Growth factors in the regulation of reparative response in the presence of peritoneal damage

In recent decades, growth factors have attracted a lot of attention in the study of the pathogenesis of various diseases and conditions because they play a crucial role in the processes of growth, development, and maintenance of cell populations. Growth factors are biologically active polypeptides that function as regulatory signals controlling cell proliferation and differentiation, and they promote cell survival [1], [2].

Most growth factors are multipotent and can affect various cell types. Although their names often reflect specific cellular types, their action might not be limited to this cell population. For example, vascular endothelial growth factor (VEGF) stimulates not only vascular growth. Still, it is also involved in the proliferation, migration, differentiation, and mobility of fibroblasts, both in physiological and reparative regeneration processes [3], [4], [5]. Despite the affinity for vascular endothelial cells, the level of VEGF significantly affects collagen production during the development of postinfarction cardiosclerosis [6]. Similarly, fibroblast growth factor 2 (FGF2) can act as an activator of angiogenesis [7], [8].

The general role of growth factors in the regulation of physiological and reparative regeneration processes response has been extensively documented. FGF and VEGF are the master regulators of connective tissue formation; they activate the repair in the damaged tissue by stimulating fibroblast migration and the growth of granulation tissue. However, some peculiarities are depending on the organ localization of its formation and tissue environment [9].

Growth factors play an essential role in repairing the peritoneal damage and have a significant impact on the development of adhesions in the abdominal cavity, for example, after surgery. Transforming growth factor-beta (TGF-β) expression has been documented from the third postoperative day and increases gradually until day 14 [10]. Conversely, blocking TGF-β1 reduces the development of peritoneal fibrosis [11], [12]. A coexpression of connective tissue growth factor (CTGF) was observed with increasing fibrosis and angiogenesis in a peritoneal adhesion model in the rodent, with a peak between postoperative days 6 and 15. Thus, CTGF is another critical molecule in fibrous adhesive disease and might be a target for future adhesion prevention [13], [14]. Intraperitoneal administration of Bevacizumab, a recombinant monoclonal antibody blocking VEGF, decreased the intensity of peritoneal adhesions in the rat model [15]. Less peritoneal adhesions developed when insulin-like growth factor I (IGF1) was blocked by administrating IGF-binding protein 4 intraperitoneally [16]. Local application of epidermal growth factor (EGF) as a gelatin film also inhibited the formation of peritoneal adhesions [17].

However, the expression of growth factors in the formation of adhesions after peritoneal damage has received relatively little attention. The purpose of this study was to investigate the response of the peritoneal tissue to injury by examining the expression of a large panel of growth factors during the development of the adhesive process.

https://pubmed.ncbi.nlm.nih.gov/33575460/