight 5616 Da, which had 33% structural homology with epidermal growth factor (EGF) (Marquardt et al, 1984) and competed with EGF for the EGF receptor (Roberts et al, 1980). There have been a number of reports of high-molecular-weight forms of 0t-TGF (Stromberg et aI., 1982;Salomon et al, 1984;Popik, 1987;Yamada & Serrero, 1989;McGeady et al, 1989;Kanno et al, 1989;Aladib et al, 1990;Okada et al, 1991); all of those tested were biologically active in promoting cell growth. 0018-2214 9 1994 Chapman & Hall ~-TGF has been found to be expressed in a number of cell lines derived from human breast carcinomas as well as in a number of human mammary tumours.…”

Section: Introductionmentioning

confidence: 99%

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Immunolocalization of alpha-transforming growth factor in the developing rat mammary gland in vivo, rat mammary cells in vitro and in human breast diseases

et al. 1994

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Immunoreactive alpha-transforming growth factor (alpha-TGF) was shown by immunocytochemistry to be present in the rat mammary gland at various stages of development, the staining being most intense in mature myoepithelial cells. Alpha-TGF was also detected in the secretions of the mammary glands of pregnant and lactating rats. alpha-TGF in the extracts of rat mammary glands at each stage of development, and in several rat mammary cell lines and in culture medium in which they had been grown, was shown by Western blotting to consist primarily of a protein of molecular weight 50 kDa. The amount of this protein was greater in the mammary gland of the lactating rat than in resting or involuting glands. alpha-TGF was also found in some, but not all, human breast carcinomas, and in benign hyperplastic breast diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Immunolocalization of alpha-transforming growth factor in the developing rat mammary gland in vivo, rat mammary cells in vitro and in human breast diseases

et al. 1994

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“…Cell-cell communication as a membrane-anchored growth factor (juxtacrine action) has been proposed (24), but some higher molecular weight species can also be released (19). These larger forms are typically 10-19 KD in size, although species of up to 70 KD have been shown (2,25,44,53). It is therefore pertinent to determine the size of the molecule recognized in any localization study of this growth factor.…”

Section: Introductionmentioning

confidence: 99%

Transforming growth factor-alpha immunoreactivity during induced hair follicle growth cycles in sheep and ferrets.

Nixon

Broad²,

Saywell³

et al. 1996

J Histochem Cytochem.

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Transforming growth factor-alpha (TGF-alpha) has been associated with cell proliferation of keratinocytes and implicated in hair growth. We therefore examined changes in the immunocytochemical localization of TGF-alpha and cell proliferation markers in the skin of two unrelated species in which hair cycles could be induced, to elucidate the role of this growth factor in the control of fiber growth. Skin was collected from melatonin-treated ferrets (Mustela putorius furo), untreated Romney sheep (Ovis aries), and New Zealand Wiltshire sheep in which interruption of wool growth had been photoperiodically induced. Immunostaining patterns were very similar in ferrets and sheep. TGF-alpha immunoreactivity was observed in epithelial tissues of the skin but was not co-localized with cell proliferation markers. In anagen follicles, specific staining was most intense in the innermost cells of the outer root sheath and cortical cells in the keratogenous zone but was absent from inner root sheath or dermal papilla. TGF-alpha immunostaining diminished during catagen, although faint staining was retained in all epithelial cells. In telogen and early proanagen follicles, staining remained faint or was restricted to cells on the margin of the brush end and follicle neck. Immunoreactivity in the outer root sheath was reestablished in late proanagen. Sebaceous glands and epidermis were stained intensely throughout the hair cycle. TGF-alpha-immunoreactive components of skin extracts, analyzed by Western blotting, showed mobility corresponding to approximately 32 KD, but not to the size of the fully cleaved peptide. These results are consistent with an epithelial autocrine or juxtacrine, but not a mitogenic, function of TGF-alpha.

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Angiotensin II and EGF receptor cross-talk in chronic kidney diseases: a new therapeutic approach

Lautrette

Li²,

Alili

et al. 2005

Nat Med

312

334

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Mechanisms of progression of chronic renal diseases, a major healthcare burden, are poorly understood. Angiotensin II (AngII), the major renin-angiotensin system effector, is known to be involved in renal deterioration, but the molecular pathways are still unknown. Here, we show that mice overexpressing a dominant negative isoform of epidermal growth factor receptor (EGFR) were protected from renal lesions during chronic AngII infusion. Transforming growth factor-alpha (TGF-alpha) and its sheddase, TACE (also known as ADAM17), were induced by AngII treatment, TACE was redistributed to apical membranes and EGFR was phosphorylated. AngII-induced lesions were substantially reduced in mice lacking TGF-alpha or in mice given a specific TACE inhibitor. Pharmacologic inhibition of AngII prevented TGF-alpha and TACE accumulation as well as renal lesions after nephron reduction. These findings indicate a crucial role for AngII-dependent EGFR transactivation in renal deterioration and identify in TACE inhibitors a new therapeutic strategy for preventing progression of chronic renal diseases.

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High molecular weight type-α transforming growth factor in the urine of patients with surgical bone wound involved in mandibular osteotomy

Cited by 3 publications

References 21 publications

Immunolocalization of alpha-transforming growth factor in the developing rat mammary gland in vivo, rat mammary cells in vitro and in human breast diseases

Immunolocalization of alpha-transforming growth factor in the developing rat mammary gland in vivo, rat mammary cells in vitro and in human breast diseases

Transforming growth factor-alpha immunoreactivity during induced hair follicle growth cycles in sheep and ferrets.

Angiotensin II and EGF receptor cross-talk in chronic kidney diseases: a new therapeutic approach

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