Platelet-Derived Growth Factor (PDGF)

Introduction of PDGF

There are four PDGF family members: PDGF-A, PDGF-B, PDGF-C, and PDGF-D. PDGFs exert their biological effects through two PDGF receptor tyrosine kinases, PDGFR-a and PDGFR-b, which can form homo- or heterodimers. Traditionally, PDGFs are considered to be potent mitogens for cells of mesenchymal origin, such as fibroblasts, smooth muscle cells (SMCs), and glial cells.

Fig.1 Structural overview of PDGF-C and PDGF-D. (Chunsik, 2018)

PDGFs and Disease

In humans, γδ T cells produce transcripts and/or proteins for several growth factors, including PDGF. PDGFs have many functions, and they have direct effects on a wide range of cell types, including stem/progenitor cells, neuronal cells, vascular endothelial cells, and inflammatory cells. They are also associated with disease.

PDGFs and Fibrosis

• In lung fibrosis, PDGFs released from alveolar macrophages promote the proliferation of alveolar fibroblasts and fibrogenesis.
• In liver fibrosis, hepatic stellate cells up-regulate PDGFR in response to transforming growth factor (TGF). PDGFs produced by resident and invading macrophages contribute to stellate cell proliferation and fibrogenesis.
• In scleroderma, PDGFs released by macrophages promote the proliferation of dermal (myo) fibroblasts. Fibroblast PDGFR and PDGF expression is up-regulated in response to IL-1 and TGF. Circulating autoantibodies that activate the PDGF receptor have been described in scleroderma patients.
• In a variety of renal diseases and disease models, PDGF-B released from invading macrophages and PDGF-D released from mesangial cells may drive mesangial cell proliferation and matrix deposition, leading to glomerulosclerosis.
• In transgenic models, the expression of PDGFs in myocardial cells drives the proliferative expansion of PDGFR-positive cardiac fibroblasts and collagen deposition, leading to severe cardiac fibrosis.

Fig.2 PDGFs and fibrosis. (Johanna, 2008)

PDGF and Atherosclerosis

PDGF expression has been reported in virtually every cell type of the atherosclerotic arterial wall, as well as in infiltrating inflammatory cells. All PDGFs (A-D) and, in particular, A and B have been found in atherosclerotic lesions at increased levels compared with the normal vessel wall.

Fig.3 PDGFs and atherosclerosis. (Johanna, 2008)

PDGF and Myocardial Infarction

Following myocardial infarction, PDGF-A and PDGF-D expression levels are increased in the infarcted area, whereas PDGF-B and PDGF-C expression levels are decreased in the normal heart surrounding the infarction. PDGF-D expression is increased in the late stages of infarction and remained elevated for 6 weeks, with strong staining detected at the border zone and infarcted myocardium. Both PDGFR-a and PDGFR-b expression levels are increased in the early and late stages of myocardial infarction. Studies using PDGFR-a and PDGFR-b neutralizing antibodies show that inhibition of these receptors leads to decreased collagen deposition in the infarcted area.

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References

1. Chunsik, Lee.; Xuri, Li. Platelet-derived growth factor-C and -D in the cardiovascular system and diseases. Molecular Aspects of Medicine. 2018, 62.
2. Johanna, Andrae.; et al. Role of platelet-derived growth factors in physiology and medicine. Johanna Andrae; Radiosa Gallini; Christer Betsholtz. 2008, 22(10).