Insulin-Like Growth Factor (IGF)-1

Short Introduction of IGF-1

IGF1 is a polypeptide hormone, which is produced mainly by the liver. It is central to the somatotropic axis, acting downstream of growth hormone (GH). IGF1 activates both the mitogen-activated protein (MAP) kinase and PI3K signaling pathways, which act in almost every tissue in the body to promote tissue growth and maturation through the upregulation of anabolic processes.

Fig.1 Schematic structures of IGFs and their receptors. (Puche, 2012)

IGF-1, γδ T Cell, and Wounds

Different T cell subsets, including γδ T cells, may have a contribution to the integrity of healthy skin and pathological conditions such as psoriasis, alopecia areata, type II diabetes, and melanoma. Epidermal T cells have been shown to play unique roles in tissue homeostasis and repair in mice through the local secretion of distinct growth factors in the skin.

In a skin organ culture model, human epidermal T cells can produce IGF-1 upon activation and promote wound healing. However, an analysis of the functional capabilities of T cells isolated from acute versus chronic wounds revealed a striking difference.

Both αβ+ and Vδ1+ T cells that were isolated from acute wounds actively produced IGF-1, which means that they are activated during tissue damage to participate in wound repair. In contrast, IGF-1 production could not be detected in T cells isolated from chronic wounds.

Epidermal invasion of IL-17 producing dermal Vγ4 cells suppresses IGF-1 production by dendritic epidermal γδ T cells (DETC) and wound healing via IL-23 and IL-1β producing keratinocytes.

IGF-1 and Cardiovascular Diseases (CVD)

Low circulating IGF-I levels have been correlated with an increased risk for CVD in humans. In cross-sectional studies, low circulating IGF-I levels were found to be associated with angiographically documented coronary artery disease and may predict fatal ischemic heart disease, a significantly increased risk of ischemic stroke and congestive heart failure in elderly patients, as well as a worse prognosis of recovery after acute myocardial infarction.

Fig.2 IGF-I receptor pathway. (Puche, 2012)

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Reference

1. Puche, J E.; Inma, Castilla-Cortázar. Human conditions of insulin-like growth factor-I (IGF-I) deficiency. Journal of Translational Medicine. 2012, 10(1): 224.