Contractile apparatus in CNS capillary pericytes.

Whether or not capillary pericytes contribute to blood flow regulation in the brain and retina has long been debated. This was partly caused by failure of detecting the contractile protein -smooth muscle actin ( -SMA) in capillary pericytes. The aim of this review is to summarize recent developments in detecting -SMA and contractility in capillary pericytes and the relevant literature on the biology of actin filaments. Evidence suggests that for visualization of the small amounts of -SMA in downstream mid-capillary pericytes, actin depolymerization must be prevented during tissue processing. Actin filaments turnover is mainly based on de/re-polymerization rather than transcription of the monomeric form, hence, small amounts of -SMA mRNA may evade detection by transcriptomic studies. Similarly, transgenic mice expressing fluorescent reporters under the -SMA promoter may yield low fluorescence due to limited transcriptional activity in mid-capillary pericytes. Recent studies show that pericytes including mid-capillary ones express several actin isoforms and myosin heavy chain type 11, the partner of -SMA in mediating contraction. Emerging evidence also suggests that actin polymerization in pericytes may have a role in regulating the tone of downstream capillaries. With guidance of actin biology, innovative labeling and imaging techniques can reveal the molecular machinery of contraction in pericytes.