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Abstract Aging is a complex biological process often characterized by increased vulnerability to disease, infection, and death. This increased vulnerability is mechanistically linked to a progressive and functional decline of the immune system. In humans, aged T cells lose their ability to effectively surveil complex microenvironments, thereby decreasing their capacity to clear infections, eradicate diseases, and maintain physiological homeostasis.
Abstract Estradiol (E2), a sex steroid hormone molecule, plays a key role in regulating the actin and shape dynamics of cells in a multitude of normal and pathophysiological conditions. While cytoskeletal rearrangements, membrane dynamics, and cellular protrusions are intimately involved in cell motility and invasiveness, little is known about the impact of E2 on these processes in estrogen-dependent epithelial cells.
1. Introduction The blood-brain barrier (BBB) is key to central nervous system health. The BBB is composed of brain microvascular endothelial cells (BMECs) lining the cerebral vessels, along with a host of supporting neural cells, such as pericytes, astrocytes, and glial cells. The BBB structure is responsible for separating the brain tissue from the contents of the brain’s blood supply [].
Cell motion is necessary for many physiological phenomena, including reproduction, development, wound healing, and the immune response. Cell motion is also involved in many pathological processes, including cancer and cardiovascular disease. Over the past decades, we have learned that cells have a variety of mechanisms for movement at their disposal.
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