Immune Functions and Properties of Resident Cells in the Heart and Cardiovascular System: Pericytes.

This chapter provides an introduction to pericyte physiology. Pericytes are smooth muscle-like cells that wrap around vessels and arterioles. Here, we discuss their structure, function, contractility and interaction with other cells including immune cells and finally their role in pathological processes.

Cardiac regeneration: All work and no repair?

Structural changes in the developing heart may influence the limited regenerative capacity of the adult heart. We examine how the workload exerted on the adult mammalian heart may limit regenerative capability and discuss recent therapies that demonstrate beneficial effects through unloading the heart.

Cardiac regeneration: epicardial mediated repair.

The hearts of lower vertebrates such as fish and salamanders display scarless regeneration following injury, although this feature is lost in adult mammals. The remarkable capacity of the neonatal mammalian heart to regenerate suggests that the underlying machinery required for the regenerative process is evolutionarily retained. Recent studies highlight the epicardial covering of the heart as an important source of the signalling factors required for the repair process.

Nonsteroidal anti-inflammatory drugs alter vasa recta diameter via pericytes.

We have previously shown that vasa recta pericytes are known to dilate vasa recta capillaries in the presence of PGE2 and contract vasa recta capillaries when endogenous production of PGE2 is inhibited by the nonselective nonsteroidal anti-inflammatory drug (NSAID) indomethacin. In the present study, we used a live rat kidney slice model to build on these initial observations and provide novel data that demonstrate that nonselective, cyclooxygenase-1-selective, and cyclooxygenase -2-selective NSAIDs act via medullary pericytes to elicit a reduction of vasa recta diameter. Real-time images of in situ vasa recta were recorded, and vasa recta diameters at pericyte and nonpericyte sites were measured offline.

Insulin-like growth factor-1 induces regulatory T cell-mediated suppression of allergic contact dermatitis in mice.

Allergic contact dermatitis (ACD) is triggered by an aberrant hyperinflammatory immune response to innocuous chemical compounds and ranks as the world's most prevalent occupational skin condition. Although a variety of immune effector cells are activated during ACD, regulatory T (Treg) cells are crucial in controlling the resulting inflammation. Insulin-like growth factor-1 (IGF-1) regulates cell proliferation and differentiation and accelerates wound healing and regeneration in several organs including the skin.