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Deposition of Transforming Growth Factor- β in the Marrow in Myelofibrosis, and the Intracellular Localization and Secretion of TGF- β by Leukemic Cells

1995; Oxford University Press; Volume: 103; Issue: 5 Linguagem: Inglês

10.1093/ajcp/103.5.574

1943-7722

James B. Johnston, Bakul I. Dalal, Sara J. Israels, Sandra Oh, Eileen McMillan, Asher Begleiter, Ginette Y. Michaud, Lyonel G. Israels, Arnold H. Greenberg,

Eosinophilic Disorders and Syndromes

The marrows of 10 patients with hematologic malignancies were examined by immunohistochemistry using anti TGF-β antibody, CC(l-30), which detects secreted TGF-β, and compared with four normal marrows. TGF-β was not demonstrated in marrows with a normal level of rcticulin fibrosis; however, TGF-β was observed within collagen in marrows having collagen fibrosis or increased reticulin fibrosis. The extent of TGF-β deposition paralleled the severity of fibrosis (P < .0001), and occurred even with normal or reduced numbers of megakaryocytes. Using another TGF-β antibody, LC(l-30), which detects intracellular TGF-β, TGF-β was detected by immunofluorescence in discrete sites in the cytoplasm of immature and mature myeloid and large granular lymphocytic leukemia cells. These sites colocalized with areas detected by an anti-granule antibody (D545) suggesting that TGF-β was stored in granules. However, neither the TGF-β mRNA content nor the degree of TGF-β secretion by these leukemic cells correlated with the extent of TGF-β deposition in the marrow. Thus, TGF-β deposition in marrow may contribute to myelofibrosis, but the source of this cytokine in the absence of megakaryocytes requires further study.