Proliferation and extracellular matrix production by human infragenicular smooth muscle cells in response to interleukin-1β

Abstract

These results suggest that interleukin-1 beta acts as a potent stimulant of the proliferation of human infragenicular VSMCs. IL-1 beta also acts to augment the production of fibronectin by these cells. Fibronectin has been implicated in the phenotypic transformation of VSMCs from the contractile to the synthetic state. Therefore, IL-1 beta may serve as an important regulatory factor in the development of atherosclerosis by stimulating the proliferation of VSMCs and their transformation to the synthetic state, two important steps in the formation of the atherosclerotic lesion.

Fenofibric Acid Reduces Fibronectin and Collagen Type IV Overexpression in Human Retinal Pigment Epithelial Cells Grown in Conditions Mimicking the Diabetic Milieu: Functional Implications in Retinal Permeability

“…Overall, these findings indicate that a higher content of basement membrane components may contribute to the impairment of barrier function, leading to excess permeability. In addition, the overexpression of basement membrane components known to be induced by inflammatory cytokines such as IL-1␤ 35,36 may be involved in hyperpermeability, which occurs in DR.…”

Blockade of Smooth Muscle Cell Migration and Proliferation in Baboon Aortic Explants by Interleukin-1β and Tumor Necrosis Factor-α Is Nitric Oxide-Dependent and Nitric Oxide-Independent

“…TNFα has been shown to inhibit [40, 41], have no effect [42]and stimulate [41, 43, 44]SMC proliferation in vitro. Several [3, 4, 22, 43, 45], but not all [5, 31, 46], studies of cultured rat, rabbit and human SMC have demonstrated mitogenic effects of IL-1β and cooperative interactions with PDGF with regard to mitogenesis. These variable reports cannot be explained by species or dosage differences.…”

Prosthetic vascular grafts: Wrong models, wrong questions and no healing

“…In situ hybridization of human explants, however, has demonstrated that interstitial macrophages and FBGCs are still secreting IL-1b even after numbers of years [190]. Although IL-1b is known to stimulate both smooth muscle cell proliferation and fibronectin deposition in atherosclerotic plaque formation [191], it has been suggested that this interleukin can also inhibit vascular smooth muscle proliferation in an autocrine fashion through nitric oxide upregulation [192]. The giant cells, therefore, may be responsible for not only affecting capillarization but also inhibiting smooth muscle cell ingrowth through persistent IL-1b secretion.…”