Introduction: This study aimed to determine the number of macrophages and apoptotic cells and perform annexin-A1 detection in patients with leishmaniasis.
Methods: Patients with Leishmania infection were admitted to Júlio Müller University Hospital.
Results: The number of apoptotic cells was higher in the exudative granulomatous reaction. The exudative cellular reaction displayed higher levels of annexin-A1 detection in macrophages and apoptotic cells. The correlation between annexin-A1 detection in apoptotic cells and macrophages was observed in exudative necrotic reaction and exudative necrotic-granulomatous reaction.
Conclusions: Our data demonstrate the relevance of annexin-A1 in the regulation of apoptosis and phagocytosis in leishmaniasis.
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http://dx.doi.org/10.1590/0037-8682-0756-2020 | DOI Listing |
Alzheimers Dement
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Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: The Neurovascular Unit is a multicellular structure of the CNS known to become dysfunctional in Alzheimer's Disease (AD) and cerebral amyloid angiopathy. Amyloidosis disrupts the function of cerebrovascular endothelial cells (cECs) via extrinsic and intrinsic apoptosis, and induction of blood brain barrier (BBB) permeability. Findings in our lab demonstrated that pan-Carbonic Anhydrase inhibitors (CAi's) prevent mitochondria-mediated apoptotic mechanisms in cECs.
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January 2023
Center for Computational Molecular Biology, Brown University, Providence, RI, USA.
Cellular senescence (CS) is a state of irreversible cell cycle arrest, and the accumulation of senescent cells contributes to age-associated organismal decline. The detrimental effects of CS are due to the senescence-associated secretory phenotype (SASP), an array of signaling molecules and growth factors secreted by senescent cells that contribute to the sterile inflammation associated with aging tissues. Recent studies, both in vivo and in vitro, have highlighted the heterogeneous nature of the senescence phenotype.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, China.
FAT atypical cadherin 1 (), which encodes an atypical cadherin-coding protein, has a high mutation rate and is commonly regarded as a tumor suppressor gene in head and neck squamous cell carcinoma (HNSCC). Nonetheless, the potential regulatory mechanisms by which FAT1 influences the progression of HNSCC remain unresolved. In this context, we reported that FAT1 was downregulated in tumor tissues/cells compared with normal tissues/cells and that it was correlated with the clinicopathological features and prognosis of HNSCC.
View Article and Find Full Text PDFJ Cancer
January 2025
Department of Pharmacology, The Yancheng Clinical College of Xuzhou Medical University, The First people's Hospital of Yancheng, Yancheng, China.
Longikaurin A (LK-A), a naturally occurring ent-kaurane diterpenoid, has been identified as a promising anti-cancer agent. This study aims to elucidate the anti-tumorigenic effects of LK-A on oral squamous cell carcinoma (OSCC) cells and to unravel its underlying mechanisms. assays, including CCK-8 and EdU, were performed to assess cell viability and proliferation.
View Article and Find Full Text PDFBiomed Rep
March 2025
Department of Biology, Xavier University of Louisiana, New Orleans, LA 70125, USA.
As a putative lung specific oncogene, the transducin-like enhancer of split 1 (TLE1) corepressor drives an anti-apoptotic and pro-epithelial-mesenchymal transition (EMT) gene transcriptional programs in human lung adenocarcinoma (LUAD) cells, thereby promoting anoikis resistance and tumor aggressiveness. Through its survival- and EMT-promoting gene regulatory programs, TLE1 may impact drug sensitivity and resistance in lung cancer cells. In the present study, a novel function of TLE1 was uncovered as an inhibitor of the antitumor effects of the epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) gefitinib in the human LUAD cell line A549, which exhibits moderate sensitivity to EGFR-TKI.
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