scholarly journals Programmed cell death recruits macrophages into the developing mouse cochlea

2021 ◽  
Author(s):  
Vikrant Borse ◽  
Tejbeer Kaur ◽  
Ashley Hinton ◽  
Kevin Ohlemiller ◽  
Mark E. Warchol
Keyword(s):  
Cell Death ◽  
Thyroid Hormone ◽  
Programmed Cell Death ◽  
Critical Role ◽  
Large Population ◽  
Developmental Time ◽  
Macrophage Recruitment ◽  
Time Period ◽  
Developmental Cell Death

AbstractProgrammed cell death (PCD) plays a critical role in the development and maturation of the cochlea. Significant remodeling occurs among cells of the greater epithelial ridge (GER) of Kölliker’s organ, leading to tissue regression and formation of the inner sulcus. In mice, this event normally occurs between postnatal days 5-15 (P5-15) and is regulated by thyroid hormone (T3). During this developmental time period, the cochlea also contains a large population of macrophages. Macrophages are frequently involved in the phagocytic clearance of dead cells, both during development and after injury, but the role of macrophages in the developing cochlea is unknown. This study examined the link between developmental cell death in the GER and the recruitment of macrophages into this region. Cell death in the basal GER begins at P5 and enhanced numbers of macrophages were observed at P7. This pattern of macrophage recruitment was unchanged in mice that were genetically deficient for CX3CR1, the receptor for fractalkine (a known macrophage chemoattractant). We found that injection of T3 at P0 and P1 caused GER cell death to begin at P3, and this premature PCD was accompanied by earlier recruitment of macrophages. We further found that depletion of macrophages from the developing cochlea (using CX3CR1DTR/+ mice and treatment with the CSF1R antagonist BLZ945) had no effects on the pattern of GER regression. Together, these findings suggest that macrophages are recruited into the GER region after initiation of developmental PCD, but that they are not essential for GER regression during cochlear remodeling.

scholarly journals Programmed Cell Death Recruits Macrophages Into the Developing Mouse Cochlea

2021 ◽  
Vol 9 ◽  
Author(s):  
Vikrant Borse ◽  
Tejbeer Kaur ◽  
Ashley Hinton ◽  
Kevin Ohlemiller ◽  
Mark E. Warchol
Keyword(s):  
Cell Death ◽  
Thyroid Hormone ◽  
Programmed Cell Death ◽  
Critical Role ◽  
Large Population ◽  
Developmental Time ◽  
Macrophage Recruitment ◽  
Time Period ◽  
Developmental Cell Death

Programmed cell death (PCD) plays a critical role in the development and maturation of the cochlea. Significant remodeling occurs among cells of the greater epithelial ridge (GER) of Kölliker’s organ, leading to tissue regression and formation of the inner sulcus. In mice, this event normally occurs between postnatal days 5–15 (P5-15) and is regulated by thyroid hormone (T3). During this developmental time period, the cochlea also contains a large population of macrophages. Macrophages are frequently involved in the phagocytic clearance of dead cells, both during development and after injury, but the role of macrophages in the developing cochlea is unknown. This study examined the link between developmental cell death in the GER and the recruitment of macrophages into this region. Cell death in the basal GER begins at P5 and enhanced numbers of macrophages were observed at P7. This pattern of macrophage recruitment was unchanged in mice that were genetically deficient for CX3CR1, the receptor for fractalkine (a known macrophage chemoattractant). We found that injection of T3 at P0 and P1 caused GER cell death to begin at P3, and this premature PCD was accompanied by earlier recruitment of macrophages. We further found that depletion of macrophages from the developing cochlea (using CX3CR1DTR/+ mice and treatment with the CSF1R antagonist BLZ945) had no effect on the pattern of GER regression. Together, these findings suggest that macrophages are recruited into the GER region after initiation of developmental PCD, but that they are not essential for GER regression during cochlear remodeling.

scholarly journals The Function, Regulation and Mechanism of Programmed Cell Death of Macrophages in Atherosclerosis

2022 ◽  
Vol 9 ◽  
Author(s):  
Chang Liu ◽  
Zecheng Jiang ◽  
Zhongjie Pan ◽  
Liang Yang
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Cells ◽  
Critical Role ◽  
Inflammatory Cells ◽  
Cerebrovascular Diseases ◽  
Atherosclerotic Plaques ◽  
Whole Process ◽  
Programmed Death

Atherosclerosis is a chronic progressive inflammatory vascular disease, which is an important pathological basis for inducing a variety of cardio-cerebrovascular diseases. As a kind of inflammatory cells, macrophages are the most abundant immune cells in atherosclerotic plaques and participate in the whole process of atherosclerosis and are the most abundant immune cells in atherosclerotic plaques. Recent studies have shown that programmed cell death plays a critical role in the progression of many diseases. At present, it is generally believed that the programmed death of macrophages can affect the development and stability of atherosclerotic vulnerable plaques, and the intervention of macrophage death may become the target of atherosclerotic therapy. This article reviews the role of macrophage programmed cell death in the progression of atherosclerosis and the latest therapeutic strategies targeting macrophage death within plaques.

The role of programmed cell death ligand-1/ programmed cell death-1 (PD-L1/PD-1) in HPV-induced cervical cancer and potential for their use in blockade therapy

2020 ◽  
Vol 27 ◽  
Author(s):  
Lifang Zhang ◽  
Yu Zhao ◽  
Quanmei Tu ◽  
Xiangyang Xue ◽  
Xueqiong Zhu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Escape ◽  
Hypoxia Inducible Factor ◽  
Hpv Infection ◽  
Advanced Cervical Cancer ◽  
Cervical Carcinogenesis ◽  
Programmed Cell Death 1

Background: Cervical cancer induced by infection with human papillomavirus (HPV) remains a leading cause of mortality for women worldwide although preventive vaccines and early diagnosis have reduced morbidity and mortality. Advanced cervical cancer can only be treated with either chemotherapy or radiotherapy but outcomes are poor. The median survival for advanced cervical cancer patients is only 16.8 months. Methods: We undertook a structural search of peer-reviewed published studies based on 1). Characteristics of programmed cell death ligand-1/programmed cell death-1(PD-L1/PD-1) expression in cervical cancer and upstream regulatory signals of PD-L1/PD-1 expression, 2). The role of the PD-L1/PD-1 axis in cervical carcinogenesis induced by HPV infection and 3). Whether the PD-L1/PD-1 axis has emerged as a potential target for cervical cancer therapies. Results: One hundred and twenty-six published papers were included in the review, demonstrating that expression of PD-L1/PD-1 is associated with HPV-caused cancer, especially with HPV 16 and 18 which account for approximately 70% of cervical cancer cases. HPV E5/E6/E7 oncogenes activate multiple signaling pathways including PI3K/AKT, MAPK, hypoxia-inducible factor 1α, STAT3/NF-kB and MicroRNAs, which regulate PD-L1/PD-1 axis to promote HPV-induced cervical carcinogenesis. The PD-L1/PD-1 axis plays a crucial role in immune escape of cervical cancer through inhibition of host immune response. creating an "immune-privileged" site for initial viral infection and subsequent adaptive immune resistance, which provides a rationale for therapeutic blockade of this axis in HPV-positive cancers. Currently, Phase I/II clinical trials evaluating the effects of PD-L1/PD-1 targeted therapies are in progress for cervical carcinoma, which provide an important opportunity for the application of anti-PD-L1/anti-PD-1 antibodies in cervical cancer treatment. Conclusion: Recent research developments have led to an entirely new class of drugs using antibodies against the PD-L1/PD-1 thus promoting the body’s immune system to fight the cancer. The expression and roles of the PD-L1/ PD-1 axis in the progression of cervical cancer provide great potential for using PD-L1/PD-1 antibodies as a targeted cancer therapy.

scholarly journals Ozone-Induced Cell Death in Tobacco Cultivar Bel W3 Plants. The Role of Programmed Cell Death in Lesion Formation

2003 ◽  
Vol 133 (3) ◽  
pp. 1122-1134 ◽  
Author(s):  
Stefania Pasqualini ◽  
Claudia Piccioni ◽  
Lara Reale ◽  
Luisa Ederli ◽  
Guido Della Torre ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Lesion Formation ◽  
Tobacco Cultivar

scholarly journals The role of reactive oxygen species and nitric oxide in programmed cell death associated with self-incompatibility

2015 ◽  
Vol 66 (10) ◽  
pp. 2869-2876 ◽  
Author(s):  
Irene Serrano ◽  
María C. Romero-Puertas ◽  
Luisa M. Sandalio ◽  
Adela Olmedilla
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Self Incompatibility

scholarly journals The role of B7 family molecules in hematologic malignancy

Blood ◽  
2013 ◽  
Vol 121 (5) ◽  
pp. 734-744 ◽  
Author(s):  
Paul Greaves ◽  
John G. Gribben
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Responses ◽  
Hematologic Malignancy ◽  
Surface Proteins ◽  
Cell Responses ◽  
Inducible Costimulator ◽  
Programmed Cell Death 1 ◽  
B7 Family

AbstractThe B7 family consists of structurally related, cell-surface proteins that regulate immune responses by delivering costimulatory or coinhibitory signals through their ligands. Eight family members have been identified to date including CD80 (B7-1), CD86 (B7-2), CD274 (programmed cell death-1 ligand [PD-L1]), CD273 (programmed cell death-2 ligand [PD-L2]), CD275 (inducible costimulator ligand [ICOS-L]), CD276 (B7-H3), B7-H4, and B7-H6. B7 ligands are expressed on both lymphoid and nonlymphoid tissues. The importance of the B7 family in regulating immune responses is clear from their demonstrated role in the development of immunodeficiency and autoimmune diseases. Manipulation of the signals delivered by B7 ligands shows great potential in the treatment of cancers including leukemias and lymphomas and in regulating allogeneic T-cell responses after stem cell transplantation.

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