No Abstract Available.
Calmodulin* ; Cell Death* ; Humans* ; Retinoblastoma*

Dying cells interact with living cells and release molecules that can signal to immune system. Based on the morphology of the dying cells, there are three types of cell death, which are apoptotic cell death (Type I), autophagic cell death (Type II) and necrotic cell death (Type III). The immune response is different according to the pathway of cell death as apoptosis or necrosis regulates immune response via caspase activation or cytokine secretion, respectively. Here, we discuss the different modes of cell death and the nature of the immune response elicited by the released molecules from the cell death.
Apoptosis ; Autophagy ; Cell Death ; Immune System ; Necrosis

Age-related rotator cuff tendon degeneration is related to tenofibroblast apoptosis. Anthocyanins reduce oxidative stress-induced apoptotic cell death in tenofibroblasts. The current study investigated the presence of cell protective effects in cyanidin and delphinidin, the most common aglycon forms of anthocyanins. We determined whether these anthocyanidins have antiapoptotic and antinecrotic effects in tenofibroblasts exposed to H₂O₂, and evaluated their biomolecular mechanisms. Both cyanidin and delphinidin inhibited H₂O₂-induced apoptosis in a dose-dependent manner. However, at concentrations of 100 μg/ml or greater, delphinidin showed cytotoxicity against tenofibroblasts and a decreased antinecrotic effect. Cyanidin and delphinidin both showed inhibitory effects on the H₂O₂-induced increase in intracellular ROS formation and the activation of ERK1/2 and JNK. In conclusion, both cyanidin and delphinidin have cytoprotective effects on cultured tenofibroblasts exposed to H₂O₂. These results suggest that cyanidin and delphinidin are both beneficial for the treatment of oxidative stress-mediated tenofibroblast cell death, but their working concentrations are different.
Anthocyanins ; Apoptosis ; Cell Death ; Rotator Cuff ; Tendons

BACKGROUND: The pathogenesis of psoriasis remains uncertain. It is known that a variety of factors take a role in its pathogenesis. One of them is the alteration of keratinocytes differentiation. The terminal differentiation of keratinocytes includes the process of the synthesis of proteins such as involucrin, filaggrin, loricrin and cornifin, and produce keratohyaline granules and a structure termed cornified cell envelope finally. And the terminal differentiation of keratinocytes is known as a process of apoptosis, programmed cell death. OBJECTIVE: In this study, we tried to clarify the pathogenetic mechanisms of psoriasis by comparing the expression patterns of several proteins(involucrin, loricrin, filaggrin) associated with keratinocyte differentiation and of bcl-2 protein, known as inhibitor of apoptosis, between lesional and non-lesional psoriatic skin. RESULTS: The results were summarized as follows, firstly early expression of involucrin in lower epidermis, secondly no or reduced expression of filaggrin and loricrin in upper epidermis and lastly no expression of bcl-2 in basal layer of psoriatic skin. CONCLUSION: This study clarified that the accelerated terminal differentiation, the shortening of cell-cycle of keratinocytes, and the increased turnover of keratinocytes may be involved in the pathogenetic role of psoriasis.
Apoptosis ; Cell Death ; Epidermis ; Keratinocytes ; Psoriasis* ; Skin

Animals ; Apoptosis ; Cell Death ; Humans ; Necrosis

Cell Death ; Hepatocytes ; cytology ; pathology ; Humans

Immunogenic Cell Death ; Prognosis ; Immunotherapy ; Neoplasms

Eosinophilia is common feature of many disorders, including allergic diseases. There are many factors that influence the production, migration, survival and death of the eosinophil. Apoptosis is the most common form of physiological cell death and a necessary process to maintain but limit cell numbers in humans and other species. It has been directly demonstrated that eosinophil apoptosis is delayed in allergic inflammatory sites, and that this mechanism contributes to the expansion of eosinophil numbers within tissues. Among the proteins known to influence hematopoiesis and survival, expression of the cytokine interleukin-5 appears to be uniquely important and specific for eosinophils. In contrast, eosinophil death can result from withdrawal of survival factors, but also by activation of pro-apoptotic pathways via death factors. Recent observations suggest a role for cell surface death receptors and mitochondria in facilitating eosinophil apoptosis, although the mechanisms that trigger each of these death pathways remain incompletely delineated. Ultimately, the control of eosinophil apoptosis may someday become another therapeutic strategy for treating allergic diseases and other eosinophil-associated disorders.
Apoptosis ; Cell Count ; Cell Death ; Eosinophilia ; Eosinophils ; Hematopoiesis ; Humans ; Interleukin-5 ; Mitochondria ; Proteins ; Receptors, Death Domain

Eosinophilia is common feature of many disorders, including allergic diseases. There are many factors that influence the production, migration, survival and death of the eosinophil. Apoptosis is the most common form of physiological cell death and a necessary process to maintain but limit cell numbers in humans and other species. It has been directly demonstrated that eosinophil apoptosis is delayed in allergic inflammatory sites, and that this mechanism contributes to the expansion of eosinophil numbers within tissues. Among the proteins known to influence hematopoiesis and survival, expression of the cytokine interleukin-5 appears to be uniquely important and specific for eosinophils. In contrast, eosinophil death can result from withdrawal of survival factors, but also by activation of pro-apoptotic pathways via death factors. Recent observations suggest a role for cell surface death receptors and mitochondria in facilitating eosinophil apoptosis, although the mechanisms that trigger each of these death pathways remain incompletely delineated. Ultimately, the control of eosinophil apoptosis may someday become another therapeutic strategy for treating allergic diseases and other eosinophil-associated disorders.
Apoptosis ; Cell Count ; Cell Death ; Eosinophilia ; Eosinophils ; Hematopoiesis ; Humans ; Interleukin-5 ; Mitochondria ; Proteins ; Receptors, Death Domain

Acute kidney injury (AKI) refers to a clinical syndrome in which renal function declines rapidly in a short period of time caused by various pathological factors. During the development of AKI, renal tubules with the functions of reabsorption and excretion are prone to cell death due to external pathological stimuli, which is an important cause of impaired renal function. In recent years, a variety of new cell death pathways have been gradually recognized. Researchers have now found that regulated cell death (RCD), such as necroptosis, pyroptosis and ferroptosis, are important regulatory mechanisms of AKI. This article will summarize the research advances of various types of RCD involved in the process of AKI, aiming to deepen the understanding of AKI and provide innovative thoughts for the clinical treatment of AKI.
Acute Kidney Injury/metabolism* ; Cell Death ; Humans ; Kidney/metabolism* ; Necroptosis ; Necrosis/pathology* ; Regulated Cell Death