Exaggerated Spontaneous Release of Platelet-Derived Growth Factor by Alveolar Macrophages from Patients with Idiopathic Pulmonary Fibrosis

Martinet, Yves; Rom, William N.; Grotendorst, Gary R.; Martin, George R.; Crystal, Ronald G.

doi:10.1056/nejm198707233170404

Cited by 379 publications

(151 citation statements)

References 47 publications

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“…Alveolar macrophages isolated from the bronchoalveolar lavage (BAL) of patients with IPF have been shown to produce PDGF [59]. Expression of PDGF messenger ribonucleic acid (mRNA) and protein localization have also been observed directly in the lung tissue [60].…”

Section: Growth Factorsmentioning

confidence: 99%

Immune-inflammatory functions of fibroblasts

Jordana¹,

Särnstrand²,

Sime³

et al. 1994

Eur Respir J

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Inflammation is a response that has evolved over millions of years to become an extremely complex process. This complexity reflects the host's need to deal effectively with a wide variety of potentially injurious agents, as well as the need to incorporate an adequate set of checks and balances. An inappropriately checked response, which occurs rarely, results in disease, either acute or chronic. However, in most instances, inflammation is a beneficial response, essential for survival. Inflammation comprises an extensive network of cellular interactions implemented by an overwhelming number of molecules. One category of signal includes soluble products, such as neuropeptide, lipid mediators, cytokines and growth factors, most of which can be produced by inflammatory/haemopoietic cells. However, resident structural cells can also produce many of these products and, on this basis only, fibroblasts, epithelial, endothelial and smooth muscle cells should be considered as active contributors to the regulation of the inflammatory response. Extracellular matrix (ECM) proteins comprise another category of signals. Whilst the most recognized activities of these proteins are those concerned with providing structural tissue integrity, it is clear that they also have powerful inductive effects. Indeed, ECM proteins can influence the shape, movement and state of activation of inflammatory cells in the tissue. Recent evidence indicates that these signals may also play substantial roles in homing of inflammatory cells to certain sites and in the handling of a number of cytokines and growth factors. In so far as fibroblasts are the main producers of ECM proteins, these new data establish an indirect but important role for fibroblasts in the regulation of the inflammatory response.

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Section: Growth Factorsmentioning

confidence: 99%

Immune-inflammatory functions of fibroblasts

Jordana¹,

Särnstrand²,

Sime³

et al. 1994

Eur Respir J

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“…The production of these growth factors is augmented at the site of fibrosis [9][10][11], which suggests potential roles for these factors in the establishment of fibrosis. Interleukin-6 (IL-6) induces, also in vitro, fibroblast proliferation and collagen production [12,13], as well as the synthesis of tissue inhibitor of metalloproteinase-1 [14].…”

Section: Introductionmentioning

confidence: 99%

Attenuated liver fibrosis and depressed serum albumin levels in carbon tetrachloride-treated IL-6-deficient mice

Natsume

Tsuji

Harada

et al. 1999

Journal of Leukocyte Biology

105

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Chronic intermittent injection of carbon tetrachloride (CCl 4 ) for more than 10 weeks induced liver fibrosis in mice, as evidenced by positive Azan staining and increased intrahepatic collagen content. Preceding the onset of liver fibrosis, interleukin-6 (IL-6) gene expression was enhanced in liver and immunoreactive IL-6 was detected in infiltrating inflammatory cells. To delineate the role of IL-6 in this process, we treated IL-6-deficient mice with CCl 4 in a similar manner for 12 weeks, after which fibrotic changes were less evident and serum albumin levels were lower in IL-6-deficient than wild-type mice. Moreover, CCl 4 -induced expression of transforming growth factor ␤ 1 and hepatocyte growth factor genes in liver was significantly reduced in IL-6-deficient mice. Thus, IL-6 may be vitally involved in fibrotic changes and maintenance of serum albumin levels, partly by modulating intrahepatic expression of these cytokines. J. Leukoc. Biol. 66: 601-608; 1999.

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“…However, the source of platelet-derived growth factor in liver fibrogenesis is unceftain. In patients with idiopathic pulmonary fibrosis, alveolar macrophages release a large amount of platelet-derived growth factor (25). In chronic liver diseases, it is possible that activated macrophages, including Kupffer cells, and/or platelets, which accumulate in hepatic inflammation (18,26), release plateletd erived growth factor.…”

Section: Discussionmentioning

confidence: 99%

Increased Release of Platelet-Derived Growth Factor from Platelets in Chronic Liver Disease

Shiraishi

Morimoto²,

Koh³

et al. 1994

Clinical Chemistry and Laboratory Medicine

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Shiraishi et al.: Plateiet-derived growth factor in platelcts in chronic liver disease Eur. J. Clin. Chem. Clin. Biochem. Vol. 32, 1994, pp. 5-9 © 1994 Walter de Gruyter & Co.Berlin · New York Summary:The concentrations of platelet-derived growth factor in serum in 7 healthy controls (61 ± 9 years; mean ± SD) and 10 patients (62 ± 8 years) with chronic liver disease (chronic hepatitis and/or liver cirrhosis) were compared.The plasma concentration of platelet-derived growth factor was below the detection limit (< 0.45 μg/l) in all the subjects studied. The peripheral blood platelet count in patients with chronic liver disease was significantly lower than that in control subjects. However, the concentration of platelet-derived growth factor in serum, which was assumed to be released from platelet, was similar in patients with chronic liver disease and control subjects. These results indicate that the mean amount of platelet-derived growth factor releasedrfrom the same number (lO 9 ) of platelets, calculated from the serum platelet-derived growth factor concentration and the peripheral blood platelet count, in patients with chronic liver disease (33 ± 11 ng/10 9 platelets) was significantly (p < 0.01) higher than that in control subjects (14 ± 5 ng/10 9 platelets).Moreover, the amount of platelet-derived growth factor released from l O 9 platelets inversely correlated with the serum concentration of pseudocholinesterase activity (r = -0.65, p < 0.01), and correlated positively (r = 0.91, p < 0.01) with the percent retention of indocyanine green in serum, in all subjects studied.These findings suggest that the amount of platelet-derived growth factor releasable from platelets of patients with chronic liver disease i$ higher than that in normal subjects and that it correlates with the severity of the disease. Platelet-derived growth factor released from platelets may be involved in the pathophysiology of chronic liver diseases s a local factor.

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Exaggerated Spontaneous Release of Platelet-Derived Growth Factor by Alveolar Macrophages from Patients with Idiopathic Pulmonary Fibrosis

Cited by 379 publications

References 47 publications

Immune-inflammatory functions of fibroblasts

Immune-inflammatory functions of fibroblasts

Attenuated liver fibrosis and depressed serum albumin levels in carbon tetrachloride-treated IL-6-deficient mice

Increased Release of Platelet-Derived Growth Factor from Platelets in Chronic Liver Disease

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