Investigating the capacity of pericytes to differentiate under inflammatory conditions.

Scar formation is an important part of the process of tissue repair after an injury. However, it can sometimes turn into pathological fibrosis, which can lead to tissue destruction and organ failure. Fibrosis is caused by chronic inflammation, oxidative stress, and ageing. Unfortunately, there are currently no effective treatments for organ fibrosis, which has a negative impact on the quality of life of patients. Dr Jill Johnson's research group has identified pericytes as the primary cause of fibrosis. Pericytes are a type of mesenchymal progenitor cell that supports capillaries throughout the body and is particularly important in maintaining healthy tissue structure. Pericytes are associated with tissue fibrosis in the lung, liver, and kidney. Recent studies have shown that pericytes contribute to fibrosis by moving away from local blood vessels, migrating to the site of inflammation, and transforming into scar-forming myofibroblasts. However, it is currently unknown how chronic inflammation affects the differentiation capacity of pericytes. Trilineage differentiation is the process by which multipotent stem cells give rise to three different lineages of specialized cells: ectoderm, mesoderm, and endoderm. Inflammation can have a significant impact on trilineage differentiation, affecting both the normal development and regeneration of tissues. Understanding the impact of inflammation on trilineage differentiation is essential for developing therapeutic strategies for conditions associated with abnormal tissue development or regeneration. It highlights the intricate relationship between inflammation, stem cell biology, and tissue homeostasis. The main objective of our investigations is to identify the mechanisms that trigger tissue fibrosis, or scar formation by examining the function of pericytes, a type of tissue-resident progenitor cell, and focusing primarily on the regulation of pericyte migration and interactions with other cells at sites of inflammation.