The amino-acid sequence of the precursor of the human tumour cell line-derived platelet-derived growth factor (PDGF) A-chain has been deduced from complementary DNA clones and the gene localized to chromosome 7. The protein shows extensive homology to the PDGF B-chain precursor. Expression of the PDGF A-chain gene is independent of that of the PDGF B-chain in a number of human tumour cell lines, and secretion of a PDGF-like growth factor of relative molecular mass 31,000 correlates with expression of A- but not B-chain messenger RNA.

cDNA sequence and chromosomal localization of human platelet-derived growth factor A-chain and its expression in tumour cell lines

Smooth muscle proliferation has been recognized as central to the pathology of both major forms of vascular disease: atherosclerosis and hypertension. Recent advances in our knowledge of mechanisms of control of proliferation suggest that events occurring in adult animals may recapitulate portions of the developmental biology of the smooth muscle cell. This review attempts to consider the current state of knowledge of the mechanisms controlling smooth muscle proliferation in these two diseases, to put that knowledge into the context of what is known about smooth muscle biology, and to offer two hypotheses on the possible roles of smooth muscle developmental biology in manifestations of atherosclerosis and hypertension in adult humans.

Replication of smooth muscle cells in vascular disease.

Communication between cells determines the steady-state composition of the lung in health and becomes a critical determinant of outcome in pathologic processes resulting in anatomic remodeling. This review presents the evolving concepts of the biology of cytokines (also known as peptide growth factors or biological response modifiers) in maintaining normal tissue growth and homeostasis. How these extracellular signaling proteins are involved in such pathologic disorders as spontaneous pulmonary fibrosis, sarcoidosis, pneumoconiosis, and the evolution and recovery from acute lung injury is also discussed. During the past decade the cytokines have come to the fore as important multifunctional mediators of cell behavior and cell-cell communication. A wide range of cellular responses are influenced or triggered when cytokines interact with cells. These include mitosis, chemotaxis, angiogenesis, cytoskeleton arrangement, immunomodulation, and extracellular matrix production. Cytokines influence cell behavior by binding to specific high affinity surface receptors on target cells. These receptors are linked in turn at the cell membrane to a complex array of intracellular signaling pathways. Individual cytokines may inhibit as well as promote cellular functions such as mitosis and thereby play a critical role in homeostasis of normal tissue elements. Hence, cytokines are intimately involved in normal tissue homeostasis as well as in processes eventuating in growth and remodeling. All cells produce and secrete cytokines at some time during their life. Each cytokine is capable of modulating more than one cellular function. Although produced by a variety of cell types, the triggers that induce a specific cytokine to be produced differ between cells. Many of the cytokines share regions of homologous nucleic acid sequences, suggesting that they are members of larger gene families. Given that tissues and cells are exposed to complex cytokine mixtures rather than to individual cytokines, recent attention has turned to understanding how cytokines interact. The combined effects of cytokine mixtures have proved to be both complex and unpredictable based on knowledge of the separate actions of the individual cytokines involved. In studies of the role of cytokines in lung disease, early research attention has focused on those cytokines released by alveolar macrophages (the so-called macrophage-derived growth factors). However, structural cells as well as immune effector cells of the lung are capable of cytokine production and release. The cytokines receiving the most attention to date in relation to pulmonary diseases include platelet-derived growth factor (PDGF), interleukin-1 (IL-1), transforming growth factor-beta (TGF-beta), tumor necrosis factor-alpha (TNF-alpha), insulinlike growth factor I (IGF-I), and, most recently, interleukin-6 (IL-6).(ABSTRACT TRUNCATED AT 400 WORDS)

Cytokines of the Lung

Silk fibroin as a vehicle for drug delivery applications.

The extracellular matrix (ECM) is the naturally occurring substrate upon which cells migrate, proliferate, and differentiate. The ECM functions as a biological adhesive that maintains the normal cytoarchitecture of different tissues and defines the key spatial relationships among dissimilar cell types. A loss of coordination and an alteration in the interactions between mesenchymal cells and epithelial cells separated by an ECM are thought to be fundamental steps in the development and progression of cancer. Although a substantial body of knowledge has been accumulated concerning the role of the ECM in most other tissues, much less is known of the structure and function of the ECM in the nervous system. Recent experiments in mammalian systems have shown that an increased knowledge of the ECM in the nervous system can lead to a better understanding of complex neurobiological processes under developmental, normal, and pathological conditions. This review focuses on the structure and function of the ECM in the peripheral and central nervous systems and on the importance of ECM macromolecules in axonal regeneration, cerebral edema, and cerebral neoplasia.

The extracellular matrix of the central and peripheral nervous systems: structure and function

Initiation of cell replication by cationic polypeptide hormones.

We report here that platelet-derived growth factor (PDGF)1–4 and pituitary-derived fibroblast growth factor (FGF)5 bind rapidly and tenaciously to tissue culture plates either coated with collagen (a major component of the extracellular matrix) or uncoated. Surface-bound PDGF resists extraction with non-ionic detergents, organic solvents and chaotropic solvents; moreover it is biologically active in situ. Our finding that immobilized PDGF is nonetheless mitogenic lends support to other observations which indicate that PDGF functions outside the cell via production of a stable intracellular second signal6. In a broader context, the observations suggest that one role of the extracellular matrix in vivo is to sequester biologically active molecules like PDGF to provide a localized and persistent stimulation.

Growth factors adherent to cell substrate are mitogenically active in situ.

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Initiation of cell replication by cationic polypeptide hormones.

Growth factors adherent to cell substrate are mitogenically active in situ.