To get anywhere, you need effective communication, be it between say construction workers building a bridge (as a human example), worker bees making honey or bats out in the dark hunting for food. The same applies in the micro scale - the cells in our body need to communicate at different stages of development so that they know what to become, where to go, whether to grow or die, among other things.
And just like many other cells in the body, adipocytes (or fat cells; a slight obsession of mine in my previous life!) communicate with a type of skin cell known as a keratinocyte, sending signals to regulate the growth of hair follicles and, ultimately, hair growth (a very complicated cycle of growth and death that you can read about here if you have access). It turns out that this line of communication actually goes both ways, as a new study published in PNAS shows that molecular signals from epidermal cells also regulate the growth of the underlying adipocyte layer.
The authors found that the thickness of the adipocyte layer under the skin actually correlated with the hair growth cycle, both in mouse and human skin, becoming thicker during the growth phase (known as anagen) and thinner during the destruction phase (known as telogen).
This is actually regulated by the signal that induces the hair follicle growth phase, known as the Wnt/β-catenin pathway: inhibiting this pathway resulted in loss of adipocytes from the skin, and activating it caused increased adipocyte differentiation. Notably, it was the Wnt/β-catenin pathway directly, rather than indirectly through its stimulation of hair follicle growth, that promoted adipocyte differentiation.
The main means of communication between cells is through secretion of proteins, sent from one cell type to the other, and this is also what was observed here: activation of the Wnt/β-catenin pathway in keratinocytes triggered the production of a large number of proteins. Among the factors identified as pro-adipogenic were bone morphogenetic protein 2 (BMP2) and BMP6 and insulin growth factor 2 (IGF2).
So it seems that hair follicle growth has to be coordinated with the growth of the underlying adipocyte layer, possibly, as speculated by the authors of this paper, because a high density of hair combined with a thick layer of fat would provide better insulation in the cold. At this point this is all speculation, and perhaps we might find out by determining what is responsible for synchronising the two processes.
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| Its good to talk. Image from https://www.flickr.com/photos/danielcoy/4175199668 |
The authors found that the thickness of the adipocyte layer under the skin actually correlated with the hair growth cycle, both in mouse and human skin, becoming thicker during the growth phase (known as anagen) and thinner during the destruction phase (known as telogen).
This is actually regulated by the signal that induces the hair follicle growth phase, known as the Wnt/β-catenin pathway: inhibiting this pathway resulted in loss of adipocytes from the skin, and activating it caused increased adipocyte differentiation. Notably, it was the Wnt/β-catenin pathway directly, rather than indirectly through its stimulation of hair follicle growth, that promoted adipocyte differentiation.
The main means of communication between cells is through secretion of proteins, sent from one cell type to the other, and this is also what was observed here: activation of the Wnt/β-catenin pathway in keratinocytes triggered the production of a large number of proteins. Among the factors identified as pro-adipogenic were bone morphogenetic protein 2 (BMP2) and BMP6 and insulin growth factor 2 (IGF2).
So it seems that hair follicle growth has to be coordinated with the growth of the underlying adipocyte layer, possibly, as speculated by the authors of this paper, because a high density of hair combined with a thick layer of fat would provide better insulation in the cold. At this point this is all speculation, and perhaps we might find out by determining what is responsible for synchronising the two processes.
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