[2] Pericytes are embedded in the basement membrane of blood capillaries, where they communicate with endothelial cells by means of both direct physical contact and paracrine signaling.

[6] In the central nervous system (CNS), pericytes wrap around the endothelial cells that line the inside of the capillary.

Many types of integrin molecules facilitate communication between pericytes and endothelial cells separated by the basement membrane.

At these interlocking sites, gap junctions can be formed, which allow the pericytes and neighboring cells to exchange ions and other small molecules.

[21] Aside from creating and remodeling blood vessels, pericytes have been found to protect endothelial cells from death via apoptosis or cytotoxic elements.

When this hormone was mixed with cerebral endothelial cells as well as astrocytes, the pericytes grouped into structures that resembled capillaries.

[22] It has also been found that pericytes contribute to the survival of endothelial cells, as they secrete the protein Bcl-w during cellular crosstalk.

This barrier is composed of endothelial cells and ensures the protection and functionality of the brain and central nervous system.

[26][27] Loss or dysfunction of pericytes is also theorized to contribute to neurodegenerative diseases such as Alzheimer's,[28][29][30] Parkinson's and ALS[31] through breakdown of the blood-brain barrier.

For the retina, movies have been published[12] showing that pericytes constrict capillaries when their membrane potential is altered to cause calcium influx, and in the brain it has been reported that neuronal activity increases local blood flow by inducing pericytes to dilate capillaries before upstream arteriole dilation occurs.

[32] It appears that different signaling pathways regulate the constriction of capillaries by pericytes and of arterioles by smooth muscle cells.

In a study involving adult pericyte-deficient mice, cerebral blood flow was diminished with concurrent vascular regression due to loss of both endothelia and pericytes.

[35] Because of their crucial role in maintaining and regulating endothelial cell structure and blood flow, abnormalities in pericyte function are seen in many pathologies.

The clinical phases of hemangioma have physiological differences, correlated with immunophenotypic profiles by Takahashi et al. During the early proliferative phase (0–12 months) the tumors express proliferating cell nuclear antigen (pericytesna), vascular endothelial growth factor (VEGF), and type IV collagenase, the former two localized to both endothelium and pericytes, and the last to endothelium.

Treatment may involve surgical removal and radiation therapy, depending on the level of bone penetration and stage in the tumor's development.

Studies have found that pericytes are essential in diabetic individuals to protect the endothelial cells of retinal capillaries.

[39] Studies have found that pericyte loss in the adult and aging brain leads to the disruption of proper cerebral perfusion and maintenance of the blood–brain barrier, which causes neurodegeneration and neuroinflammation.

Immunohistochemical studies of human tissue from Alzheimer's disease and amyotrophic lateral sclerosis show pericyte loss and breakdown of the blood-brain barrier.

In conditions of stroke, pericytes constrict brain capillaries and then die, which may lead to a long-lasting decrease of blood flow and loss of blood–brain barrier function, increasing the death of nerve cells.

Through lineage tracking studies, these subtype of pericytes were followed after stroke, revealing that they contribute to the glial scar by differentiating into myofibroblasts and depositing extracellular matrix.

[51][52] The emerging evidence (as of 2019) suggests that neural microvascular pericytes, under instruction from resident glial cells, are reprogrammed into interneurons and enrich local neuronal microcircuits.