Fat Cells Migrate to Wounds to Drive Repair

Fat Body Cells Are Motile and Actively Migrate to Wounds to Drive Repair and Prevent Infection – Science Direct – Feb 2018 – free full-text article

I just found this interesting: the body fat cells that we so want to get rid of actually have a critical role in wound healing.

Highlights

  • Fat body cells actively migrate to wounds using a peristaltic mode of motility
  • Fat body cells tightly seal the gap by forming lamellipodia around the wound margin
  • Fat body cells collaborate with macrophages to clear wound debris
  • Fat body cells locally release antimicrobial peptides at infected wounds

Adipocytes have many functions in various tissues beyond energy storage, including regulating metabolism, growth, and immunity.

However, little is known about their role in wound healing. Here we use live imaging of fat body cells, the equivalent of vertebrate adipocytes in Drosophila, to investigate their potential behaviors and functions following skin wounding.  

We find that pupal fat body cells are not immotile, as previously presumed, but actively migrate to wounds using an unusual adhesion-independent, actomyosin-driven, peristaltic mode of motility.

Once at the wound, fat body cells collaborate with hemocytes, Drosophila macrophages, to clear the wound of cell debris; they also tightly seal the epithelial wound gap and locally release antimicrobial peptides to fight wound infection.

Thus, fat body cells are motile cells, enabling them to migrate to wounds to undertake several local functions needed to drive wound repair and prevent infections.

The article gives detailed descriptions of this process, but it’s far more technical than I understand.

Discussion

The observation that FBCs are motile cells that actively migrate to wounds is unexpected and has not previously been made for adipocytes in any other organism. However, our findings raise the interesting question as to whether vertebrate adipocytes might also have the capacity to migrate.

The mode of motility we observe for FBCs moving through the hemolymph to wounds is unusual, since it does not appear to involve the use of standard lamellipodia or blebs, utilized by most known migrating cells as they crawl in an adhesion-dependent fashion over substrates and through a milieu of extracellular matrix

Adhesion-independent migration has recently emerged as an alternative migration mode that has now been described for several other types of cells, including ameba, lymphocytes, and some cancer cells (Paluch et al., 2016).

Similar to FBCs, several other cell types have been reported to migrate by swimming, when they are required to move through viscous fluid: amebae and neutrophils have been shown to swim when in viscous solution (Barry and Bretscher, 2010) and lymphocytes are known to migrate using contraction waves when in suspension (Haston and Shields, 1984).

However, the exact mechanism by which these swimming cells generate internal forces and how these forces are transduced to the extracellular environment to generate forward movement is still unknown.

However, it still remains unclear how such an intracellular force might be transduced to the extracellular environment to drive forward movement of FBCs.

Although we have not observed contacts, it is possible that the close proximity of FBCs with other cells and tissues en route to a wound might enable them to occasionally generate additional frictional forces

Our study shows that FBCs play multiple local roles in driving wound repair and preventing wound infection.

Given our finding that hemocytes and FBCs collaborate during the wound repair process to clear cell debris and fight infection, it is tempting to speculate that these two cell types communicate with each other during vertebrate wound healing also.

Interestingly, in recent years several mammalian studies have uncovered complex interactions between adipocytes and macrophages in white adipose tissue (WAT), with important implications for tissue regeneration and disease.

Thus interactions between adipocytes and immune cells appear to be key in many diseases, including type 2 diabetes, and we believe that important insights into these links may be provided by future studies of the functional relationship and communication between FBCs and hemocytes during pupal wound repair in flies.

Now we have reason to be thankful that we have body fat!

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