Transforming growth factor beta-1 (TGF-β1) stimulates collagen synthesis in cultured rainbow trout cardiac fibroblasts

Abstract

Cold acclimation of rainbow trout, , causes collagen to increase within the extracellular matrix (ECM) of the myocardium, while warm acclimation has the opposite effect. The mechanism responsible for this remodelling response is not known. In mammals, transforming growth factor beta-1 (TGF-β1) stimulates collagen deposition within the myocardial ECM. Therefore, we hypothesized that TGF-β1 regulates trout myocardial ECM turnover and predicted that TGF-β1 would induce collagen deposition in cultured rainbow trout cardiac fibroblasts. We found that treatment of trout cardiac fibroblasts with 15 ng ml human recombinant TGF-β1 caused an increase in total collagen at 48 and 72 h and an increase in collagen type I protein after 7 days. We also found that TGF-β1 treatment caused an increase in the transcript abundance of tissue inhibitor of metalloproteinase 2 () and matrix metalloproteinase 9 () at 24 h. Cells treated with TGF-β1 also had lower levels of the gene transcript for after 48 h and higher levels of the gene transcript for collagen type I α1 () after 72 h. These changes in gene expression suggest that the increase in collagen deposition is due to a decrease in the activity of matrix metalloproteinases and an increase in collagen synthesis. Together, these results indicate that TGF-β1 is a regulator of ECM composition in cultured trout cardiac fibroblasts and suggest that this cytokine may play a role in regulating collagen content in the trout heart during thermal acclimation.

Atrophic acne scar: a process from altered metabolism of elastic fibres and collagen fibres based on transforming growth factor‐β1 signalling

“…TGF‐β1 participates in scar formation by directly regulating fibrosis or manipulating keratinocyte proliferation. It has been recognized that TGF‐β1 drives ECM synthesis and fibroblast proliferation, as well as myofibroblast differentiation, which are responsible for tissue contraction during scarring . Also, TGF‐β1 can restrict keratinocyte proliferation through disturbing transcription of c‐Myc or inducing transcription of p21 .…”

“…It has been recognized that TGF-b1 drives ECM synthesis and fibroblast proliferation, as well as myofibroblast differentiation, which are responsible for tissue contraction during scarring. [42][43][44] Also, TGF-b1 can restrict keratinocyte proliferation through disturbing transcription of c-Myc or inducing transcription of p21. 23,45 As keratinocytes actively crosstalk with cutaneous immunity by expressing cytokines, and interact with fibroblasts in a double paracrine manner, they play a pivotal role in wound healing.…”

Exogenous supply of Hsp47 triggers fibrillar collagen deposition in skin cell cultures in vitro

“…Hsp47 has a regulatory role during scar formation in neonatal mouse skin after injury, which indicates that its expression during healing is up regulated in situ, in response to injury [63]. These facts indicate that Hsp47 could be an interesting therapeutic target in collagen-related skin disorders, as alternative to non-specific collagen inducers such as TGF β [64], VEGF [65] or ascorbic acid [17,18]. Therapeutic use of these molecules to enhance collagen deposition influences other cellular functions such as proliferation [17,18,66,67], differentiation [66] and angiogenesis [68], leading to undesired side effects.…”

Exogenous supply of Hsp47 triggers fibrillar collagen deposition in skin cell cultures in vitro

“…Hsp47 has a regulatory role during scar formation in neonatal mouse skin after injury, which indicates that its expression during healing is up regulated in situ, in response to injury [67]. These facts indicate that Hsp47 could be an interesting therapeutic target in collagenrelated skin disorders, as alternative to non-specific collagen inducers such as TGF β [68], VEGF [69] or ascorbic acid [17,18]. Therapeutic use of these molecules to enhance collagen deposition influences other cellular functions such as proliferation [17,18,70,71], differentiation [70] and angiogenesis [72], leading to undesired side effects.…”