Despite the effectiveness in controlling the progression of brain tumors, cranial irradiation often causes neuropsychological deficits in cancer survivors. Inflammation is considered a major cause of tissue injury from irradiation. The caspase-1 activation complexes (inflammasomes) can facilitate caspase-1 and IL-1β processing, which amplifies the inflammatory response. In the present study we examined whether caspase-1 activation contributes to irradiation-induced damage to neural stem and progenitor cells (NSPCs). We found that X-ray irradiation induced activation of caspase-1 in NSPCs in vitro and in vivo. Next, using a caspase-1 inhibitor (Ac-YVAD-CMK) to block caspase-1 activation in vitro and in vivo, we further demonstrated that X-ray irradiation may inhibit proliferation, induce senescence of NSPCs through caspase-1 activation. Together, our results suggest that caspase-1 activation is involved in irradiation-induced damage to NSPCs.
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http://dx.doi.org/10.1016/j.neulet.2014.11.028 | DOI Listing |
Biochim Biophys Acta Mol Basis Dis
January 2025
Department of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital of Hainan Medical University, No. 48 Baishuitang Road, Haikou City 570100, Hainan Province, China. Electronic address:
Background: Programmed cell death protein 5 (PDCD5) is involved in apoptosis and is regarded as a tumor suppressor in various tumors. However, its role and underlying molecular mechanisms in hepatocellular carcinoma (HCC) remain unclear.
Methods: PDCD5-overexpressing cell and xenograft tumor models were developed.
Life Sci
January 2025
School of Life Sciences, Anhui University, Hefei, Anhui, China; Key Laboratory of Human Microenvironment and Precision Medicine of Anhui Higher Education Institutes, Anhui University, Hefei 230601, Anhui, China; Anhui Province Joint Construction Discipline Key Laboratory of Nanobody Technology, Hefei, China; Anhui Healcurer Heath Biotech Co., Ltd. - Anhui University Joint Postgraduate Training Base of Anhui Province, Hefei, China. Electronic address:
Aflatoxin B1 (AFB1) is a prevalent contaminant in food and feed matrices, known for its hepatotoxic effects. Its metabolic breakdown generates reactive oxygen species (ROS), leading to oxidative stress and subsequent liver damage. Mitigating oxidative stress is, therefore, essential for ameliorating the hepatocellular damage and systemic toxicity caused by AFB1.
View Article and Find Full Text PDFExp Neurol
January 2025
Department of Clinical Laboratory Medicine, Zhuzhou Kind Cardiovascular Disease Hospital, Hunan Province, China. Electronic address:
Parkinson's disease is the second most common neurodegenerative disease, characterized by substantial loss of dopaminergic (DA) neurons, the formation of Lewy bodies (LBs) in the substantia nigra, and pronounced neuroinflammation. The nucleotide-binding domain like leucine-rich repeat- and pyrin domain-containing protein 3 (NLRP3) inflammasome is one of the pattern recognition receptors (PRRs) that function as intracellular sensors in response to both pathogenic microbes and sterile triggers associated with Parkinson's disease. These triggers include reactive oxygen species (ROS), misfolding protein aggregation, and potassium ion (K) efflux.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2025
Department of Biological Sciences, College of Liberal Arts and Sciences, Wayne State University, Detroit, MI 48202.
The mammalian Hippo kinases, MST1 and MST2, regulate organ development and suppress tumor formation by balancing cell proliferation and death. In macrophages, inflammasomes detect molecular patterns from invading pathogens or damaged host cells and trigger programmed cell death. In addition to lytic pyroptosis, the signatures associated with apoptosis are induced by inflammasome activation, but how the inflammasomes coordinate different cell death processes remains unclear.
View Article and Find Full Text PDFInflammation
January 2025
Department of Nephrology, the First Affiliated Hospital of Bengbu Medical University, No. 287, Changhuai Road, Longzihu District, Bengbu, 233000, Anhui Province, China.
Primary membranous nephropathy (PMN) is a prevalent renal disorder characterized by immune-mediated damage to the glomerular basement membrane, with recent studies highlighting the significant role of pyroptosis in its progression. In this study, we investigate the molecular mechanisms underlying PMN, focusing on the role of Tumor necrosis factor receptor-associated factor 6 (TRAF6) in promoting disease advancement. Specifically, we examine how TRAF6 facilitates PMN progression by inducing the ubiquitination of Transforming growth factor-beta-activated kinase 1 (TAK1), which in turn activates the Gasdermin D (GSDMD)/Caspase-1 axis, leading to podocyte pyroptosis.
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