We have previously shown that long-term treatment of primary cultured astrocytes with TGF beta 1 induces morphological changes accompanied by increases in actin and GFAP synthesis, and a profound rearrangement of the cytoskeleton. The present report describes the short-term reorganization of actin filaments induced by TGF beta 1 in rat cerebellum cultured astrocytes and in an astrocytic cell line. TGF beta 1 caused the appearance of new actin and vinculin organizations, without protein synthesis. This cytoskeletal rearrangement was followed by altered cell-cell interactions. All these changes induced by TGF beta 1 were different and slower than those induced by serum, PDGF, and endothelin. TGF beta 1 induced the appearance of lamellipodia, organelles found at the cell front of motile cells in low-density cultures of immortalized astrocytes. These results indicate that the changes in the astrocyte cytoskeleton induced by TGF beta 1 are probably associated with cell movement. The events promoted by TGF beta 1 might help to clarify its action in the brain during embryogenesis and in tissue repair.
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http://dx.doi.org/10.1002/glia.440130405 | DOI Listing |
BMC Pediatr
January 2025
Department of Orthodontics, University Hospital Bonn, Medical Faculty, Welschnonnenstr. 17, 53111, Bonn, Germany.
Background: Children with non-syndromic cleft lip with or without palate (CL ± P) may present alterations in dental development. The purpose of this cross-sectional study was to compare the dental age (DA) between children with and without CL ± P, and whether single nucleotide polymorphisms (SNPs) in genes encoding growth factors are associated with DA variations.
Methods: Children aged between 5 and 14 years with and without CL ± P were recruited to participate in this study.
BMC Pregnancy Childbirth
January 2025
Obstetrics and Gynecology Center, Department of Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510280, China.
Background: Preeclampsia, characterized by hypertension and proteinuria during pregnancy, poses significant risks to both mother and fetus. The complement system's aberrant activation, notably the C3AR1, is important to the pathogenesis of preeclampsia, although the precise mechanisms are not fully understood.
Materials And Methods: Utilizing the Comparative Toxicogenomics Database (CTD) and Molecular Signatures Database (MSigDB), we identified complement system targets associated with preeclampsia and environmental pollutants.
J Adv Res
January 2025
Department of Biotechnology, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou 510006, China; Guangdong Provincial Key Laboratory of Advanced Drug Delivery, Guangdong Provincial Engineering Center of Topical Precise Drug Delivery System, Guangdong Pharmaceutical University, Guangzhou 510006, China. Electronic address:
Introduction: Although it is believed that chronic inflammatory and degenerative diseases of the central nervous system are mediated by autoimmune Th17 cells, the underlying mechanisms remain largely unexplored. Recent studies and our research have revealed that Sp3 was blocked in multiple sclerosis (MS) patients and experimental autoimmune encephalomyelitis (EAE). However, it remained unclear why it is silent and how it regulates Th17 cell differentiation in MS.
View Article and Find Full Text PDFBiochim 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.
Pharmacol Res
January 2025
Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai 200241, China. Electronic address:
Gastric cancer remains a significant global health burden, characterized by regional variations in incidence and poor survival prospects in advanced stages. Natural killer (NK) cells play a crucial role in the body's anti-cancer defense, and chimeric antigen receptor (CAR)-NK cell therapy is gaining attention as a cutting-edge and promising treatment method. This study aims to tackle the challenge of TGF-β-mediated tumor immune evasion within the immunosuppressive tumor microenvironment by designing a novel chimeric cytokine receptor TRII/21R, which consists of extracellular domains of TGF-β receptor II (TRII) and transmembrane and intracellular domains of IL-21 receptor (21R) and can convert the immunosuppressive signal from TGF-β in the tumor microenvironment (TME) into an NK cell activation signal through the IL-21R-STAT3 pathway.
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