Barbara Hissa

By Barbara Hissa and Luciana O. Andrade

Lysosomes are acidic organelles that are not only involved in degradation processes but also participated in other cellular functions, such as specialized secretion and plasma membrane (PM) resealing. When the PM is ruptured, Ca2+ flows from the extracellular milieu toward the cytoplasm potentially triggering cell death. In order to escape from the apoptotic route, cells developed an elegant mechanism in which lysosomes are recruited to the sites of injuries in a Ca2+-dependent fashion. Lysosomes, fuse with the PM releasing their enzymatic content. Acid sphingomyelinase (ASM), one of the secreted enzymes, cleaves sphingomyelin into ceramide, inducing compensatory endocytosis and internalization of the membrane-damaged site. Trypanosoma cruzi, the etiological agent of Chagas disease, relies heavily on lysosomes to successfully invade mammalian cells. By mechanically injuring the host PM, T. cruzi evokes lysosome exocytosis, and subsequently, compensatory endocytosis. The latter drives the parasite into the host cell, where it can replicate. This early association with lysosomes prevents T. cruzi evasion from the host cells allowing colonization of host intracellular milieu. This review chapter will summarize the main contributions in the field exploring the crosstalk between PM repair and T. cruzi invasion and how the understanding of these mechanisms evolved throughout the years.

Part of the book: Lysosomes

By Barbara Hissa and Bruno Pontes

Atherosclerosis is a chronic inflammatory process that initiates with accumulation of apolipoprotein B containing lipoproteins (LPs) in the subendothelium (intima), especially in areas where the laminar flow is disturbed. LP retention triggers an inflammatory response leading to activation of endothelial and vascular smooth muscle cells that culminates with recruitment of leukocytes. Atherosclerosis is the leading cause of vascular disease worldwide being its major clinical manifestations ischemic heart disease, ischemic stroke, and peripheral arterial disease. Even though a lot has been done to unravel the role of turbulent flow and mechanotransduction for atherosclerosis development, little is known about the role of plasma membrane (PM) cholesterol in this process. This chapter is going to be focused on exploring what has been done so far to decipher the role of PM cholesterol in regulating actin architecture, cellular mechanical properties, and cellular contractility in muscle and nonmuscle cells.

Part of the book: Cholesterol