More than 20 human diseases involve the fibrillation of a specific protein/peptide which forms pathological deposits at various sites. Hereditary lysozyme amyloidosis is a systemic disorder which mostly affects liver, spleen and kidney. This conformational disorder is featured by lysozyme fibril formation. In vivo lysozyme fibrillation was simulated under in vitro conditions using a strong denaturant GdHCl at 3 M concentration. Sharp decline in the ANS fluorescence intensity compared to the partially unfolded states, almost 20-fold increase in ThT fluorescence intensity, increase in absorbance at 450 nm suggesting turbidity, negative ellipticity peak in the far-UVCD at 217 nm, red shift of 50 nm compared to the native state in Congo red assay and appearance of a network of long rope-like fibrils in transmission electron microscope (TEM) analysis suggested HEWL fibrillation. Anti-fibrillation potency of baicalein against the preformed fibrils of HEWL was investigated following ThT assay in which there was a dose-dependent decrease in ThT fluorescence intensity compared to the fibrillar state of HEWL with the maximum effect observed at 150-μM baicalein concentration, loss of negative ellipticity peak in the far-UVCD region, dip in the Rayleigh scattering intensity and absorbance at 350 and 450 nm, respectively, together with a reduction in the density of fibrillar structure in TEM imaging. Thus, it could be suggested that baicalein could prove to be a positive therapeutics for hereditary human lysozyme amyloidosis.
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http://dx.doi.org/10.1080/07391102.2015.1108232 | DOI Listing |
Langmuir
January 2025
Department of Chemistry, Indian Institute of Technology Bombay, Powai, Mumbai 400076, India.
It is crucial to comprehend protein misfolding and aggregation in the domains of biomedicine, pharmaceuticals, and proteins. Amyloid fibrils are formed when proteins misfold and assemble, resulting in the debilitating illness known as "amyloidosis". This work investigates lysozyme fibrillation with pluronics (F68 and F127).
View Article and Find Full Text PDFSpectrochim Acta A Mol Biomol Spectrosc
February 2025
Department of Chemical Engineering and Biotechnology, Tatung University, Taipei 104, Taiwan. Electronic address:
There are currently over forty degenerative diseases that are correlated with abnormal accumulation of peptide/protein aggregates in the human body, such as Alzheimer's disease. Due to their unique physiochemical properties (e.g.
View Article and Find Full Text PDFNat Commun
November 2024
Institute of Protein Biochemistry, Ulm University, Ulm, Germany.
Systemic ALys amyloidosis is a debilitating protein misfolding disease that arises from the formation of amyloid fibrils from C-type lysozyme. We here present a 2.8 Å cryo-electron microscopy structure of an amyloid fibril, which was isolated from the abdominal fat tissue of a patient who expressed the D87G variant of human lysozyme.
View Article and Find Full Text PDFInt J Biol Macromol
November 2024
Laboratory of Structural Dynamics, Stability and Folding of Proteins, Institute of Cytology of the Russian Academy of Sciences, 4 Tikhoretsky ave., 194064 St. Petersburg, Russia. Electronic address:
Biosensors (Basel)
August 2024
Department of Biotechnology and Bioinformatics, Korea University, Sejong 30019, Republic of Korea.
Quantifying the formation and decomposition of amyloid is a crucial issue in the development of new drugs and therapies for treating amyloidosis. The current technologies for grasping amyloid formation and decomposition include fluorescence analysis using thioflavin-T, secondary structure analysis using circular dichroism, and image analysis using atomic force microscopy or transmission electron microscopy. These technologies typically require spectroscopic devices or expensive nanoscale imaging equipment and involve lengthy analysis, which limits the rapid screening of amyloid-degrading drugs.
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